Composition of crystalloids.
\r\n\tIn sum, the book presents a reflective analysis of the pedagogical hubs for a changing world, considering the most fundamental areas of the current contingencies in education.
",isbn:"978-1-83968-793-8",printIsbn:"978-1-83968-792-1",pdfIsbn:"978-1-83968-794-5",doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!1,hash:"b01f9136149277b7e4cbc1e52bce78ec",bookSignature:"Dr. María Jose Hernandez-Serrano",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/10229.jpg",keywords:"Teacher Digital Competences, Flipped Learning, Online Resources Design, Neuroscientific Literacy (Myths), Emotions and Learning, Multisensory Stimulation, Citizen Skills, Violence Prevention, Moral Development, Universal Design for Learning, Sensitizing on Diversity, Supportive Strategies",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:null,numberOfDimensionsCitations:null,numberOfTotalCitations:null,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"September 14th 2020",dateEndSecondStepPublish:"October 12th 2020",dateEndThirdStepPublish:"December 11th 2020",dateEndFourthStepPublish:"March 1st 2021",dateEndFifthStepPublish:"April 30th 2021",remainingDaysToSecondStep:"3 months",secondStepPassed:!0,currentStepOfPublishingProcess:4,editedByType:null,kuFlag:!1,biosketch:"Dr. Phil. Maria Jose Hernandez Serrano is a tenured lecturer in the Department of Theory and History of Education at the University of Salamanca, where she currently teaches on Teacher Education. She graduated in Social Education (2000) and Psycho-Pedagogy (2003) at the University of Salamanca. Then, she obtained her European Ph.D. in Education and Training in Virtual Environments by research with the University of Manchester, UK (2009).",coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"187893",title:"Dr.",name:"María Jose",middleName:null,surname:"Hernandez-Serrano",slug:"maria-jose-hernandez-serrano",fullName:"María Jose Hernandez-Serrano",profilePictureURL:"https://mts.intechopen.com/storage/users/187893/images/system/187893.jpg",biography:"DPhil Maria Jose Hernandez Serrano is a tenured Lecturer in the Department of Theory and History of Education at the University of Salamanca (Spain), where she currently teaches on Teacher Education. She graduated in Social Education (2000) and Psycho-Pedagogy (2003) at the University of Salamanca. Then, she obtained her European Ph.D. on Education and Training in Virtual Environments by research with the University of Manchester, UK (2009). She obtained a Visiting Scholar Postdoctoral Grant (of the British Academy, UK) at the Oxford Internet Institute of the University of Oxford (2011) and was granted with a postdoctoral research (in 2021) at London Birbeck University.\n \nShe is author of more than 20 research papers, and more than 35 book chapters (H Index 10). She is interested in the study of the educational process and the analysis of cognitive and affective processes in the context of neuroeducation and neurotechnologies, along with the study of social contingencies affecting the educational institutions and requiring new skills for educators.\n\nHer publications are mainly of the educational process mediated by technologies and digital competences. Currently, her new research interests are: the transdisciplinary application of the brain-based research to the educational context and virtual environments, and the neuropedagogical implications of the technologies on the development of the brain in younger students. Also, she is interested in the promotion of creative and critical uses of digital technologies, the emerging uses of social media and transmedia, and the informal learning through technologies.\n\nShe is a member of several research Networks and Scientific Committees in international journals on Educational Technologies and Educommunication, and collaborates as a reviewer in several prestigious journals (see public profile in Publons).\n\nUntil March 2010 she was in charge of the Adult University of Salamanca, by coordinating teaching activities of more than a thousand adult students. She currently is, since 2014, the Secretary of the Department of Theory and History of Education. Since 2015 she collaborates with the Council Educational Program by training teachers and families in the translation of advances from educational neuroscience.",institutionString:"University of Salamanca",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"0",totalChapterViews:"0",totalEditedBooks:"0",institution:{name:"University of Salamanca",institutionURL:null,country:{name:"Spain"}}}],coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"23",title:"Social Sciences",slug:"social-sciences"}],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. From chapter submission and review to approval and revision, copyediting and design, until final publication, I work closely with authors and editors to ensure a simple and easy publishing process. I maintain constant and effective communication with authors, editors and reviewers, which allows for a level of personal support that enables contributors to fully commit and concentrate on the chapters they are writing, editing, or reviewing. I assist authors in the preparation of their full chapter submissions and track important deadlines and ensure they are met. I help to coordinate internal processes such as linguistic review, and monitor the technical aspects of the process. As an ASM I am also involved in the acquisition of editors. Whether that be identifying an exceptional author and proposing an editorship collaboration, or contacting researchers who would like the opportunity to work with IntechOpen, I establish and help manage author and editor acquisition and contact."}},relatedBooks:[{type:"book",id:"6942",title:"Global Social Work",subtitle:"Cutting Edge Issues and Critical Reflections",isOpenForSubmission:!1,hash:"222c8a66edfc7a4a6537af7565bcb3de",slug:"global-social-work-cutting-edge-issues-and-critical-reflections",bookSignature:"Bala Raju Nikku",coverURL:"https://cdn.intechopen.com/books/images_new/6942.jpg",editedByType:"Edited by",editors:[{id:"263576",title:"Dr.",name:"Bala",surname:"Nikku",slug:"bala-nikku",fullName:"Bala Nikku"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"1591",title:"Infrared Spectroscopy",subtitle:"Materials Science, Engineering and Technology",isOpenForSubmission:!1,hash:"99b4b7b71a8caeb693ed762b40b017f4",slug:"infrared-spectroscopy-materials-science-engineering-and-technology",bookSignature:"Theophile Theophanides",coverURL:"https://cdn.intechopen.com/books/images_new/1591.jpg",editedByType:"Edited by",editors:[{id:"37194",title:"Dr.",name:"Theophanides",surname:"Theophile",slug:"theophanides-theophile",fullName:"Theophanides Theophile"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3092",title:"Anopheles mosquitoes",subtitle:"New insights into malaria vectors",isOpenForSubmission:!1,hash:"c9e622485316d5e296288bf24d2b0d64",slug:"anopheles-mosquitoes-new-insights-into-malaria-vectors",bookSignature:"Sylvie Manguin",coverURL:"https://cdn.intechopen.com/books/images_new/3092.jpg",editedByType:"Edited by",editors:[{id:"50017",title:"Prof.",name:"Sylvie",surname:"Manguin",slug:"sylvie-manguin",fullName:"Sylvie Manguin"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3161",title:"Frontiers in Guided Wave Optics and Optoelectronics",subtitle:null,isOpenForSubmission:!1,hash:"deb44e9c99f82bbce1083abea743146c",slug:"frontiers-in-guided-wave-optics-and-optoelectronics",bookSignature:"Bishnu Pal",coverURL:"https://cdn.intechopen.com/books/images_new/3161.jpg",editedByType:"Edited by",editors:[{id:"4782",title:"Prof.",name:"Bishnu",surname:"Pal",slug:"bishnu-pal",fullName:"Bishnu Pal"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"72",title:"Ionic Liquids",subtitle:"Theory, Properties, New Approaches",isOpenForSubmission:!1,hash:"d94ffa3cfa10505e3b1d676d46fcd3f5",slug:"ionic-liquids-theory-properties-new-approaches",bookSignature:"Alexander Kokorin",coverURL:"https://cdn.intechopen.com/books/images_new/72.jpg",editedByType:"Edited by",editors:[{id:"19816",title:"Prof.",name:"Alexander",surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"1373",title:"Ionic Liquids",subtitle:"Applications and Perspectives",isOpenForSubmission:!1,hash:"5e9ae5ae9167cde4b344e499a792c41c",slug:"ionic-liquids-applications-and-perspectives",bookSignature:"Alexander Kokorin",coverURL:"https://cdn.intechopen.com/books/images_new/1373.jpg",editedByType:"Edited by",editors:[{id:"19816",title:"Prof.",name:"Alexander",surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"57",title:"Physics and Applications of Graphene",subtitle:"Experiments",isOpenForSubmission:!1,hash:"0e6622a71cf4f02f45bfdd5691e1189a",slug:"physics-and-applications-of-graphene-experiments",bookSignature:"Sergey Mikhailov",coverURL:"https://cdn.intechopen.com/books/images_new/57.jpg",editedByType:"Edited by",editors:[{id:"16042",title:"Dr.",name:"Sergey",surname:"Mikhailov",slug:"sergey-mikhailov",fullName:"Sergey Mikhailov"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"371",title:"Abiotic Stress in Plants",subtitle:"Mechanisms and Adaptations",isOpenForSubmission:!1,hash:"588466f487e307619849d72389178a74",slug:"abiotic-stress-in-plants-mechanisms-and-adaptations",bookSignature:"Arun Shanker and B. Venkateswarlu",coverURL:"https://cdn.intechopen.com/books/images_new/371.jpg",editedByType:"Edited by",editors:[{id:"58592",title:"Dr.",name:"Arun",surname:"Shanker",slug:"arun-shanker",fullName:"Arun Shanker"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"878",title:"Phytochemicals",subtitle:"A Global Perspective of Their Role in Nutrition and Health",isOpenForSubmission:!1,hash:"ec77671f63975ef2d16192897deb6835",slug:"phytochemicals-a-global-perspective-of-their-role-in-nutrition-and-health",bookSignature:"Venketeshwer Rao",coverURL:"https://cdn.intechopen.com/books/images_new/878.jpg",editedByType:"Edited by",editors:[{id:"82663",title:"Dr.",name:"Venketeshwer",surname:"Rao",slug:"venketeshwer-rao",fullName:"Venketeshwer Rao"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"4816",title:"Face Recognition",subtitle:null,isOpenForSubmission:!1,hash:"146063b5359146b7718ea86bad47c8eb",slug:"face_recognition",bookSignature:"Kresimir Delac and Mislav Grgic",coverURL:"https://cdn.intechopen.com/books/images_new/4816.jpg",editedByType:"Edited by",editors:[{id:"528",title:"Dr.",name:"Kresimir",surname:"Delac",slug:"kresimir-delac",fullName:"Kresimir Delac"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"62743",title:"Fluids and Sodium Imbalance: Clinical Implications",doi:"10.5772/intechopen.79121",slug:"fluids-and-sodium-imbalance-clinical-implications",body:'The serum sodium (sNa) concentration and thus serum osmolality (sOsm) are closely controlled by water homeostasis, which is mediated by thirst, arginine vasopressin, and the kidneys. A disruption in this delicate balance is manifested as an abnormality in the sNa concentration—hyponatremia or hypernatremia and/or hemodynamic instability.
Fluid administration is an integral part of the clinician’s armamentarium to manage a wide variety of clinical conditions, which range from mild dehydration to more life-threatening conditions like shock or trauma.
The goal of this review is to provide a concise discussion regarding fluids and sodium imbalance with an attempt to answer practical clinical questions on those areas. We focus in discussing basics physiological principles, and addressing the most common clinical challenges encountered by the practicing clinician.
The human body is composed of approximately 60% of water of which two-third are in the intracellular space and one-third in the extracellular space. The extracellular space is composed by the intravascular compartment (~8%), the interstitial compartment (~25%) and the transcellular compartment like cerebrospinal, pericardial fluid, which is very small [1, 2]. In the healthy individual, the extracellular fluid (ECF) and intracellular fluid (ICF) are in osmotic equilibrium, water moves from areas of greater solute concentration to establish equilibrium. Additionally, osmotically active substance shifts water from lower osmolarity to higher osmolarity areas. This is an important concept to understand when we administer intravenous fluids (IVF), as the distribution of fluids is based on the type of fluid administered.
There is a delicate and complicated transport system of water through cell membranes to maintain fluids and electrolyte balance. Sodium is the predominant cation in the extracellular compartment, which is electro-neutralized by chloride (Cl) and bicarbonate (HCO3) as anions. In the intracellular space, potassium (K) is the major intracellular cation that is neutralized by many organic and nonorganic anions. The differential distribution of Na and K is tightly regulated by the sodium pump (Na-K ATPase) [1, 2]. Most osmotically active Na and K are dissolved and are sourced mostly from food intake. The body’s ability to store sodium in tissues (bone, cartilage, connective tissue, etc.) prevents large fluctuations in the sNa levels despite erratic sodium intake [3, 4]. Most of the components in the intracellular compartment are too large to be able to cross membranes exerting little osmotic pressure.
Estimating the ECF volume based on sNa is highly prone to errors in clinical judgment. The volume in both, intracellular and extracellular fluids is primarily determined by the concentration of effective solutes that attract water by osmosis. Sodium and its attendant monovalent anions are the most prevalent effective solutes in ECF volume. The concentration of Na is determined by content of Na as well as volume of water. The primary tonicity receptor is located in the hypothalamic osmoreceptor, which is in charge to regulate the antidiuretic hormone (ADH) or vasopressin. The absence of ADH prevents aquaporin insertion on the luminal surfaces of collecting ducts in the nephrons forming hypotonic urine. The osmoreceptor is linked to both the thirst center and the vasopressin release center via nerve connections. There is a genetic susceptibility to hyponatremia linked to the gene coding for TRPV4 [2, 5, 6, 7, 8]. Disease states releasing ectopic vasopressin or affecting vasopressin receptors will present with hyponatremia. Less prominent but important trigger for the regulation of vasopressin is large changes in effective arterial blood volume and blood pressure. Baroreceptors or stretch receptors in the carotid sinus and aortic arch are surrogates that detect changes in effective arterial blood volume. Nausea, pain, stress, and a number of other stimuli, including some drugs can also cause release of vasopressin [5].
Intravenous fluids are one of the commonest used medications in hospitalized patients. They can be broadly categorized as crystalloids and colloids. Crystalloid solutions contain water, electrolytes with or without glucose. Colloids solutions contain albumin, starch, or other blood products. Fluids can be isotonic, hypotonic, or hypertonic.
Crystalloids: Common crystalloid solutions include 0.9%-normal saline (NS), 0.45%NS, lactated Ringers solutions (LR), Plasma-Lyte, and dextrose in water. Solutions with electrolyte compositions closer to that of plasma are called balanced fluids. Composition of commonly used crystalloids can be seen in Table 1.
Solution | Na+ (mEq/L) | Cl− (mEq/L) | K+ (mEq/L) | Ca++ (mEq/L) | Lactate (mEq/L) | Glucose (g/l) | pH | Osmolarity (mOsm/L) |
---|---|---|---|---|---|---|---|---|
0.9%NS | 154 | 154 | 0 | 0 | 0 | 0 | pH 5.6 (4.5–7.0) | 308 |
0.45 saline (1/2 saline) | 77 | 77 | 0 | 0 | 0 | 0 | 5.0 (4.5–7) | 154 |
3% saline | 513 | 513 | 0 | 0 | 0 | 0 | 5.0 (4.5–7) | 1026 |
Ringers lactate | 130 | 109 | 4 | 3 | 28 | 0 | 6.5 | 272 |
Plasma-Lyte A* | 140 | 98 | 5 | 0 | 8 | 0 | 7.4 | 294 |
5% dextrose | 0 | 0 | 0 | 0 | 0 | 50 | 5.0 | 260 |
Composition of crystalloids.
Also contains magnesium 3 mEq/L, acetate 27 mEq/L, gluconate 23 mEq/L.
Colloids: They can be divided into natural or synthetic. Natural colloidal solutions include red blood cells, fresh frozen plasma, and human albumin. Indications for the use of packed red cell and fresh frozen plasma are specific; they provide oxygen carrying capacity and clotting factors, respectively. Discussion regarding the use of red blood cells and plasma is beyond the scope of this review.
Synthetic colloidal solutions include hetastarch and dextran. They are used for volume expansion and include hetastarch and dextran.
Colloids can be categorized as hypo oncotic (e.g., gelatins, 4 or 5% albumin) and hyper oncotic (e.g., dextrans, hydroxyethyl starches (HES), and 20 or 25% albumin) solutions. Table 2 describes the composition of commonly used colloids.
Fluid | Na+ (mEq/L) | Cl− (mEq/L) | Colloidal oncotic pressure (mm Hg) | Osmolarity (mOsm/L) |
---|---|---|---|---|
Albumin 5% | 130–160 | 130–160 | 20 | 308 |
Albumin 25% | 154 | 154 | 100 | 308 |
Hetastarch (6%)-NaCl | 154 | 154 | 30 | 310 |
Gelatins (gelofusine 4%) | 154 | 154 | 33 | 310 |
Dextran 70 + NaCl | 154 | 154 | 60 | 310 |
Composition of colloids.
Indications for the use of either crystalloids or colloids depend of the clinical condition. Volume expansion by fluids is dependent on their osmolality and oncotic pressure. Isotonic fluids will distribute equally to all fluid compartments without a significant shift across cellular or vascular planes. However, hypertonic solutions will move fluids from intracellular and interstitial space into the intravascular compartment, while hypotonic fluids will result in shift of fluids from intravascular space to interstitial and intracellular compartments. Volume expansion of the intravascular compartment with colloids depends on the oncotic pressure.
The most common clinical indications for fluid administration are:
Replacement of volume losses
Maintenance of fluids and electrolyte balance
Correction of electrolyte or acid-base disorders
Persistent hypoglycemia or hyperglycemia
Provision of a source of fuel (glucose)
Intravenous administration of medication.
Fluid resuscitation in critically ill patients in shock is the mainstay of therapy to maintain effective circulating blood volume. Timing of fluid resuscitation plays an important role in resuscitation and is based on the pathophysiology of shock [9, 10]. A long-standing controversy exists between proponents of colloids versus crystalloids for those patients. Supporters of crystalloids argue about risks of anaphylaxis, hemostasis impairment, and need for renal replacement therapy (RRT) with colloids as well as the potential to accumulate in tissues; whereas the colloid proponents argue with the risk of edema associated with crystalloids.
A recent Cochrane analysis concluded that there was no difference in mortality for hospitalized patients with trauma, burns, or following surgery when colloids were compared with crystalloids [11]. The use of HES may be associated with increased mortality; when they are compared to crystalloids, there was a higher incidence of adverse events and need for RRT [12, 13].
In the Crystalloid versus Hydroxyethyl Starch Trial (CHEST), involving 7000 adults in the ICU, the use of 6% HES (130/0.4), as compared with 0.9NS, was not associated with a significant difference in the rate of death at 90 days.
However, there was an increase in the rate of RRT and more adverse events in HES group [12]. The Colloids versus Crystalloids for the Resuscitation of the Critically Ill (CRISTAL) trial compared the effects of colloids versus crystalloids on mortality in patients presenting with hypovolemic shock [14]. There was no difference in mortality between the two groups at 28 days although 90-day mortality was lower in patients receiving colloids.
Low albumin levels are associated with all-cause mortality in both medical and surgical patients [15, 16]. Contrary to the belief that using albumin as a resuscitation fluid could improve mortality, a Cochrane review of 24 studies involving a total of 1419 patients, suggested that administration of albumin-containing fluids resulted in a 6% increase in the absolute risk of death when compared with use of crystalloid solutions [17]. This lead to the SAFE trial that showed similar outcomes between albumin and 0.9NS for resuscitation [18] No trial has consistently revealed superiority of albumin over crystalloids as resuscitative fluid.
In summary, there is no advantage of colloids versus crystalloids or vice versa. Considering the cost and adverse effect profile of colloids, crystalloids may be preferred over colloids. When colloids are used, care must be taken not to exceed recommended dose by regulatory agencies and avoid their use in patients with renal failure.
Normal saline is also referred as physiological or isotonic saline, neither of which is accurate. The sodium and chloride concentration of 154 mEq/L and the pH of 5.6 are certainly abnormal in “normal saline.” The strong ion difference (SID) is the difference between the positively- and negatively-charged strong ions in plasma. Disturbances that increase the SID increase the blood pH while disorders that decrease the SID lower the plasma pH. This may also occur with volume resuscitation with 0.9NS (>30 cc/kg/h) due to excessive chloride administration impairing bicarbonate resorption in the kidneys resulting in hyperchloremic metabolic acidosis [19]. Other potential effects of 0.9NS include renal vasoconstriction with worsening renal function [20], increased postoperative complications, coagulation abnormalities [21], and an increased risk of death [22, 23, 24].
Lactated ringer, Plasma-Lyte, and Normosol are often called ‘balanced fluids’ as their electrolyte contents are closer to human plasma. These balanced crystalloids are also nearly isotonic but have a chloride concentration less than 110 mEq/L and a SID close to plasma.
Several trials comparing 0.9NS to balanced fluids have reported multiple outcomes. Outcomes have ranged from renal failure to mortality. Among critically ill adults with sepsis, resuscitation with balanced fluids was associated with a lower risk of in-hospital mortality [25]. In a meta-analysis of 11 RCTs (8 trials in operation room and 3 in ICU) involving 2703 patients, the in-hospital mortality, occurrence of acute kidney injury (AKI), and need for RRT was not different between balanced solutions and 0.9NS, irrespective of the location of the patients [26]. In a before and after trial comparing 0.9NS with LR solution, use of saline was a safe, viable alternative to LR in the trauma population [27]. In ICU patients requiring crystalloid fluid therapy, the use of a buffered crystalloid compared with saline did not reduce the risk of AKI or mortality [28]. Data regarding best fluid for the perioperative period is still inconclusive [29]. In patients undergoing renal transplants, balanced electrolyte solutions were associated with less hyperchloremic metabolic acidosis compared to 0.9NS, but there were no difference in graft outcomes [30]. Among critically ill adults, the use of balanced crystalloids for IVF administration resulted in a lower rate of the composite outcome of death from any cause, new RRT or persistent renal dysfunction when compared to 0.9NS [31] Among noncritically ill adults treated with IVFs in the emergency department, there was no difference in hospital-free days between treatment with balanced crystalloids compared with saline [32].
Some myths about Ringers lactate:
Ringers lactate in renal failure: In a study comparing acid-base status in kidney transplant patients, LR compared with 0.9NS may lead to a lower serum potassium level and a lower risk of acidosis [33]. In a randomized, double-blind comparison of LR’s solution and 0.9%NS during renal transplantation, LR was associated with less hyperkalemia and acidosis compared with 0.9NS [34].
Ringers lactate in hepatic failure: LR is avoided in patients with hepatic failure with the fear of inducing or worsening lactic acidosis. However, lactate is given as sodium lactate, which is a base rather than an acid. There are no data describing LR causing worse outcomes compared to saline in patients with hepatic dysfunction.
In summary, 0.9%NS is not superior to balanced fluids in volume resuscitation in both critically ill and noncritically ill patients, perioperative patients and posttrauma. Studies suggest that use of balanced crystalloids for IVF administration results in a lower rate of the composite outcome of death from any cause, new RRT, or persistent renal dysfunction than the use of 0.9%NS in critically ill patients. Balanced fluids are not harmful compared to 0.9%NS and seem to be the fluid of choice. However, caution is advised when balanced solutions are used in patients with renal failure and hyperkalemia. Normal saline is an ideal choice in patients with metabolic alkalosis and chloride deficits who are vomiting or have nasogastric tube to suction.
The classical indication for 3% saline is symptomatic severe hyponatremia. This is discussed in detail later in this chapter. Other indication for hypertonic saline is resuscitation in patients with traumatic brain injury (TBI). In patients with TBI, osmotic agents to reduce cerebral edema are recommended [35]. Common osmotic agents are mannitol and hypertonic saline. Hypertonic saline decreases intracranial pressure (ICP), improves microcirculation, and acts as anti-inflammatory [36]. A retrospective study comparing effectiveness of mannitol versus hypertonic saline revealed that hypertonic saline given in boluses may be more effective than mannitol in lowering ICP but no difference was found in short-term mortality [37]. A comparison of effects in coagulation function or increase in the risk of intracranial rebleeding in patients with moderate TBI when using 3% hypertonic saline versus 20% mannitol for the control of ICP showed no differences [38]. A comparison of pharmacologic therapeutic agents used for the reduction of intracranial pressure after traumatic brain injury concluded that hypertonic saline exhibits beneficial advantages compared with the other medications as a first-line treatment of intracranial hypertension in patients with severe TBI [39]. Complications of hypertonic saline use include hypernatremia, hyperchloremia, and renal failure. Mannitol and hypertonic saline in equiosmolar concentrations produced comparable effects on ICP reduction, brain relaxation, and systemic hemodynamic [40].
Hypertonic saline has been advocated in patients with volume loss after trauma, whereas TBI seems to be an indication to decrease cerebral edema, use of hypertonic saline in other situations is still unclear. In a meta-analysis, use of hypertonic saline showed no differences in clinical outcomes for hypotensive injured patients compared to isotonic fluid in the prehospital setting [41]. There is no evidence that hypertonic saline provides any additional benefit over isotonic crystalloid solutions for trauma resuscitation [42].
In summary, hypertonic saline can be used to decrease intra cranial pressure in patients with moderate to severe TBI. Care must be taken to avoid hypernatremia, hyperchloremia, and renal failure.
In severe sepsis and septic shock, early volume resuscitation is indicated to save lives [43, 44, 45]; however, the best choice of fluids is unclear.
In a multicenter ICU trial of patients with severe sepsis randomly assigned to either 6% HES 130/0.42 or ringers acetate, patients receiving 6% HES 130/0.42 had a significant increase in the rate of death at 90 days and need for RRT. Several meta-analyses have shown that albumin does not provide a mortality benefit or decrease the need for RRT in critically ill patients, including those with hypoalbuminemia and sepsis [46, 47, 48]. A recent trial comparing albumin in addition to crystalloids versus crystalloids alone did not confer survival benefit in patients with severe sepsis or septic shock [49].
The early 2000s saw a resurgence in the use of hypertonic saline for sepsis resuscitation. Small volume resuscitation with hypertonic saline was postulated to achieve hemodynamic normalization by recruitment of fluid from the intracellular space, limiting interstitial edema [50]. Additional advantages included improved microcirculatory flow and favorable immunomodulatory effects. Two clinical trials have investigated the use of hypertonic saline in adult septic patients and there was no mortality difference [51, 52].
In the risk-adjusted inverse probability weighting analyses including 60,734 adults admitted to 360 ICUs across the United States between January 2006 and December 2010, the hospital mortality was 17.7% in the balanced fluid group, 19.2% in the 0.9%NS plus balanced fluids plus colloid group, 20.2% in the 0.9NS group ,and 24.2% in the saline plus colloid group. Balanced crystalloids were consistently associated with lower mortality. The authors concluded that when compared with exclusive use of 0.9%NS during resuscitation, coadministration of balanced crystalloids is associated with lower in-hospital mortality and no difference in LOS or costs per day. When colloids are coadministered, LOS and costs per day are increased without improved survival [53].
In summary, balanced fluids may be preferred over 0.9%NS in the resuscitation of patients with severe sepsis or septic shock without renal/liver or potassium issues. Hypertonic saline and other colloids including albumin are likely of no benefit over crystalloids. Use of starch is associated with adverse effects including increased need for RRT.
Patients with diabetic ketoacidosis (DKA) present with high anion gap metabolic acidosis, dehydration, and fluid deficits. Caution is advised in use of 0.9%NS due to two reasons. First, cerebral edema is a risk factor for death in patients with DKA. When a saline bolus is administered, it will distribute initially in the plasma that reaches the blood-brain barrier before equilibrating with the extracellular compartment. This has the potential to increase the interstitial volume of the brain ECF compartment and leads to cerebral edema. Second, chloride load in 0.9%NS can trigger nonanion gap metabolic acidosis.
A large bolus of 0.9%NS should be given only in emergent situations. It is advised to limit the amount of sodium ions infused in the first 120 min of therapy to about 3 mmol/kg body weight.
In a multicenter retrospective analysis of adults admitted for DKA to the ICU, which received almost exclusively Plasma-Lyte or 0.9%NS infusion up to 12 h, patients with PL had faster initial resolution of metabolic acidosis and less hyperchloremia, with a transiently improved blood pressure profile and urine output [54].
In summary: caution should be used using 0.9%NS in DKA and it is prudent to limit its use. If continued fluid resuscitation is needed, choice of fluids should be based on sNa levels. In patients with eunatremia or hypernatremia 0.45%NS is preferred and should be infused at 4–14 ml/kg/h, 0.9%NS is preferred in hyponatremia patients [55, 56].
Maintenance fluid therapy is indicated in patients who are unable to eat for prolonged period of time in order to provide for fluids, electrolytes, and possibly some nutrition. The goal is to provide enough fluid and electrolytes to meet insensible losses and enable renal excretion of waste products. On an average, 2500 ml of water is ingested daily of which 60% is in form of fluids. Maintenance fluids should be a short-term measure since inappropriate therapy risks volume overload and electrolyte and acid-base disturbance. It is recommended to use 25–30 ml/kg/day water, 1 mmol/kg/day sodium, potassium, chloride, and 50–100 g/day glucose daily [57].
Higher insensible losses and hence higher maintenance of fluids needs to be considered in patients with ongoing losses, fever, burns, and third space losses especially in post-operative surgical patients. There is no evidence to use one kind of crystalloids over the other, hypotonic solutions should be avoided to avoid hyponatremia and avoidance of excessive sodium overload with 0.9%NS. Monitoring and avoidance of development of electrolyte imbalance is critical. Daily weights will prevent volume overload. Continuation of maintenance fluids should be critically reviewed in a daily bases.
An ideal resuscitative fluid should have an electrolyte composition close to plasma, should not accumulate in tissue, and must be completely metabolized. An ideal fluid does not exist and fluids should be treated as any other medication—indications, duration, effects, and adverse effects. Deciding which fluids are appropriate for each patient depends on the type of fluid lost and the body compartment(s) that require additional volume. It is advisable to consider patients comorbid conditions, acid-base and electrolyte status, and the indication for fluids before making a final selection. Timing of therapy is based on clinical context, delayed resuscitation is not only resuscitation denied but could have a detrimental effect.
Education of use of fluids to the health care providers, especially those who usually initiate care on hospital admission is paramount to improve outcomes and decrease morbidity and mortality.
Pearls:
Treat IVF like medications and consider risks, benefits, alternatives, and risks of alternatives.
In most instances, balanced solutions may be adequate.
Normal saline is probably the fluid of choice in patients with metabolic alkalosis due to vomiting or gastrointestinal losses with volume and chloride deficits.
In critically ill adults, the use of 0.9%NS for IVF administration results in a higher rate of the composite outcome of death from any cause, new RRT, or persistent renal dysfunction.
In patients with DKA, use of 0.9%NS should be restricted to 1–1.5 L unless a compelling indication.
Hypertonic saline or colloids are fluids of choice in TBI with cerebral edema.
Role of hypertonic saline in trauma other than TBI, severe sepsis, septic shock, and hemorrhagic shock is uncertain.
HES is a risk factor for renal injury and need for RRT.
If a synthetic colloid is chosen, do not exceed the manufacturer recommended maximal dose.
Use maintenance fluids only when indicated and review need daily.
Hyponatremia is a common laboratory abnormality; it is usually defined as a sNa of less than 136 mmol/L. The sNa cut offs to define hyponatremia varies from 125 to 135 mmol/L depending on different studies [58, 59].
Hyponatremia have been reported in 8% of the general population and in up to 60% of hospitalized patients [60]. Patients in ambulatory setting have a lower rate compared with hospital or skill nursing facility setting. Miller et al. reported an 11% incidence of hyponatremia in the ambulatory setting among elderly population with a median age of 78 years [61, 62].
The importance of hyponatremia is related not only to the absolute sNa value, but to the underlying conditions leading to it; it can be the tip of a serious condition. Severity of hyponatremia or its management can impact the patient’s outcomes. Hyponatremia is not a disease, but a manifestation of an underlying disorder. The main focus of the management of hyponatremia is to elucidate the etiology and correction of laboratory abnormalities when levels are life threatening [59, 63].
Two major international guidelines attempted to address best practices in the management of this condition. The United States guidelines were published in 2013, however, they did not include grade of evidence due to scarce clinical evidence and resorted to expert panel recommendations [64]. In 2014, the European guidelines were published and included quality of evidence grades [65, 66, 67]. Rather than the absolute value of the sNa levels, the acuity of development of hyponatremia and its correction are of prime importance because the rate of change in sNa levels is associated with mortality, morbidity, and LOS [68, 69]. Mortality associated with hyponatremia has been reported as high as 30% [69].
A summary of relevant publications addressing prevalence of hyponatremia can be seen in Table 3. The serum cut off values for sodium in all those studies was between 130 and 138 and most of the studies were randomized control studies [58, 59].
Reference | Frequency (%) | Sample size | Outcome |
---|---|---|---|
Ambulatory setting | |||
Hawkins et al. | 0.14 | 24,027 | NA |
Liamis et al. | 7.7 | 5179 | ↑ Mortality |
Gankam Kengne et al. | 6 | 3551 | ↑ Mortality |
Mohan et al. | 2.5 | 14,697 | NA |
Hospital | |||
Hawkins et al. | 42.6 | 43,249 | NA |
Hoorn et al. | 30 | 5437 | NA |
Wald et al. | 30 | 34,761 | ↑ Mortality |
Wakar et al. | 14.5 | 98,411 | ↑ Mortality |
Congestive heart failure | |||
Gheorghiade | 20 | 47,647 | ↑ Mortality |
Liver cirrhosis | |||
Angeli et al. | 49 | 997 | ↑ Mortality |
Dawas | 11 | 5152 | ↑ Mortality |
HIV infection | |||
Tang | 38 | 259 | ↑ Mortality |
Cusano et al. | 31 | 96 | ↑ Mortality |
Non-dialysis kidney failure | |||
Covesdy et al. | 13 | 655,493 | ↑ Mortality |
Pneumonia | |||
Zilberberg et al. | 8 | 7965 | ↑ Mortality |
Hyponatremia can be classified based in:
Severity: this is based only in the absolute level of sNa. Mild 130–135 mmol/L, moderate 125–130 mmol/L, and severe when sNA is lower than 125 mmol/L.
Time interval of development: acute-less than 48 h and chronic if more than 48 h. This information is occasionally difficult to obtain, but causes are usually different for acute and chronic hyponatremia.
Measured osmolarity: it is fundamental to differentiate between the true hypotonic state from the isotonic and hypertonic state. Isotonic hyponatremia is usually due to pseudohyponatremia secondary to high plasma concentrations of triglycerides or proteins [70]. Expected changes in sNa in hypertriglyceridemia (TG) can be calculated as TG × 0.0002 = decrease in sNa in mEq/L; for plasma proteins (PP), PP in gm/dl – 8 × 0.25 = decrease in sNa in mEq/L.
Commonest causes of hypertonic hyponatremia are hyperglycemia, administration of mannitol or other agents; the osmotic shift of water from ICF to ECF increases the total plasma volume diluting the sNa levels. Each increase in serum glucose levels by every 100 mg/dl after 150 mg/dl, decreases the sNa by approximately 1.6 mmol/L [71].
Volume status: hypovolemia, euvolemia, and hypervolemia [72]. This is the most common classification used in the United States [64]. However, this classification is intrinsically flawed as there are no reliable, readily available and highly sensitive clinical tools to differentiate volume status, especially to differentiate hypovolemia from euvolemia [73, 74, 75]. Euvolemia itself is considered to be a misnomer as loss of sodium cannot happen without loss of water [2]. Clinical assessment is more reliable in cases of hypervolemia [2].
Erroneous classification of patients into these categories can have detrimental outcomes [76].
Symptoms of hyponatremia are initially subtle, nonspecifics, and difficult to recognize. They mostly manifest as neurological changes, which ranges from altered personality, lethargy and confusion to seizures, coma and death in severe cases [2, 77]. Symptomatic differences between acute severe and chronic hyponatremia have been reported. Symptoms of acute severe hyponatremia include nausea, vomiting, headache, seizure, coma, respiratory failure, and death, which are manifestations of brain edema. In chronic hyponatremia, main symptoms are fatigue, gait and attention deficit, osteoporosis, and fractures. Nausea and vomiting are seen in both, acute severe and chronic hyponatremia [78, 79]. Older patients with comorbid conditions tend to develop symptoms of hyponatremia at an earlier onset than young healthier patients. Premenopausal women are prone for cerebral edema from acute hyponatremia, it is hypothesized that this could be secondary to the action of estrogen and progesterone inhibiting Na+K+-ATPase and decreasing solute expel from brain cells; if not recognized early, it will lead to neurological complications. The nonneurological manifestations are often due to the dysregulation in the volume status [5, 80].
The best approach to evaluate causes of hyponatremia is to first decide if we are dealing with acute versus chronic hyponatremia.
Acute hyponatremia: the underlying etiological mechanism primarily causes large input of water. Normal individuals with intact thirst center and mental function develop aversion to large volume water intake. Table 4 shows most common causes of acute hyponatremia.
Ingestion of large volume of water | Infusion of large volume of 5% dextrose | Infusion of large volume of hypotonic lavage fluid | Generation and retention of electrolyte-free water (“desalination”) |
---|---|---|---|
|
|
|
|
Causes of acute hyponatremia.
Chronic hyponatremia: slow onset of hyponatremia, usually more than 48 h. The underlying etiology is lower rate of water excretion and involves release of vasopressin. In some case, decreased volume of filtered solute and residual water permeability play a role [5]. Table 5 shows most common causes of chronic hyponatremia and Table 6 shows the most common laboratory findings in the most common causes of hypotonic hyponatremia.
Lower rate of water excretion due to low volume of distal delivery of filtrate | Lower rate of water excretion due to vasopressin actions |
---|---|
|
|
Volume status | Clinical conditions | Urine Osm | Urine Na | Serum uric acid | FENA |
---|---|---|---|---|---|
Hypovolemic (appropriate ADH response) | Extrarenal losses | Elevated | <10–20 | Elevated >4 | <1 |
Renal losses deficiency of mineralocorticoids | Elevated | >20 | Elevated | >1 | |
Hypervolemic (appropriate ADH response) | Heart failure, liver cirrhosis, nephrotic syndrome | Elevated | <20 | Low/normal | <1 |
Renal failure | Decreased | >20 | Variable | >1 | |
Euvolemia | Reset osmostat | Variable | |||
SIADH | Elevated >100–300 | >30–40 | Decreased <4 | >1 | |
Primary polydipsia | Decreased | Decreased | Low/normal | >1 | |
Hypothyroidism, deficiency of mineralocorticoids | Elevated | >20 | Low/normal | >1 |
Laboratory findings in most common causes of hypotonic hyponatremia.
Evaluation of hyponatremia still remains to some extent controversial and occasionally cumbersome.
In an attempt to avoid the pitfalls of volume evaluation recommended in the 2012 guidelines, the European guidelines were released in 2014. They prioritized the use of urine sodium (uNa) levels and urine osmolality (uOsm) over assessment of volume status [67]. Conditions leading to a false low or high uNa levels like low sodium diet or recent diuretic use and chronic kidney disease respectively were addressed [66, 81, 82].
Role of vasopressin and copeptin levels: measurement of vasopressin levels seems logical for the investigation of hyponatremia, but its unstable nature when not bound to plasma, low accuracy, and not readily available makes it use unsuitable. Moreover, uOsm is a readily available, accurate, and inexpensive surrogate [83]. Vasopressin is degraded into neurophysin and copeptin by enzymatic cleavage. Copeptin has been considered also a reasonable surrogate for vasopressin. Copeptin levels were reported to be increased in hypo and hypervolemic hyponatremia but not in syndrome of inappropriate secretion of antidiuretic hormone (SIADH). A ratio of serum copeptin to uNa with a cut off value of 30 pmol/mmol had an AUC of 0.88 in identifying hypovolemia from euvolemia [84].
Other biomarkers like apelin and midregional proatrial natriuretic peptide (MR-ProANP) have been evaluated in hyponatremia. Apelin counteract vasopressin in homeostasis. MR-ProANP increases to a larger extent in hypo or hypervolemic hyponatremia rather than in SIADH. The true diagnostic potential of these biomarkers are yet to be validated [85, 86, 87, 88].
Based on existing guidelines and trying to overcome limitations of clinical evaluation of volume status, we suggest the following steps when evaluating a patient with hyponatremia:
Measurement of serum osmolarity to differentiate between hypotonic hyponatremia from iso- and hypertonic.
Hypotonic hyponatremia: clinical evaluation of volume status. In general, identification of hypervolemia is more accurate than differentiating between euvolemic and hypovolemic state.
Measurement of urine osmolarity (uOsm) and urinary sodium (uNa). This is conjunction with sOsm and examination should narrow down the diagnosis. For example, a threshold of uOsm of >100 mOsm/kg predicts the action of ADH on the collecting tubules, which in case of hyponatremia is not the appropriate response. This together with elevated uNa >20–30 mmol/L strongly suggests the presence of SIADH [2].
Needs to consider the presence of more than one disorder leading to hyponatremia [89].
Management should ideally address correction of sNa levels as well as the underlying condition leading to it.
Delayed or unavailability of sOsm is one of the major limiting factors during evaluation of hyponatremia as addressed by the United States guidelines, potentially leading to misclassification of patients based on clinical assessment of volume status.
Some experts suggest that a limited work up including sOsm, uNa, uOsm, and infusion of isotonic saline 1–2 l over 24 h may be sufficient for an accurate diagnosis in most cases of hypotonic hyponatremia [2]. Increase in sNa after trial of volume expansion suggests hypovolemic hyponatremia. However, this can be also seen in SIADH [75, 90, 91, 92].
Volume expansion should be cautiously done in certain conditions like immediate post-operative period, where isotonic saline can worsen the hyponatremia by a process called desalination, as presence of vasopressin makes the urine hypertonic by water resorption [93]. In addition, patients with hypervolemic states like heart failure or liver cirrhosis could deteriorate with the additional fluid administration.
Figure 1 shows a flow diagram for initial evaluation of hyponatremia.
Algorithm for initial evaluation of hyponatremia. Based in the USA and European guidelines [64, 65, 66, 67].
Goal should ideally focus in the prevention of hyponatremia knowing its association with significant morbidity and mortality. There is no data available regarding the effects of treating asymptomatic mild to moderate hyponatremia [2, 94, 95].
Patients presenting with severe, acute, or chronic hyponatremia should be treated in a monitor setting as those patients are at risk for adverse outcomes [2]. Acute respiratory failure from damage of the respiratory center or noncardiogenic pulmonary edema has been reported [96, 97]. Identification of patients at higher risk for osmotic demyelination remains a challenge during treatment; risks factors for development of osmotic demyelination include presence hypokalemia, alcoholism, malnutrition, and liver disease [64, 98]. Table 7 shows basic management of patients presenting with hyponatremia and comparison of the two major existing guidelines.
Conditions | General agreement in guidelines | Disagreement between guidelines |
---|---|---|
Acute or symptomatic hyponatremia—less 48 h | Severe symptoms: bolus 3% NaCl: 100–150 ml over 10–20 min × 2–3 as needed | Minimal—just in amount of fluids 50 ml difference |
Moderate symptoms: continuous infusion 3% NaCl 0.5–2 ml/kg/h or bolus 3% NaCl: 100–150 ml over 20 min × 1 | ||
Chronic hyponatremia—more 48 h | ||
SIADH | First line: fluid restriction | None |
Second line: demeclocycline, urea, or vaptan | European guidelines do not recommend vaptans when sNa > 130 and recommend against when sNa > 125. Recommends against demeclocycline Suggest oral NaCl or loop diuretics | |
Hypovolemic hyponatremia | Isotonic saline or balanced crystalloid solution | Minimal/none |
Hypervolemic hyponatremia | Fluid restriction—500—1 L/day Vaptans | European guidelines recommend against vaptan |
Correction rates | Minimum-only USA guidelines: 4–8 mmol/L/day, 4–6 mmol/L/day in high risk of neurological complications | European guidelines have no minimum |
Limits: 10–12 mmol/L/day, 8 mmol/L/day in high risk patients | None | |
Management of overcorrection | Baseline sNa ≥ 120 mmol/L: probably unnecessary | European guidelines suggest to start once limit is exceeded |
Baseline sNa < 120 mmol/L: relower with electrolyte-free water or desmopressin after correction exceeds 6–8 mmol/L/day | Expert consultations recommended by European guidelines |
Management of hypotonic hyponatremia and comparison between existing guidelines.
Modified from [72].
Areas of concern with guidelines: caution must be excised when following guidelines. Areas of concern in the management of hyponatremia are:
There is no clear evidence regarding the 48 h cut off to differentiate between acute and chronic hyponatremia, neither to clearly differentiate risk for osmotic demyelination in those patients.
Clinically difficult to be certain regarding acuity of hyponatremia; in asymptomatic patients with hyponatremia, it could be assumed to be chronic.
Limited evidence regarding the best and safer correction rate. A lower correction rate of 6 mEq/L/24 h could be safer.
When to treat a patient with mild to moderate hyponatremia and none/minimal neurological symptoms remain a gray zone and depends on the clinical situation. Fluid restriction is the most common, cost effective, and safer modality of treatment [2, 72]. Fluid restriction of 500–1000 ml/day has been suggested and should be based in volume assessment. Urine Na to serum electrolyte ratio (uNa + urine K/sNa) >1 indicates antidiuretic phase and a ratio <1 suggests aquaretic phase. Fluid restrictions to less than 500 ml/day in antidiuretic phase and 1000 ml/day in aquaretic phase have been recommended; however, adherence is a problem [72].
Use of Vaptans. Vaptans are vasopressin type 2 receptor antagonist, present in the collecting duct and they induce excretion of hypotonic urine. Its use has been recommended in a subgroup of patients with hyponatremia secondary to excess vasopressin [99, 100]. There are many vaptans available including tolvaptan, satavaptan, lixivaptan, and conivaptan, which are been successful at increasing sNa and relieving symptoms in conditions like SIADH, congestive heart failure, and liver cirrhosis [101, 102, 103]. Sodium overcorrection is a concern and it was reported in 25% of 61 patients included in a study [103]. Side effects including liver injury, risk of overcorrection, and lack of long-term sodium improvement are some of limitations [101, 102, 104].
Demeclocycline and lithium have low quality evidence to support front line management of hyponatremia. Demeclocycline is thought to inhibit adenylate cyclase activity upon binding of vasopressin to its receptor in the collecting tubule. The adverse effects associated with the drugs make them less desirable for treatment [2, 105].
Complications of hyponatremia can be divided in those caused by hyponatremia per se and those caused by the treatment of hyponatremia. In general, worse outcomes are associated with sNa levels of less than 115 mEq/L and with faster rate of fall in sNa [2].
Complications of hyponatremia range from chronic debilitating symptoms like gait deficit and neuromuscular symptoms to a more severe and life-threatening presentation of brain edema. Chronic and mild-moderate hyponatremia have been associated with attention or gait deficits, increased risk of falls, and bone fractures. Bone is a reservoir for Na. Observational retrospective cross sectional and epidemiological surveys have established an association between chronic hyponatremia and osteoporosis and major osteoporotic fracture [106, 107, 108, 109, 110, 111].
Unfortunately, there is a lack of evidence to suggest that osteoporosis is reversed with correction of hyponatremia [2].
The brain which is contained in the hard skull is not able to accommodate any swelling or increase in brain volume. This is evident especially in patients who develop acute hyponatremia. Cerebral edema occurs when cells within the brain swell, when there is an increase in extracellular fluid volume in the brain or both. Brain cells swell when there is a large osmotic force favoring an intracellular shift of water, owing to a higher effective osmolality in brain cells than the effective osmolality in plasma in capillaries near the blood–brain barrier [112, 113, 114, 115]. The elevated intracranial pressure with the resultant acute cerebral edema can potentially lead to serious symptoms that ranges from seizures, coma to brain herniation causing irreversible midbrain damage and death [116, 117]. Incidence of fatal brain damage secondary to severe hyponatremia is unknown, majority of the cases have been reported during the perioperative period secondary to infusion of hypotonic fluids or self-water intoxication like marathon runners and psychiatric patients [118].
Most cases of hyponatremia in the ambulatory setting are mild. An sNa of less than 125 mmol/L was seen in 0.14% in Hawkin et al. study [60]. The Dallas heart study, a large prospective multiethnic cohort study of 3551 ambulatory individuals with median age of 43 year/age and from diverse ethnicity, found that mild hyponatremia (median 133 mmol/L) was significantly associated with increased risk of death [119]. A large cross sectional observational study by the National Health and Nutrition Examination Survey in the United States with 15,000 individuals demonstrated that hyponatremia was an independent risk for increased mortality across age, gender, and comorbid conditions. Overall prevalence was around 2%. They also showed that prevalence of hyponatremia increased with age and was more frequent among women than men [120].
Others studies looking at the association of hyponatremia with specific comorbid conditions like heart failure, HIV, pneumonia, renal failure among others, concluded that hyponatremia is an independent risk factor for mortality regardless the levels of sNa [58, 121, 122, 123, 124, 125, 126, 127, 128, 129]. Among patients presenting with acute pulmonary emboli, hyponatremia is common and several studies has shown to be an independent risk factor for increased short-term mortality. This result could be encountered as a variable in determining of pulmonary emboli severity and mortality [130, 131].
Among the hospitalized population, many studies have estimated the prevalence of hyponatremia from 8 to 40% [60, 69, 89, 132]. In Wald et al. study evaluating more than 50,000 patients, he established that irrespective of onset of hyponatremia-community, hospital aggravated or hospital acquired, all were associated with increased mortality, length of stay, and discharge to a facility; and this was independent of the underlying comorbid conditions. Mortality was increased among older patients. The operational definition for normal sNa in this study was 138–142 mEq/L. In patients with hospital acquired hyponatremia, the risk of mortality was 15 times higher among patients with first serum sodium level of 127 mEq/L or less [69]. A larger prospective study by Waiker and colleagues with approximately 100,000 individuals followed up to 5 years showed that irrespective of the severity of hyponatremia, presence of hyponatremia independently increased risk of dead with an odd ratio of 1.47, 1.32, and 1.33 at the time of admission, 1 and 5 year follow-up, respectively. It was more pronounced among patients admitted with cardiovascular disease, metastatic cancer, and those admitted for procedures related to the musculoskeletal system. They also showed that resolution of hyponatremia attenuated the increased risk of mortality [132].
There are no many studies evaluating outcomes of treatment of hyponatremia. Two studies evaluated the impact of treatment on mortality among patients with congestive heart failure and concluded that treatment confers no mortality benefit, however, there was symptomatic improvement and decreased length of stay [94, 95]. Other studies suggested that correction of mild hyponatremia could reverse attention and gait deficits [133, 134].
When hyponatremia develops over a slower rate, 24–48 h, the brain cells are able to adapt to expel enough of anions and organic solutes along with water to maintain its size. Rapid correction of hyponatremia can lead to inability to regain the organic solutes causing osmotic demyelination, a process still poorly understood [5].
Osmotic demyelination syndrome (ODS) and central pontine myelinolysis (CPM) are terms usually used interchangeably, but they represent separate, not well understood and highly feared complications of the treatment of hyponatremia. The effect of rapid correction of hyponatremia is termed as ODS and it is specific to the central nervous system and not always localized to the pontine region. Extrapontine myelinolysis is as frequent as CPM [135, 136]. Risk factors making patients more susceptible to the development of ODS include severity and chronicity of hyponatremia, the increment of sNa, the treatment used for sodium correction, concomitant hypokalemia, presence of liver disease and the nutritional status [98]. A small study of 33 patients showed that an increase in sNa to normal or hypernatremic levels in the first 48 h, a change in the sNa concentration of >25 mmol/L in the first 48 h, a hypoxic-anoxic episode, and an elevation of sNa to hypernatremic levels in patients with hepatic encephalopathy were associated with CMP. However, rate of correction was not associated with demyelination [118].
The clinical manifestations of ODS are variable depending on the location of demyelination. They range from pontine and bulbar symptoms such as dysarthria, dysphagia, and dystonia to more severe forms like locked-in state and coma [137]. In the past, prognosis of ODS and CMP was considered to be very poor; however, several studies have reported near complete neurological recovery. In addition, ODS/CMP are associated with other complications like aspiration pneumonia, urinary tract infection, deep venous thrombosis, and pulmonary embolism [137, 138, 139].
In the absence of an absolute threshold for the rate of correction, it is well accepted that the safest rate of correction of hyponatremia is 6–8 mEq/L/day. Brain demyelination has been reported over a range of rate of sNa correction of 8–12–18 mEq/L/day [2, 72]. Some investigators in small, nonrandomized studies suggest concomitant use of desmopressin and hypertonic saline for better control of the rate of sNa correction in hyponatremia [140, 141]. Experiments on rats have shown little success with the combination regimen of D5W and desmopressin for the treatment of overcorrection of hyponatremia [142, 143]. The role of urea for ODS have not been well studied.
A difference of the complexity of hyponatremia, the finding of hypernatremia invariably denotes hypertonic hyperosmolality and always causes cellular dehydration. It is usually defined as a sNa of more than 145 mmol/L. It can be a frequent finding in hospitalized patients or high risk patients with poor access to water like the elderly, infants, patients on mechanical ventilation, and patients with altered mental status. In the elderly, a physiologic decrease in the thirst mechanism have been reported; however, there can be a pathological decrease in free water intake as well [60].
In general, clinical manifestations of hypernatremia correlate with the severity of sodium abnormalities and are related to central nervous system dysfunction and ranges from weakness, confusion to seizure and coma. In addition, sign of hypovolemia and hemodynamic abnormalities can be found on examination.
The complications of hypernatremia vary from mild to life threatening [144]. Brain shrinkage induced by hypernatremia can cause vascular rupture, with cerebral bleeding, subarachnoid hemorrhage, and permanent neurologic damage or death.
Causes of hypernatremia can be loose classified in two: either net water losses due to gastrointestinal or renal etiologies or hypertonic solution administration [144, 145].
The focus of management is addressing the underlying cause leading to hypernatremia and the correction of serum sodium. Initial evaluation includes evaluation of vital signs. In hemodynamically unstable patients, administration of isotonic 0.9% normal saline or balance fluids is advised, irrespective of sNa. Goal in those patients is fluid resuscitation hemodynamic stabilization. Patient who are hemodynamically stable can be managed with oral or IVF replacement. The preferred route for fluid administration is the oral route or a feeding tube; otherwise IVF are required. Only hypotonic fluids are recommended, including pure water, 5% dextrose, and 0.2 or 0.45% sodium chloride. The more hypotonic the infusate, the lower the infusion rate required. An easy and efficient way to calculate this is by using Adrogue-Madias formula, which allows to calculate rate of infusate [144].
Correction rates: similar to management of hyponatremia, and to avoid sudden changes in tonicity, the target recommended fall in the sNa concentration is 8–10 mmol/L/day for patients with hypernatremia with a goal to reduce the sNa to 145 mmol/L [145, 146].
Pearls:
Serum sodium abnormalities are common and carry significant morbidity and mortality.
Evaluation of sodium abnormalities should focus in the underlying condition as well as management.
Following recommended algorithms for evaluation of hyponatremia is advised.
Evaluation of volume status in patients with sodium disorders can be a challenge.
Needs to keep in consideration the presence of more than one disorder.
Resuscitation of an unstable patient takes precedence over correction of sodium levels.
There is no rush to correct sNa levels, risk of overcorrection, or rapid increase in sNa can lead to serious complications.
We reviewed issues related to fluids and sodium disturbance and the clinical implications of these issues. The dysregulation of fluid and sodium homeostasis leads to many direct and indirect effects and carries significant morbidity and mortality in a wide variety of patients and clinical settings. Those range from mild cases of dehydration to more severe cases of patients in shock or with severe hypo- or hypernatremia.
Since the high prevalence of these disorders, clinicians in virtually every medical specialty will interact with patients requiring fluid administration and need for electrolyte evaluation and correction. Appropriate and timely administration of fluids and electrolyte correction with focus in avoidance of complications and improvement of outcomes is fundamental.
The authors have no conflict of interest.
ECF | extracellular fluid |
ICF | intracellular fluid |
IVF | intravenous fluids |
RRT | renal replacement therapy |
HES | hydroxyethyl starches |
SID | strong ion difference |
TBI | traumatic brain injury |
For the last decades, the demand for renewable energy has been increasing intensively due to the crude-oil crisis and the alert of global warming. Among the alternatives for fossil fuels to generate heat, biomass is an abundant neutral carbon source, of which its conversion to heat does not break the balance of the atmosphere’s air contents [1]. Combustion of biomass has been the most direct and simple process to produce energy. However, the traditional combustion of biomass, such as wood, charcoal, straw, husks, etc., often leads to the emission of smoke, dust, fumes, volatile compounds and toxic gases due to incomplete reactions and fine particles dragged out of the system by the flue gas [2]. Although several combustion methods were invented to increase efficiency and reduce emission of pollutants, such as fixed bed rocket type, and fluidized bed technology, the direct combustion of solid fuels is still one of the major causes of the industrial air pollutant in the world [3].
\nIn contrast, gasification of biomass can minimize the emission of pollutants. Syngas produced from gasification of biomass can be optionally purified before being combusted. Ultimately, the combustion of gaseous fuels inherently has higher efficiency than that of solid matters. That is because the oxidation of a solid object in oxygen/air is gradually happening from its outer surface into the inner layers, which can be described as a heterogeneous process, while a combustive gas like syngas can be burned at a very high mass transfer rate in a homogeneous process. A comparison is presented in Table 1.
\n\n | Combustion of syngas from gasification of biomass | \nDirect combustion of solid biomass | \n
---|---|---|
Type of reactions | \nHomogeneous | \nHeterogeneous | \n
Uniformity | \nVery high | \nNone | \n
Process nature | \nSimple | \nComplex | \n
Mass transfer rate | \nAlmost instant | \nSlow, depending on the solid surface – oxygen/air contact | \n
Combustion of syngas vs. combustion of solid biomass.
The gasification phenomenon of carbonaceous materials was possibly observed in the human history as very early as the invention of fire. Gasification was found as the ignition and combustion of smoke released from smoldering coal, wood, straw, grass, or other organic substances in the lack of oxygen. In 1792, the first industrial gasification system to generate electricity was reported [4]. Gasification is a thermal decomposition process of solid or liquid substances to syngas in the presence of gasification agents through a series of chemical reactions mentioned in the following sections. This technology can help converting variable low-energy-density fuels to combustive gases. It attracts significant interests in both academic and industrial fields. Figure 1 shows a very strong flame torch produced by gasification of oil-extracted cashew nut shell.
\nGasification of oil-extracted cashew nut shell at Laboratory of Biofuel and Biomass Research, Ho chi Minh City University of Technology (HCMUT).
Gasification is an advanced technology to convert biomass to syngas fuel under different atmospheres (oxygen/air, steam, H2, CO2). The product syngas can also be used as precursors to synthesize valuable chemicals via Fischer-Tropsch (F-T) reactions [5]. Table 2 highlights some key differences between gasification and direct combustion of biomass.
\n\n | Gasification of biomass | \nDirect combustion of biomass | \n
---|---|---|
Input feedstock | \nLow-energy-density and wet biomass is still feasible | \nThe biomass fuel must have acceptable moisture content and relatively flammable to guarantee a sustainable operation. | \n
Output flame | \nSmokeless, free of dust and toxic gases if the syngas is purified. | \nSmoky and dusty with fly ash. | \n
Impact to the heat exchangers’ surface | \nMinimized | \nSilica fume, dusty aerosol, and corrosive gases can shorten the lifetime of equipment. | \n
Applicability for internal combustion engines | \nYes | \nNo | \n
Equipment design complexity | \nComplex | \nSimple | \n
Heat receiver arrangement | \nMobile | \nFixed to the burner | \n
Side product | \nChar, ash (solids), tar, bio-oil, wood vinegar (liquids) | \nAsh | \n
A brief comparison between biomass gasification and combustion.
The combustion of a solid fuel is a thermal and oxidation decomposition with the involvement of oxygen in air. Generally, for biomass, it can be simply expressed as:
\nThis process can be observed with two visual phenomena: first, thermal decomposition on the outer surface of the solid phase to release volatile and combustive components, which join thermal reactions in the gas phase secondly, as the formation of flames [6]. Differing from direct combustion, gasification limits the process at the first step to produce syngas. Conventionally, oxygen/air is used as gasification agent in this case. However, other gasification agents also can be employed to enhance the conversion efficiency as presented followings.
\nIn this context, to simplify the theory, biomass can be formulated with its main general composition CaHbOc due to the much lower contents of other elements, such as N, S, P, and halogens. The involvement of inorganic compounds is not considered.
\nThe thermal decomposition of biomass in insufficient presence of oxygen/air, known as incomplete combustion, is the most conventional gasification. Logically, the whole process can be described below as rearranged from theory [7].
\nDrying: firstly, once entering the reactor, the biomass is dried due to heat.
\nCombustion: secondly, a part of the solid biomass, which was ignited and in contact with locally excess oxygen/air, is combusted to generate heat as the energy source for later reactions to occur.
\nPyrolysis: heat from the combustion zone is transferred via radiation, conduction, and convective hot streams to the surrounding biomass where oxygen/air is not sufficient or absent. Due to the heat, pyrolysis occurs to form CO2, CO, CH4, C2H4, H2O, char (C), and other organic solids and liquids as primary tar (2).
\nReduction: after the above two steps, hot reactants react in situ with the biomass and with each other via a series of reactions.
\nThe main weakness of gasification by oxygen/air is due to a large portion of inert nitrogen in the agent (79–80%), which makes the resulted syngas diluted. It can be roughly estimated that syngas from this type of gasification mainly contains around 30–60% of nitrogen and 10–15% of CO2 since its heating value is typically between 4 and 6 MJ/m3 (for comparison, HHV of H2 = 12.76 MJ/m3, CO = 12.63 MJ/m3, CH4 39.76 MJ/m3 and CH4 is commonly much less than CO and H2) [7, 8, 9]. Low quality syngas is the main disadvantage of this technique for applications which require high temperature and steady operation, such as internal combustion engine, metallurgy, and melting glass industries.
\nAir-based gasification processes are sensitive and complex, which are influenced by a number of factors, such as biomass composition and particle geometry, gasification agent composition and flow rate, equipment design, etc. Among these, the ratio of actual air-fuel ratio to the stoichiometric air-fuel ratio (ER) is used as a parameter to calculate and to simulate the process [10].
\nGasification ER is theoretically usually from 0.19 to 0.43, and a range of 0.25–0.29 was studied to be considered as the optimum ER in gasification of some popular biomass [11].
\nTo obtain more concentrated syngas, nitrogen must be limited from the gasification agent in air-based systems while sufficient oxygen is still guaranteed for combustion to generate heat [12]. This method does not change the nature of the gasification process since nitrogen is an inert gas not involved in the reactions. Several techniques were introduced to remove nitrogen, thus increase oxygen content in the input air stream, such as pressure swing adsorption (PSA) [13], temperature swing adsorption [14], carbon membranes [15], etc. Oxygen concentration in studies on gasification with oxygen- enriched air is found limited by less than 50%, and no study on 100% oxygen gasification, possibly because of a high risk of explosion [16, 17, 18].
\n\nFigure 2 shows the visual change in an air-based syngas flame (wood pellet as feedstock) when oxygen concentration in the gasifying agent increased from that of normal air to 30%. With normal air, the syngas flame is thinner with smoke, while oxygen-enriched air makes the flame stronger, thicker, and less smoke. The flame temperature was measured as 874 and 933°C, respectively.
\nExperimental gasification of wood pellet (a) showing the flame of syngas when using (b) normal air (21% vol. as O2) and (c) oxygen-enriched air (30% vol. as O2)
Water gas (3) and water gas shift (6) reactions are the reasons steam can be introduced to oxygen/air gasification or wet biomass is accepted, of which moisture is more tolerated than that in direct combustion. Higher generation yields of H2 and CO are obtained so the final syngas mixture gets higher heating value. However, these two reactions are endothermic while the vaporization enthalpy of water has a large value (at atmospheric pressure that is 40.65 kJ/mol) so saturated steam or water can make the pyrolysis zone lose heat, drop temperature, leading to lower conversion yield. Lower quantity becomes a contrast to higher quality of syngas formation in this case. Subsequently, the process even gets faded if sufficient heat is not guaranteed. To achieve both quantity and quality of syngas, heat should be redeemed by using superheated steam instead of saturated steam or water in wet biomass so that the gasification temperature is maintained above 750–800°C [19].
\nThe ratio of steam to carbon content of the biomass fuel (SCR) is used as a crucial operating parameter in biomass gasification with steam feeding [20]:
\nSteam flow rate (kg/s) to biomass (kg/s) ratio (S/B) is also used like SCR [21]. Steam feeding makes the ratio of hydrogen to carbon in the whole reaction mixture increase, which was found to yield more H2, and increase the heating value of the syngas, while tar content decreases significantly [22]. This technique is positively meaningful in biomass gasification because it does not only increase the quality of the syngas but also reduce tar-clogging problems to sustain the process.
\nNot many studies on gasification by hydrogen and carbon dioxide were found although these two agents are reactants in methanation (4) and Boudouard (7) reactions.
\nMethanation reaction can be increased when more H2 exists in the reaction zone of a gasifier. Since methanation is exothermic, hydrogen can be mixed with air in air-based gasification or can be used as the only gasification agents without slagging problems in the gasifiers like conventional oxygen/air gasification. Pure hydrogen gasification is expected to be able to run at lower temperature and milder conditions because less heat is generated from methanation reaction (ΔH = −87.5 kJ/mol) than from combustion step in air-based gasification [23], which may lead to the absence of oils and tars [24]. However, catalysts are needed because the reaction rates are very low [25]. Otherwise, hydrogen gasification should be carried out in high H2 pressure, which rises several safety concerns.
\nCO2 is a Boudouard reactant, as well as it can react with H2 in the mixture via reverse water gas shift reaction. Hot flue gas is a popular product in industry, which includes steam, CO2, and heat from direct combustion of fuel, thus can be considered as a gasification agent [26]. This technique is available if a combustion process is combined with gasification because air-based gasification already has its combustion zone. CO2 utilization and enhancement of CO formation can be the purposes of CO2-gasification [27].
\nThe reactions in gasification can proceed with higher yields and less energy input if appropriate catalysts are employed. Catalysts can facilitate the process by reducing slagging problems, by which in severe cases, gasifiers need to be shut down for maintenance. Together with slagging of low-melting-point inorganic compounds, tar and soot formation also interrupts the operation because matters can be vaporized at high temperature, then condense at cooler zones and clog the systems. Catalysis helps limit the formation of such undesired side-products or decompose them to workable substances by cracking reactions. The mechanism of tar catalytic cracking can be assumed as follows [28]:
Organic and hydrocarbon compounds are dissociated from the biomass and absorbed on the catalytic sites.
Catalytic dehydrogenation reactions happen.
Water is hydroxylated to OH radicals, which oxidize the hydrocarbon fragments.
Syngas, CH4, and lighter hydrocarbons are formed then.
In contrast, catalytic gasification has some disadvantages, such as material costs and fading catalyst performance over reaction time. Theoretically, catalysts can be recovered after the process. But in fact, they are easily poisoned and contaminated by variable products, which are formed from the complex interactions in gasification.
\nAlkali metal salts seem to be the earliest catalysts to be examined for gasification [29]. Alkali elements were studied to catalyze gasification of char and biomass, and they were proved to reduce the formation of tar and soot [30, 31]. The employment of catalysts is preferred for entrained-flow gasifiers, which will be discussed later [32].
\nNatural minerals, precious metal and synthetic catalysts are also studied for their application in biomass gasification, as well as coal and syngas conversion [33, 34, 35].
\nPlasma, which can be produced by an electric arc discharged to a gas, is a very hot and highly ionized gaseous mixture. The initial gas interacts with the electric arc to become dissociated into electrons and ions at temperatures often exceeding thousands of Celsius degree. When biomass and a non-oxidizing gasifying agent are fed into a plasma reactor, the gasification can proceed at high temperatures without combustion to generate heat as in conventional process. Therefore, plasma gasification can convert organic substances to syngas that preserve all its chemical and heat energy, while converts inorganic mineral ash to inert vitrified glass or slag. As a result, contamination and dilution of syngas are minimized and the process control is easy to yield expected syngas composition [36, 37].
\nMicrowave was also used to generate plasma in plasma gasification [38]. However, microwave plasma system is not easy to scale up for industrial purposes like electric arc type.
\nWith the principle of supplying intensive heat for endothermic reactions, plasma gasification was used to produce hydrogen with steam injection as discussed in Section 2.3 [20]. Carbon dioxide gasification was studied with a various biomass feedstock to show input plasma energy was lowest while syngas formation yield was highest [39]. Experimental results showed that steam or catalysts added to plasma gasification can significantly reduce the formation of tars [40].
\nGasification is a complicated process, which is influenced by many factors, among which equipment design plays a very important role. Popular types of gasifiers are listed and briefly discussed as bellows.
\nThere are three ways of arrangement for biomass and gasifying agents entering to react with each other in the reactors: updraft, downdraft, and cross draft as illustrated in Figure 2a–c.
Updraft gasifiers (Figure 3a): in this type of reactor, biomass is fed downward from the top and gasifying agents is fed upward from the bottom in a counter flow arrangement. Ash is collected at the bottom of the equipment with air-lock design. The biggest weakness of updraft gasifiers is the accumulation of tar, moisture, and soot on the top of the reactors, which becomes hard clogging blocks inside the equipment. Figure 4 is the actual photo of a very thick and hard layer of tar and soot attached to the inner wall on the top of an updraft biomass gasification reactor (the photos were taken at the Laboratory of Biofuel and Biomass Research, Ho Chi Minh City University of Technology, HCMUT). This counter flow process also makes syngas from updraft gasifiers carries much contamination. In contrast, the operation of updraft gasifiers is the easiest among the three types of fix-bed gasifiers above. Its design is also simple and available for multi-feed stock purpose.
Downdraft gasifiers (Figure 3b): a narrow throat at the combustion zone is the typical design of this type of equipment. Since syngas is obtained at the bottom of the reactor, biomass and gasifying agents move in a co-current direction and get in contact for combustion at the device throttle. The flow rate of the gasifying agent gets maximum at this position due to the decreasing cross-sectional area of the orifice. As a result of this structure, the combustion increased sharply at the throttle while the amount of feeding agents is still. Downdraft gasifiers have higher conversion yield than that of their updraft models [41]. Syngas from downdraft gasifiers have much less tar and incomplete decomposed substances because they have to pass the combustion zone before exit with the syngas. However, downdraft gasifiers cannot be scaled up easily due to difficulties in controlling the movement of solid fuels through the throttle. Another difficulty in designing and fabricating downdraft gasifiers is “bridging problems” for feedstock with low densities [42]. The downward flow of the solid fuel is dictated by gravity while the pyrolysis zone is right above the narrow throat. The melting and adhesivity of lignin in biomass, as well as the local condensation of volatile substances, also facilitate the formation of stiff domes above the device throat, blocking the coming feedstock. It was observed that a rice husk downdraft gasifier kept stop working within some minutes of operation due to this problem and it was not an easy job to remove the bridging dome of “melting” rice husk inside the equipment (Figure 5).
Crossdraft gasifiers (Figure 3c): as an intermediate between downdraft and updraft design, crossdraft gasifiers has the simplest design when biomass is fed from the top, gasifying agent from the rear side, and syngas is withdrawn from the other rear side of the reactor. Thanks to this arrangement, the pyrolysis zone is separated from reduction zone, where syngas is obtained, and between them is the combustion zone to reduce tar and soot. Bridging problem is not a concern in this case, and scaling up is feasible.
Fix-bed gasifier types. (a) Updraft gasifier. (b) Downdraft gasifier. (c) Crossdraft gasifier.
(a) an updraft gasifier converting rice husk to syngas, (b) the inside wall of the top opening is clogged with a thick layer of condensed tar and soot.
Fixing a downdraft gasifier after a bridging problem happened.
Fluidization is an advance technique for solid fuel combustion. It is also applied for gasification. Inert materials (sand, dolomite, crushed stone, etc.) are employed to hold fluidization. The gasifying agents enter the reactor from the bottom upward to the top at velocities of 1–3 m/s through the biomass + inert material bed. Gasification reactions occur inside the bed then the resulted gases drag the particle before going up like “bubbling”. This technique provides the mixture a uniformity for heat exchange. Cyclones are installed to collected solid particles and return them to the reactors. With high gasification efficiency, fluidized bed gasifiers are known for tar and char reduction [43].
\nThe operating temperature of fluidized-bed gasifiers is limited to the melting point of the inert medium. The gasifying agents also play a role as fluidization fluids so the input flow rate must be high enough. Therefore, gasification agents in fluidized bed gasifiers are usually rather than only oxygen/air, which need to be at a limited mass ratio to the biomass [44, 45].
\nEntrained flow gasifiers are applied for biomass with small particle sizes so that the specific contact area with gasifying agents is large enough for suitable reaction rate. Simply described as illustrated in Figure 6a, the solid and the gas agents are fed co-currently to the reactor in the same downward direction. The agent surrounds the solid particles and react to convert the biomass to syngas. At the end of the falling routine to the bottom of the reactor of the feed, only ash and slag are expected to be remained solid collected in cyclone systems while syngas is passing through. The operation is carried out at high temperature and in high pressure. The extremely turbulent flow of the aerosol mixture causes rapid conversion and allows high throughput [46].
\n(a) Entrained flow gasifier, (b) rotary drum gasifier.
To reach uniformity of the biomass during gasification without combustion (using gasifying agents rather than oxygen/air), mechanical mixing can be applied as rotary kiln type reactor (Figure 6b). In this rotating cylinder, biomass is well mixed in contact with gasifying agents. Differing from fluidized bed and entrained flow equipment, the gasifying agents’ flow rates can be at any value in rotary drum gasifiers.
\nGasification is a big subject in biomass and chemical engineering. Among the renewable technologies converting biomass to fuels and energy with environmental preservation concern, gasification is superior over combustion with variable feasible application. Gasification process includes many reactions, which make it complex and sensitive to many factors. The diversity in the thermochemistry of gasification gives researchers and engineers a big space for creativity in R&D. This context introduced some brief theory and technical discussion on gasification technology with a humble hope to contribute to that vision.
\nThis research was funded by Vietnam National University Ho Chi Minh City (VNU-HCM) under grant number B2018-20-02. We acknowledge the support of time and facilities from Ho Chi Minh University of Technology (HCMUT), VNU-HCMUT for this study. We also acknowledge the technical support and consultancy from Tin Thanh Group for Laboratory of Biofuel and Biomass Research in the last 5 years of this study.
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