Country | Developed countries* | |||||||||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
USA | UK | Australia | New Zealand | Italy | Slovenia | |||||||||||||||
Study | (2000) | (2000) | (2017) | (2000) | (2019) | |||||||||||||||
Sample size | 127 | 120 | 63 | 26 | 127 | 124 | 92 | 92 | 55 | 134 | ||||||||||
Scale used | 1–7 | 1–7 | 1–7 | 1–7 | 1–7 | 1–7 | 1–7** | 1–7** | 1–7 | 1–7 | ||||||||||
Mean | Rank | Mean | Rank | Mean | Rank | Mean | Rank | Mean | Rank | Mean | Rank | Mean | Rank | Mean | Rank | Mean | Rank | Mean | Rank | |
ABC/M** | NA | 3.54 | 6 | NA | NA | 4.02 | 3 | NA | 3.51 | 12 | 3.27 | 9 | NA | NA | ||||||
Attribute costing | 2.37 | 10 | NA | 1.91 | 10 | 1.71 | 15 | NA | 2.54 | 9 | 5.28 | 1 | NA | 4.03 | 11 | 3.60 | 9 | |||
LCC** | 2.73 | 9 | 2.73 | 10 | 2.60 | 8 | 2.21 | 12 | NA | 2.43 | 10 | 3.19 | 14 | 2.92 | 11 | 4.29 | 10 | 2.90 | 12 | |
Quality costing | 3.07 | 8 | 3.07 | 9 | 3.11 | 6 | 1.67 | 16 | NA | 3.46 | 5 | 4.31 | 7 | 4.12 | 4 | 4.60 | 8 | 4.31 | 2 | |
Strategic costing | 3.43 | 5 | NA | 3.72 | 5 | 3.33 | 7 | NA | 3.44 | 6 | 4.42 | 6 | NA | NA | 4.13 | 4 | ||||
Target costing | 3.19 | 6 | 3.19 | 7 | 2.90 | 7 | 2.00 | 14 | 4.16 | 2 | 3.16 | 7 | 3.84 | 9 | 3.62 | 6 | 4.92 | 5 | 3.64 | 8 |
VCC** | 3.15 | 7 | 3.15 | 8 | 2.60 | 8 | 2.63 | 9 | 2.40 | 5 | 3.15 | 8 | 3.67 | 11 | 3.43 | 8 | 5.03 | 4 | 3.90 | 7 |
CCA** | 4.09 | 4 | 4.09 | 4 | 4.37 | 4 | 3.96 | 4 | NA | 3.91 | 4 | 4.14 | 8 | 3.95 | 5 | 4.54 | 9 | 3.38 | 10 | |
CPM** | 4.93 | 1 | 4.93 | 1 | 5.20 | 1 | 4.40 | 1 | NA | 4.95 | 1 | 4.84 | 4 | 4.69 | 2 | 5.56 | 2 | 4.31 | 2 | |
CPAFS** | 4.50 | 2 | 4.50 | 3 | 4.78 | 2 | 4.04 | 3 | NA | 4.17 | 3 | 4.61 | 5 | 4.44 | 3 | 4.63 | 7 | 4.47 | 1 | |
CPA** | NA | NA | NA | 3.50 | 6 | NA | NA | 4.99 | 2 | 4.86 | 1 | NA | 3.90 | 7 | ||||||
LTCPA** | NA | NA | NA | 2.35 | 11 | NA | NA | NA | NA | NA | 2.70 | 13 | ||||||||
VCA** | NA | NA | NA | 2.17 | 13 | NA | NA | NA | NA | NA | 2.08 | 14 | ||||||||
Benchmarking | NA | 4.59 | 2 | NA | 4.36 | 2 | 4.53 | 1 | NA | 3.82 | 10 | 3.61 | 7 | NA | 3.92 | 6 | ||||
Brand valuation | 2.35* | 11 | NA | 2.50 | 9 | 2.52 | 9 | NA | 2.16 | 11 | NA | NA | 4.74 | 6 | 3.34 | 11 | ||||
IPM/BSC** | NA | 4.00 | 5 | NA | 2.83 | 8 | 3.16 | 4 | NA | 3.43 | 13 | 3.17 | 10 | 5.34 | 3 | 3.94 | 5 | |||
Strategic pricing | 4.36 | 3 | NA | 4.73 | 3 | 3.88 | 5 | NA | 4.63 | 2 | 4.91 | 3 | NA | 5.72 | 1 | 4.29 | 3 |
Country | Developed countries | |||||||||
---|---|---|---|---|---|---|---|---|---|---|
USA | UK | New Zealand | Australia | |||||||
Study | (2000) | (2000) | (2000) | |||||||
Sample size (Final) | 127 | 63 | 112 | 124 | 124 | |||||
Scale used | 1–7 | 1–7 | 1–7 | 1–7 | 1–7 | |||||
Mean | Rank | Mean | Rank | Mean | Rank | Mean | Rank | Mean | Rank | |
ABC/M** | NA | NA | NA | NA | NA | |||||
Attribute costing | 3.56 | 9 | 3.13 | 11 | NA | 3.65 | 9 | NA | ||
LCC** | 3.76 | 8 | 3.58 | 8 | NA | 3.38 | 10 | NA | ||
Quality costing | 4.10 | 7 | 3.98 | 6 | NA | 4.65 | 6 | NA | ||
Strategic costing | 4.93 | 5 | 4.94 | 5 | 4.86 | 5 | 4.86 | 5 | NA | |
Target costing | 4.35 | 6 | 3.40 | 9 | NA | 3.83 | 8 | NA | ||
VCC** | 4.35 | 6 | 3.96 | 7 | NA | 4.37 | 7 | NA | ||
CCA** | 5.26 | 4 | 5.49 | 3 | 5.16 | 3 | 5.16 | 3 | NA | |
CPM** | 5.70 | 1 | 5.85 | 1 | 5.69 | 1 | 5.69 | 1 | NA | |
CPAFS** | 5.36 | 3 | 5.72 | 2 | 5.05 | 4 | 5.05 | 4 | NA | |
CPA** | NA | NA | NA | NA | 5.08 | 1 | ||||
LTCPA** | NA | NA | NA | NA | 4.38 | 2 | ||||
VCA** | NA | NA | NA | NA | 4.19 | 3 | ||||
Benchmarking | NA | NA | NA | NA | NA | |||||
Brand valuation | 3.45 | 10 | 3.21 | 10 | NA | 3.28 | 11 | NA | ||
IPM/BSC** | NA | NA | NA | NA | NA | |||||
Strategic pricing | 5.62 | 2 | 5.38 | 4 | 5.32 | 2 | 5.32 | 2 | NA |
Study | Country (sample size) | Theory applied | SMA techniques considered | Factors considered | Findings |
---|---|---|---|---|---|
New Zealand (112 largest public and private companies) | Contingency theory | Competitor cost assessment Competitive position monitoring Competitor performance appraisal Strategic costing Strategic pricing | Strategic mission Competitive strategy Company size Industry | Companies pursuing “build” strategic mission adopts strategic pricing and strategic costing techniques The usage rates of competitor cost assessment, competitive position monitoring and competitor performance appraisal are higher in “prospector” companies The usage rates of all the SMA techniques, except strategic pricing, are higher in larger companies Industry variations do not affect the usage rates except for competitor cost assessment in Oil, gas, mineral and electricity industry | |
USA (120) | Contingency theory | 15 SMA techniques (ABC, attribute costing, brand valuation, competitor cost assessment, competitive position monitoring, competitor performance appraisal, life cycle costing, quality costing, strategic costing, strategic pricing, target costing and value chain costing, benchmarking and IPM) | Eight subdimensions of competitive strategy (R&D, product quality, product technology, product range, service quality, price level, adverting expenditure level and market coverage) | SMA usage rate is higher in companies pursuing “Research and Development” and “Broad market coverage” strategy | |
Australia (124 top listed companies, measured in terms of market capitalization) | Contingency theory | Customer accounting Customer segment profitability analysis Customer profitability analysis Lifetime customer profitability analysis Valuation of customers as asset | Intensity of competition Market orientation Company size | Customer accounting, lifetime customer profitability analysis and valuation of customers as asset are positively associated with market orientation Intensity of competition is positively associated only with customer segment profitability analysis Company size is positively associated only with customer accounting | |
Italy (92 largest manufacturing companies) | Contingency theory | 14 SMA techniques (ABC/M, attribute costing, competitor cost assessment, competitive position monitoring, competitor performance appraisal, customer accounting, life cycle costing, quality costing, target costing, value chain costing, strategic costing, strategic pricing,benchmarking and IPM/BSC) | Strategic pattern Strategic mission Strategic positioning Company size Industry | The usage of target costing is positively associated with strategic mission (build) The usage of life cycle costing, strategic costing, ABC/M and value chain costing is greater in companies pursuing “cost leaders” strategy The usage of competitor cost assessment and strategic pricing is negatively associated with company size The association between SMA usage and types of industry is diversified | |
Slovenia (193 largest companies, in terms of total revenue) | Contingency theory | 16 SMA techniques (attribute costing, brand valuation, competitor cost assessment, competitive position monitoring, competitor performance appraisal, life cycle costing, quality costing, strategic costing, strategic pricing, target costing and value chain costing, benchmarking and IPM, customer profitability analysis, lifetime customer profitability analysis and valuation of customers as assets) | Business strategy (prospector/defender) Deliberate strategy formulation Market orientation Company size | SMA usage is positively associated with adopting a prospector strategy, deliberate strategy formulation, company size and accountants' participation in strategic decision-making | |
Italy (92 largest manufacturing companies) | Contingency theory | 11 SMA techniques (ABC/M, competitor cost assessment, competitive position monitoring, competitor performance appraisal, customer accounting, life cycle costing, quality costing, target costing and value chain costing, benchmarking and IPM/BSC) | Strategic pattern Strategic mission Strategic positioning Company size | Costing-oriented SMA usage rates are higher in “defenders” than in “prospectors” Customer-oriented SMA usage rate is higher in companies pursuing “build” strategic mission Costing-oriented SMA usage rates are higher in “cost leaders” than in “differentiators” Weak association between company size and SMA usage | |
(2013) | Germany (116 hospitals) | Strategic management | 11 SMA techniques based on (2000) | Structural characteristics (size, ownership and legal form) | The use of SMA techniques varies among hospitals based on their structural characteristics |
(2017) | Australia (127 public sector organizations) | Contingency theory | 8 (of which 5 are SMA techniques as per the scope of this study) (ABC, benchmarking, BSC, value chain analysis, strategic cost management) | Interactive use and diagnostic use of MCS | SMA usage is positively associated with interactive and diagnostic use of MCS |
Greece (94 manufacturing companies) | Upper echelons theory and role theory | 8 SMA techniques (Attribute costing, competitor cost assessment, competitor performance appraisal, customer profitability analysis, strategic pricing, brand valuation, value analysis and benchmarking) | Historical financial performance Top management team (TMT) age TMT tenure TMT educational background TMT creativity Economic crisis' perception Perceived environmental uncertainty | Firms with low profitability in the past (arising due to economic crisis) use SMA techniques more extensively SMA usage is positively associated with TMT educational background and creativity SMA usage is negatively associated with TMT tenure of service | |
Austria (72) Germany (283) Switzerland (22) Total (377) | Contingency theory | 10 SMA techniques (ABC, brand valuation, CPM, target costing, LCC, value chain costing, benchmarking, IPM, CPA, LTCPA) | Stages of firm life cycle, firm size, interdependence, degree of centralization and product quality | Firms in the maturity, revival and growth stages are more likely to use SMA techniques. Firm size, product quality and interdependence are also positively associated with SMA usage | |
(2019) | Italy (55 large manufacturing companies) | Contingency theory | 11 SMA techniques (attribute costing, brand valuation, CCA, CPM, CPAFS, target costing, LCC, value chain costing, benchmarking, BSC, strategic pricing) | Strategy type, geographic orientation, and environmental uncertainty and competitive forces | National firms adopting differentiation strategy make greater use of brand valuation. SMA usage is also positively associated with environmental uncertainty and competitive forces |
(2017) | Malaysia (121 SMEs) | Contingency theory and upper echelons theory | 16 SMA techniques of plus value stream costing and customer segment profitability analysis | CEO education CEO experience Involvement in networks | SMA usage is positively associated with CEO education and involvement in network |
Thailand (103) | Agency, resource dependency, and stewardship theory | 16 SMA techniques based on | CEO duality, board independence, board size, board meeting, audit committee independence and meeting, size, leverage, strategy type | Separation of CEO role from chairman, board independence, and frequency of audit committee meetings are positively associated with SMA usage, whereas independent chairmen and board size negatively associated with SMA usage |
Effects of the adoption of SMA techniques on firm performance
Study | Country (sample size) | Theory applied | SMA techniques considered | Performance measures used | Findings |
---|---|---|---|---|---|
Slovenia (193 largest companies, in terms of total revenue) | Contingency theory | 16 SMA techniques under 5 categories (costing, competitor, customer, strategic-decision-making, planning, control and performance measurement) | Perception of respondent (1–7 scale) on: ROI, margin on sales, capacity utilization, customer satisfaction, product quality, development of new product and market share | SMA usage is positively (significantly) associated with firm's performance | |
Slovenia (109 largest manufacturing companies) | Configurational theory | 16 SMA techniques identical to above | Perception of respondent (1–7 scale) on: Return on investment, development of new product and market share | Limited support is found for the configurational proposition that internally consistent strategy and SMA system configurations are associated with higher firm's performance Consistent with equifinality proposition, different strategic and structural alternatives are associated with similar performance levels | |
Turkey (229 medium- and large-size business) | Strategic management | 16 SMA techniques based on | Perceived qualitative and quantitative performance | Competitors and customer-oriented SMA techniques displayed significant positive effect on the perceived qualitative performance | |
(2017) | USA (95 hotel properties) | Contingency theory | 9 SMA techniques (CPA, benchmarking, CCA, strategic pricing, VCC, IPM, CPAPFS, attribute costing, strategic costing) | Hotel property customer performance and financial performance | Hotel property SMA use mediates the relationship between hotel property market orientation business strategy and hotel property financial performance |
(2017) | Malaysia (121 SMEs) | Contingency theory and upper echelons theory | 16 SMA techniques of plus value stream costing and customer segment profitability analysis | SMA usage has indirect positive effect on company performance in relation of CEO education and involvement in networks | |
Saudi Arabia (435 accounting managers from 124 listed companies) | Contingency theory | Five facets of SMA practices | Financial performance (market share, sales growth, profit growth, return on equity, cash-flow and return on assets) Nonfinancial performance (customer satisfaction, adaptive ability to a changing environment, innovative performance, employee satisfaction, product quality and new product/service offers) | SMA facets significantly (and positively) affect both financial and nonfinancial performance |
Summary of findings
Issues of SMA practices | Developed economies | Developing economies |
---|---|---|
Adoption status | Competitor-focused SMA techniques and strategic pricing have been highly and moderately adopted in most of the developed countries (e.g. USA, UK, Australia and New Zealand) Benchmarking is highly adopted in USA and Australia Customer accounting is considerably popular among the Italian manufacturing companies | No prior studies have focused on the adoption status of SMA practices (as a package) in the context of developing countries ABC, BSC and target costing have been moderately and lowly adopted in several developing countries |
Perceived benefits | Competitive position monitoring, strategic pricing and competitor performance appraisal are perceived highly beneficial by the adopting companies Several customer-oriented SMA practices are also perceived beneficial to Australian companies | Akin to the adoption status, no prior studies have focused on the perceived benefits from the use of SMA practices (as a package) in the context of developing countries |
Influencing factors | Strategic mission, positioning and pattern have mixed effect on SMA usage; positive association between SMA usage and “build”, “prospector” and “cost leader” strategy followers are more apparent R&D, broad market coverage strategy and deliberate strategy formulation are also positively associated with SMA usage The effect of firm size and industry on SMA usage is mixed with mostly positive in nature Market orientation and intensity of competition, TMT education and creativity also have positive influence on SMA usage | Positive association between SMA usage and CEO education and involvement in network |
Effects of SMA usage | Positive association between SMA usage and firm's performance | Positive effect of SMA usage on firm's performance in relation to CEO education and network is apparent |
The study uses the World Factbook (of Central Intelligence Agency) to isolate developed countries from that of developing countries ( The World Factbook, 2020 ).
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Does your assignment or publication require that you write a literature review? This guide is intended to help you understand what a literature is, why it is worth doing, and some quick tips composing one.
What is a literature review .
Typically, a literature review is a written discussion that examines publications about a particular subject area or topic. Depending on disciplines, publications, or authors a literature review may be:
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Locate patterns, relationships, connections, agreements, disagreements, & gaps in understanding Identify methodological and theoretical foundations Identify landmark and exemplary works Situate your voice in a broader conversation with other writers, thinkers, and scholars
The Literature Review will aid your research process. It will help you to:
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The Literature Review structure and organization may include sections such as:
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The body of a literature review may be organized in several ways, including:
Chronologically: organized by date of publication Methodologically: organized by type of research method used Thematically: organized by concept, trend, or theme Ideologically: organized by belief, ideology, or school of thought
1. Purpose and Scope
To help you develop a literature review, gather information on existing research, sub-topics, relevant research, and overlaps. Note initial thoughts on the topic - a mind map or list might be helpful - and avoid unfocused reading, collecting irrelevant content. A literature review serves to place your research within the context of existing knowledge. It demonstrates your understanding of the field and identifies gaps that your research aims to fill. This helps in justifying the relevance and necessity of your study.
To avoid over-reading, set a target word count for each section and limit reading time. Plan backwards from the deadline and move on to other parts of the investigation. Read major texts and explore up-to-date research. Check reference lists and citation indexes for common standard texts. Be guided by research questions and refocus on your topic when needed. Stop reading if you find similar viewpoints or if you're going off topic.
You can use a "Synthesis Matrix" to keep track of your reading notes. This concept map helps you to provide a summary of the literature and its connections is produced as a result of this study. Utilizing referencing software like RefWorks to obtain citations, you can construct the framework for composing your literature evaluation.
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Focus on searching for academically authoritative texts such as academic books, journals, research reports, and government publications. These sources are critical for ensuring the credibility and reliability of your review.
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Instead of merely summarizing sources, identify and discuss key themes that emerge from the literature. This involves interpreting and evaluating how different authors have tackled similar issues and how their findings relate to your research.
4. Critical Evaluation
Adopt a critical attitude towards the sources you review. Scrutinize, question, and dissect the material to ensure that your review is not just descriptive but analytical. This helps in highlighting the significance of various sources and their relevance to your research.
Each work's critical assessment should take into account:
Provenance: What qualifications does the author have? Are the author's claims backed up by proof, such as first-hand accounts from history, case studies, stories, statistics, and current scientific discoveries? Methodology: Were the strategies employed to locate, collect, and evaluate the data suitable for tackling the study question? Was the sample size suitable? Were the findings properly reported and interpreted? Objectivity : Is the author's viewpoint impartial or biased? Does the author's thesis get supported by evidence that refutes it, or does it ignore certain important facts? Persuasiveness: Which of the author's arguments is the strongest or weakest in terms of persuasiveness? Value: Are the author's claims and deductions believable? Does the study ultimately advance our understanding of the issue in any meaningful way?
5. Categorization
Organize your literature review by grouping sources into categories based on themes, relevance to research questions, theoretical paradigms, or chronology. This helps in presenting your findings in a structured manner.
6. Source Validity
Ensure that the sources you include are valid and reliable. Classic texts may retain their authority over time, but for fields that evolve rapidly, prioritize the most recent research. Always check the credibility of the authors and the impact of their work in the field.
7. Synthesis and Findings
Synthesize the information from various sources to draw conclusions about the current state of knowledge. Identify trends, controversies, and gaps in the literature. Relate your findings to your research questions and suggest future directions for research.
Practical Tips
Brown University Library (2024) Organizing and Creating Information. Available at: https://libguides.brown.edu/organize/litreview (Accessed: 30 July 2024).
Pacheco-Vega, R. (2016) Synthesizing different bodies of work in your literature review: The Conceptual Synthesis Excel Dump (CSED) technique . Available at: http://www.raulpacheco.org/2016/06/synthesizing-different-bodies-of-work-in-your-literature-review-the-conceptual-synthesis-excel-dump-technique/ (Accessed: 30 July 2024).
Study Advice at the University of Reading (2024) Literature reviews . Available at: https://libguides.reading.ac.uk/literaturereview/developing (Accessed: 31 July 2024).
Further Reading
Frameworks for creating answerable (re)search questions How to Guide
Literature Searching How to Guide
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Speaker 1: A literature review is a summary of the existing research on a particular topic. It's typically done at the beginning of a research project and I did one for my undergraduate thesis, for my master's thesis and for my PhD thesis. And in this video I'm going to answer all of your literature review related questions. The first thing is how do you start a literature review? Well, to start a literature review, surprisingly or not surprisingly, you need literature. Where do you find that literature? Well, there's a ton of places. The first place I would go to is illicit.com. This is a new AI tool which allows you to ask a research question and get all of the papers related to that question. For example, here I can say how effective are conditional cash transfer programs? It will go away and search more than 125 million academic papers and here are the first four abstracts here. And here are all of the different researched peer-reviewed papers and that means that experts in the field have looked at these papers and said, yes, they are true. They are something that is a valuable contribution to the research field. So that's why you should be reading them. And we can go through and see that we've got a little summary and we just click through all of these and we can go and read them individually. That's one way, semantic searching. The next thing you can do is use Litmaps. Litmaps creates a map of literature for you to search. We can go in and create a map. Here I've created a map from one of my peer-reviewed papers that I wrote during my PhD and you can see I get a nice map of all of the other stuff that I need to read. You can do this with a single seed paper or you can put in a load of different papers in this tab in Discover to find out a load of different papers that you need to read about. Then you can also use something like Google Scholar. This is old school. This is like OG science and research. You'd go in, you just type keywords. For example, charge transport in OPV. So I'll click here and then here are all of the different papers that I should consider reading. Clearly, you don't need to read all of them but we'll get into that in a minute. But this is where you start. You start by searching the literature. You can have a look since 2024, since 2023 and this is the foundational activity for any literature review. Get comfortable searching the literature and you'll become a power user of all of the literature that you're about to write about. Before you start reading any literature, you need to have a literature review outline to work with. So this is the general structure of nearly every literature review for any field. It goes like this. First of all, we start with an introduction at the top. This introduction gives background information about the research field that you are investigating. It's in a reverse pyramid shape because this is the very, very broad step. This is where we're just sort of like looking at the overarching umbrella of our research field. Then optionally, we can talk about background and methods that are used to look for the research that we're going to talk about in the literature review. For example, you may want to say we looked at these databases, we looked at these sort of questions and background is the background of the field that you're specifically interested in. So we're going a little bit deeper, which is why it's the next step down on the inverse pyramid. Then we need all of the main text and this is all of the literature that you found searched by either theme. So you sort of group it together as like, this is a group of research that I can talk about because it's under one theme. Here's another theme or here's another theme and you've put research under that. So in here, you may have one, two, three plus themes under which you will talk about literature or, which is very uncommon I think these days, but you may be lucky that you may be able to sort this based on time, which means initially these people did this and then they did this and then they did this and that's how you structure your literature review. So you say they did this first, here's all the literature in the initial stages of that research, then they did this, here's the next stage of research, the evolution of that research field, here's the next stage. So it may be theme or time, it's completely up to you which one you use, but most people use theme. Once you've outlined all of the main themes and you've talked about the literature under that theme, then you need to have a discussion to bring it all together. This is where you're looking at all of the research themes and you're talking about your specific research question. Why are you doing this research into this literature and how does it help you sort of like answer the research question or the interest you have in a particular research field and why you're looking at the literature in the first place. And then you're looking at conclusions. Based on all of the stuff that you've read, all of the individual themes, all of the chronological studies, all of the papers you've included in this literature review, what conclusions can you make specifically about the current state of the field? And that is the general structure of nearly every literature review ever produced. Now, there's an easier way to do it obviously. What I like to do is go to ChatGPT and I just say, create a literature review outline for a study about and then whatever I'm interested in. Here I've got an example where it says, the effect of climate change on plants. And as you can see, it says introduction, background and here it says I want basic concepts of climate change. Then it says general impacts of climate change. Then we want direct effects of climate change on plants. So you can see we've started broad and we're getting narrower and narrower as the literature review goes on. And then we've got different themes. So we've got indirect effect of climate change on plants. So altered pests and disease dynamics, that's a theme. Changes in land use and habitat, that's a theme. And then we've got other themes underneath. So this is how you can easily structure and get a first kind of draft of the structure of any literature review that you're writing for nearly any subject. It's just amazing. And as you can see down here, the last one is conclusion, summary of key findings and then final thoughts on the importance of further research. So this is how we can use ChatGPT to structure our literature review outline. Nice stuff. Once you've got all of the literature you need to read and you've got a structure under which to put that literature, then you need to just write. You type out all of the stuff in your literature review. Before you do that, you may want to have a look at something like explainpaper.com that allows you to quickly understand peer-reviewed papers. Peer-reviewed papers are notoriously hard to read. They're dense, they're thick in academic language. And here, it's a really nice way to just get the simple summary. And I think this is one of the most powerful ones, explainpaper.com. All you need to do is highlight a certain area and over here, it will say, okay, explain your explanation. As a middle schooler, we can move this up and down and then we just click explain. And underneath, it will tell you the undergrad explanation of what you've just highlighted. A really great way, particularly if you're early on in your academic career, if you're undergraduate, if you're in high school, this is a great way to unlock all of the power that's behind the horrible language found in peer-reviewed academic papers. Once you understand what's actually in all of this, you've collected them into themes, you need to write it. There are a few tools that you can use. So you can use jenny.ai, that's an auto-writer for research papers and literature reviews. You can use yomoo.ai. And that is another sort of like auto-writer for peer-reviewed and papers. But to be honest with you, the best thing you can do is sit there with a Word document, with a Google document, Google, what do you even call that? Google Docs? Google Word? I completely forgot. Anyway, you know what I mean. You sit there with a word processor and you start typing. You put in your structured headlines and then you say under each one, what literature you're going to mention and you start fleshing it out. It takes ages and ages and many, many revisions. Make sure that you get someone you trust or your supervisor to look over it as you're writing it. Maybe each chapter or each theme that you write, you get someone to look over it and then at the end they look over everything all together. It's a really, really long process. It takes such a long time. For my thesis, it probably took a good few weeks to get all of the information into a sensible structure and literature review. So here we are, here's one of the themes. Overview of photocurrent generation in organic photovoltaic devices. So that's just one of many, many themes in this thesis and depending on what stage of study you're at, it could be long, it could be short but let's talk about that next. Okay, how long should a literature review be? Well, there are no hard and fast rules but I like to think about it like this. Is there enough in your literature review to provide enough context to what you're doing and what you're researching? Is there enough context for you to understand the problem that your literature review is looking at and addressing and also, is there enough data in there to talk about the up-to-date research and where the current state of the field is? That's really what we're looking at but here's some rules of thumb. So if you're doing it for an assignment, one thing I recommend that you look at is about 3,000 to 10,000 words. That's normally good enough to get an overview. For example, in my undergraduate thesis, it's only about seven pages. There's not much in there. There's some fancy diagrams, there's lots of references but ultimately, it's about seven pages. So it's not much. So 3,000 to 10,000 words is all you need for a small assignment or an undergraduate thesis whereas for master's and master's theses and PhD dissertations, one thing I recommend is you look at what's normal for your field. In some fields, it's like 10 pages. In other fields, it can be up to 40 pages but ultimately, as long as you have enough information and literature to be able to provide context to your problem and you provide an up-to-date representation of that research field, then you've got enough in there. Like I said, I like to use just the guide of what is normal for my research field before I start writing my thesis so I can say, okay, normally it's about 20 pages and therefore, I need to fill 20 pages worth of stuff and that is a good starting point for almost any literature review. So there we have it. That's the introduction to literature reviews. I'd love to know what you think and also, I have got so many videos on this very channel about literature reviews with AI, how to find literature using AI tools, how to write it in seconds using tools that are available online. I'll put all of the links below in the description so you can sort of build on the knowledge that we've gained in this video but if you really want to go look at a powerful video, go check out this one where I talk about how to write an exceptional literature review using AI. You won't be disappointed. Go check it out.
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Wandering spleen complicated by thrombocytopenia, acute appendicitis, and sepsis: a case report and literature review.
3. case presentation, 4. discussion, 5. conclusions, supplementary materials, author contributions, institutional review board statement, informed consent statement, data availability statement, conflicts of interest.
Click here to enlarge figure
Author (Year) | Sex and Age (Year) | Associated Comorbidities | Surgery | Outcome |
---|---|---|---|---|
Dangen (2020) [ ] | F, 17 | CDH and splenic torsion | Closure of hernia and splenectomy | Post-operative pneumothorax but recovered well |
Mirkes (2011) [ ] | F. 21 (16 weeks pregnant) | Thrombocytopenia | None | Low platelet even after delivery |
Zhao (2022) [ ] | M, 18 | Appendicitis and splenic torsion | Laparoscopic removal of spleen and appendix | Discharged seven days after surgery |
Pelizzo (2001) [ ] | F, 12 | CDH | Diaphragmatic repair with simple medial dislocation of the spleen | Recovered well |
Moll (1996) [ ] | F, 30 | Thrombocytopenia | Splenectomy | Recovered well and no longer has thrombocytopenia |
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Inggriani, S.; Sulay, C.B.H.; Octavius, G.S. Wandering Spleen Complicated by Thrombocytopenia, Acute Appendicitis, and Sepsis: A Case Report and Literature Review. Reports 2024 , 7 , 73. https://doi.org/10.3390/reports7030073
Inggriani S, Sulay CBH, Octavius GS. Wandering Spleen Complicated by Thrombocytopenia, Acute Appendicitis, and Sepsis: A Case Report and Literature Review. Reports . 2024; 7(3):73. https://doi.org/10.3390/reports7030073
Inggriani, Sri, Callistus Bruce Henfry Sulay, and Gilbert Sterling Octavius. 2024. "Wandering Spleen Complicated by Thrombocytopenia, Acute Appendicitis, and Sepsis: A Case Report and Literature Review" Reports 7, no. 3: 73. https://doi.org/10.3390/reports7030073
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BMC Nephrology volume 25 , Article number: 282 ( 2024 ) Cite this article
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This article provides a comprehensive overview of electrolyte and water homeostasis in pediatric patients, focusing on some of the common serum electrolyte abnormalities encountered in clinical practice. Understanding pathophysiology, taking a detailed history, performing comprehensive physical examinations, and ordering basic laboratory investigations are essential for the timely proper management of these conditions. We will discuss the pathophysiology, clinical manifestations, diagnostic approaches, and treatment strategies for each electrolyte disorder. This article aims to enhance the clinical approach to pediatric patients with electrolyte imbalance-related emergencies, ultimately improving patient outcomes.
Trial registration This manuscript does not include a clinical trial; instead, it provides an updated review of literature.
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Homeostasis is a process by which an organism can preserve internal stability while adjusting to changing external conditions which involves complex interactions of multiple mechanisms and reactions in the body [ 1 ]. Electrolytes play a pivotal role in essential body functions. Electrolyte abnormalities are associated with prolonged hospital stays and higher in-hospital mortality among acutely ill children [ 2 , 3 , 4 , 5 ]. A comprehensive understanding of electrolyte pathophysiology is imperative for the effective management of these pediatric cases. Anticipating changes in plasma electrolyte concentration is crucial for preventing life-threatening emergencies. Anticipation can be achieved through continuous clinical assessment, recognizing symptoms of imbalance, understanding patient history, and appropriate laboratory tests. Additionally, cautious laboratory monitoring and early intervention can decrease the risk of severe complications. This article offers a comprehensive overview of electrolyte and water homeostasis, while also exploring the treatment strategies linked to electrolyte imbalance-related emergencies.
Sodium (Na +) plays a crucial role as the primary extracellular cation, contributing to the maintenance of cellular homeostasis, regulation of ion and water metabolism, and the control of blood pressure. Plasma sodium concentration is maintained within narrow limits despite variable dietary intake and physical activity. Sodium and water balance are tightly linked. Children have higher total body water content compared to adults. In premature newborns, water makes up to 80% of body weight. Total body weight (TBW) decreases to 70% in term newborns, however, once children reach the age of 1 they have 60% of TBW which is similar to adults. About two-thirds of TBW is in the intracellular compartment and the remaining one-third is extracellular fluid, which consists of interstitial, intravascular, and transcellular fluid (cerebrospinal, ocular, synovial, and peritoneal fluid) [ 6 ]. These various fluid compartments are depicted in Fig. 1 .
Body fluid compartments. Illustration of the fluid compartments within the body. ECF-extracellular fluid, ICF-intracellular fluid, ISF-interstitial fluid, IVF-intravascular fluid, TCF-transcellular fluid
Abnormalities of plasma sodium are one of the most common electrolyte disorders. Complex neurohumoral mechanisms play a crucial role in maintaining sodium and water balance. Renin is released from juxtaglomerular cells in response to hypovolemia, sympathetic nerve activation, or decreased renal perfusion or delivery of sodium chloride to the distal tubule. Renin functions to enhance reabsorption of sodium and water in the proximal convoluted tubule (PCT) [ 7 ]. The synthesis of antidiuretic hormone (ADH) is conducted within the hypothalamus. ADH is secreted from the neurohypophysis and plays a role in water regulation. ADH acts on V2 receptors in the distal nephron to facilitate water reabsorption. Increased effective plasma osmolality stimulates cerebral osmoreceptors, leading to ADH release and inducing thirst. Hypotension is associated with a significant reduction of effective intravascular volume and is a strong stimulus for ADH release that may even supersede osmotic stimuli [ 8 ]. Additionally, hypotension decreases the baroreceptor firing rate leading to an increased heart rate, vasoconstriction, and activation of the renin–angiotensin–aldosterone system (RAAS) along with decreased production of natriuretic peptides. Collectively, these changes can enhance tubular sodium and water reabsorption [ 9 ]. Additionally, fluid and water intake can impact sodium concentration, therefore managing fluid intake is important in maintaining sodium balance.
Hyponatremia in children is defined as plasma sodium concentration < 135 mmol/L. In pediatric patients younger than 4 years of age, hyponatremia is considered the most common serum electrolyte abnormality (SEA). However, in patients older than 4 years, hypokalemia is the most common SEA. Gastrointestinal, renal, and endocrine diseases are the predominant causes of SEAs in children [ 10 ]. Hyponatremia is typically encountered in patients with excessive intake of free water paired with an inability of the kidney to excrete free water. The majority of cases of hyponatremia are associated with decreased osmolality. The various etiologies and differential diagnoses of hyponatremia are summarized in Table 1 and Fig. 2 . Severe hyponatremia may lead to cerebral edema and hyponatremic encephalopathy. Early symptoms of hyponatremia include headache, nausea, vomiting, lethargy, and confusion. In more severe cases, altered consciousness, seizures, coma, respiratory arrest, and myocardial ischemia can develop [ 11 ]. Brain edema secondary to increased intracranial pressure may cause noncardiogenic pulmonary edema which can lead to hypoxia and impairment of brain volume regulation, known as Ayus-Arieff syndrome [ 12 ]. Children with cerebral edema are at an increased risk for developing herniation given a higher ratio of brain volume to skull size compared to adults.
Algorithm for differential diagnosis of hyponatremia, modified according to Zieg, J [ 13 ]. Low plasma osmolality is diagnostic for hypotonic hyponatremia, therefore pseudohyponatremia and translational hyponatremia must be excluded first. The next step is to assess the current volume status. The diagnostic workup should include basic measurement of plasma and urinary sodium and creatinine to calculate FENa. Both volume status and value of FENa are used to determine the cause of hyponatremia. SIADH- syndrome of inappropriate antidiuretic hormone, AKI- acute kidney injury, CKD- chronic kidney disease, FENa- fractional excretion of sodium (urinary sodium × serum creatinine)/(urinary creatinine × serum sodium) × 100
Hyponatremic encephalopathy is a medical emergency that requires early recognition and treatment with hypertonic saline 3% NaCl bolus 2 ml/kg with a maximum of 100 mL. If symptoms persist, the bolus should be repeated no more than two times [ 14 ]. Before pursuing additional diagnostic evaluations, it is essential to administer appropriate therapy to avoid potential harm to the patient due to treatment delays. In cases of symptomatic hyponatremia, it is recommended to aim for a safe increase of approximately 5–6 mmol/L in serum sodium concentration within the first one or two hours. However, it is crucial to avoid correcting serum sodium levels by more than 10 mmol/L within the first 24 h of therapy and by more than 20 mmol/L within 48 h to prevent potential complications [ 11 ]. Overcorrection of hyponatremia can lead to cerebral demyelination with severe neurologic symptoms. However, this complication primarily manifests in cases of chronic hyponatremia as there have been no reported instances of cerebral demyelination in children treated with hypertonic saline for hyponatremia [ 11 ]. For patients with subacute or chronic hyponatremia, cerebral edema is prevented by the adaptive mechanism of the brain. Therefore, rapid correction of sodium is not necessary in chronic hyponatremia.
The approach for the management of hyponatremia depends on the patient’s volume status. Hypervolemic hyponatremia is typically attributed to an excess of total body water due to conditions such as nephrotic syndrome or heart, liver, and kidney failure. Euvolemic hyponatremia is caused by various conditions including Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH), polydipsia, or hypothyroidism as there is a stable total body sodium level alongside an increase in total body water. Various risk factors for SIADH include central nervous system disturbances, lower respiratory tract infections, drugs, and certain malignancies [ 15 ]. Hypovolemic hyponatremia is due to a depletion of total body sodium, often caused by gastrointestinal losses, the use of diuretics, and mineralocorticoid insufficiencies. Patients experiencing hypovolemic hyponatremia with shock require fluid resuscitation using 0.9% saline, Ringers, Plasmalyte, or other isotonic solutions to restore hemodynamic stability. Treatment for hypervolemic hyponatremia varies depending on the etiology. For example, heart failure may be treated with diuretics whereas dialysis can be used to treat patients with end-stage kidney disease (ESKD) [ 16 ]. Patients presenting with euvolemic hyponatremia, such as in the instance of SIADH or psychogenic polydipsia must undergo fluid restriction. However, in cases of hypothyroidism, the underlying condition should be addressed for treatment. Iatrogenic hyponatremia is another concern in pediatric patients undergoing treatment with intravenous fluids. The 2018 American Academy of Pediatrics (AAP) guidelines recommend using isotonic fluids, such as 0.9% saline or Ringer’s lactate, to maintain proper sodium levels and prevent the development of iatrogenic hyponatremia [ 17 ].
Hypernatremia is characterized by a plasma sodium concentration greater than 145 mmol/L. Hypernatremia is a less common SEA and generally affects children less than 4 years old [ 10 ]. This condition typically arises from decreased free water intake or increased loss of solute-free water and viral gastroenteritis is the leading cause. Additionally, a less common cause is salt poisoning. Importantly, hypernatremic dehydration can result from excessive water loss due to conditions including osmotic diuresis or urinary concentration defects. Determining the cause of the hypernatremic state is crucial for effective management and is depicted in Fig. 3 . When the FENa is less than 1% and the patient demonstrates weight loss, this can be either attributed to free water loss or insufficient water intake. Free water loss in a hypernatremic state is attributed to extrarenal causes such as vomiting and diarrhea or renal losses such as antidiuretic hormone (ADH) resistance or osmotic diuresis. Furthermore, if a patient demonstrates a FENa of greater than 2% with weight gain, this is typically attributed to salt excess. Additionally, Table 2 demonstrates the various causes of hypernatremia in children.
Algorithm for differential diagnosis of hypernatremia, modified according to Bockenhauer et al. and Zieg, J [ 18 , 19 ]. After excluding pseudohypernatremia, early management is tailored to the volume status and weight of the patient. While free water loss and insufficient water intake are associated with weight loss and low urine sodium, children with salt intoxication gain weight and their urine sodium is high. Measurement of plasma and urine osmolality is important in determining the cause of hypernatremia
Hypernatremia may lead to neurologic symptoms due to the shift of water from the intracellular compartment, resulting in cellular shrinkage. These symptoms include irritability, fever, and weakness. Severe cases may present with lethargy, focal neurologic deficits, altered mental status, coma, seizures, and death [ 20 , 21 ]. Children with hypernatremic dehydration should first receive intravenous isotonic solutions to restore intravascular volume and tissue perfusion, followed by solutions containing higher free water content to correct hypernatremia. The free water deficit can be estimated using the formula: 4 ml x weight (kg) x desired change in serum sodium (mmol/L). This formula can be applied for patient management in situations where children are experiencing hypernatremia dehydration and require fluid supplements. It is essential to correct hypernatremia gradually with a recommended correction rate of below 1 mmol/L/h and 15 mmol/24 h to prevent the development of cerebral edema. Some experts recommend administering solutions with slightly higher sodium content (10–15 mmol/L lower) in children with severe hypernatremia (greater than 175 mmol/L) to avoid the risk of rapid decline in serum sodium due to excessive free water intake [ 22 ]. Regular monitoring of serum sodium is necessary to avoid a rapid drop in serum sodium levels [ 19 ]. Following fluid replacement for losses, hypotonic solutions with lower sodium content (Na 75 mmol/L) are recommended for severe hypernatremia and (Na 30 mmol/L) for mild cases to help control and gradually adjust the sodium concentration [ 22 ]. Rehydration strategies are different in children with renal concentration defects to control sodium levels according to specific needs. Individuals with nephrogenic diabetes insipidus should be given hypotonic solutions (dextrose), whereas those with central diabetes insipidus require replacement of water loss with hypotonic fluids alongside desmopressin administration. However, caution is exercised with these treatments as they potentially lead to hyponatremia in cases of renal impairment affecting electrolyte balance. Therefore, careful monitoring of electrolyte levels is essential when administering desmopressin and hypotonic fluids to prevent the development of hyponatremia. In hemodynamically unstable patients, rapid correction of intravascular volume with isotonic saline should be initially used to stabilize the patient. Once stability is achieved, transitioning to hypotonic solutions may be considered [ 23 , 24 ].
Potassium (K) plays a pivotal role as the primary intracellular cation, contributing significantly to maintaining membrane voltage, nerve excitation, and acid–base balance. The normal plasma concentration is regulated within the range of 3.5 to 5 mmol/L. The potassium concentration gradient across cell membranes is essential for establishing resting cell potential and ensuring the normal function of excitable cells [ 25 ]. Potassium homeostasis is maintained by a balance between intake and excretion. Both excessively high and low potassium plasma concentrations increase the risk for life-threatening complications, including cardiac arrhythmias, cardiopulmonary arrest, and neuromuscular dysfunctions [ 26 ]. The kidney assumes a central role in regulating external potassium balance and is responsible for excreting almost 90% of this electrolyte into urine daily [ 27 ]. In individuals with significantly reduced kidney function, enhanced potassium elimination through the colon becomes a significant contributor to overall potassium elimination. Interestingly, increased plasma potassium concentrations can stimulate elevated potassium excretion which indicates the existence of direct gastrointestinal-renal kaliuretic signaling [ 28 ]. Evidence from animal models demonstrates the concept of feedforward mechanisms which suggest the presence of potassium receptors in the gastrointestinal tract [ 29 ]. Potassium excretion follows a cyclic pattern directed by the circadian oscillator in the hypothalamus. Internal potassium balance hinges on maintaining a functional Na/K ATP pump and a constant difference between intracellular and extracellular potassium levels. Additionally, hormones including insulin, catecholamines, and mineralocorticoids, as well as drugs such as loop diuretics, thiazide diuretics, and beta-adrenergic agonists can stimulate tissue uptake of potassium, resulting in a decrease in plasma potassium levels [ 30 ]. Furthermore, the balance of potassium concentration is linked to acid–base equilibrium. For example, alkalosis results in hypokalemia due to increased potassium secretion and diminished potassium reabsorption in the collecting duct, whereas acidosis produces the opposite effect [ 31 ].
Hypokalemia in children may be categorized based on the severity: mild (3–3.5 mmol/L), moderate (2.5–3 mmol/L), and severe (< 2.5 mmol/L). In a retrospective study of pediatric patients with SEAs, hypokalemia was the most common in those older than 4 years old, accounting for 38.4% of patients [ 10 ]. The etiology of hypokalemia is diverse, with common causes stemming from extrarenal conditions such as diarrhea, malabsorption, protracted gastric suction, vomiting, refeeding syndrome, drug side effects, and excessive sweating. Other additional causes include endocrine disorders and tubulopathies which are demonstrated in Table 3 . Comprehensive medical history and basic laboratory examinations play a crucial role in the differential diagnosis of hypokalemic states. The urinary K/creatinine ratio and transtubular potassium gradient (TTKG) are useful tools to assess potassium urinary wasting. Importantly, TTKG is valid only if urinary osmolality exceeds plasma osmolality [ 18 ]. Mild hypokalemia may manifest with nonspecific symptoms such as weakness, fatigue, nausea, vomiting, confusion, and diarrhea. Severe hypokalemia can lead to more serious consequences including paralysis, respiratory failure, and arrhythmias. ECG changes associated with hypokalemia include ST depression along with PR and QT prolongation. Prominent U waves recognized as positive deflections after T-wave and T-wave inversions are typical for severe hypokalemia. Both tachyarrhythmias and bradyarrhythmias- atrioventricular block or cardiac arrest may occur [ 32 ].
The primary goal of managing severe hypokalemia involves the reduction of further potassium wasting by addressing the identified cause (e.g. medication), treating the underlying disease, and administration of potassium to prevent further episodes of hypokalemia [ 34 ]. Administering oral potassium therapy is the safest approach and should be utilized when possible. The recommended dosage is 1–2 mEq/kg orally every few hours, with periodic serum potassium checks every 4 h. In situations where oral potassium therapy is not feasible due to patient status, in children with severe hypokalemia (< 2.5 mmol/L), and/or in the presence of arrhythmias, intravenous correction is a necessary option [ 18 ].
A recent study indicates that infusing 1 mmol/kg of potassium chloride over 1–2 h is likely safe for young children in intensive care units with mild to moderate hypokalemia, however, those with severe hypokalemia may require additional supplementation [ 35 ]. When administering potassium via peripheral veins, the concentration should not exceed 40 mmol/L to prevent phlebitis and pain. For higher concentrations, central venous lines are recommended, however, this does not apply to life-threatening conditions. Importantly, potassium dextrose-containing solutions must be avoided, as dextrose stimulates insulin secretion and can potentially worsen hypokalemia [ 26 ]. Additionally, it is important when removing dextrose from intravenous fluids in ill children not eating as this can also increase the risk of hypoglycemia. Regular monitoring of blood glucose levels is necessary to manage potential hypoglycemia in these patients. Potassium replacement should be scaled back when the serum potassium concentration exceeds 3.5 mmol/L. During this replacement approach, serum potassium checks are recommended every 1–2 h. Continuous ECG monitoring is essential, along with regular monitoring of blood gases and potassium levels. Additionally, concurrent hypomagnesemia in children with hypokalemia requires attention as it contributes to potassium wasting and lowers tubular potassium reabsorption. Management should focus on correcting low magnesium levels since hypokalemia is refractory until magnesium levels are within the range of 0.7–1 mmol/L. In specific conditions such as correcting electrolyte imbalances or acid–base disorders, alternative forms of potassium supplementation may be considered. These scenarios include potassium phosphate in diabetic ketoacidosis or potassium citrate in renal tubular acidosis [ 36 ].
Hyperkalemia in children is defined as plasma potassium greater than 5.5 mmol/L. A retrospective study demonstrated that hyperkalemia constitutes nearly 22.4% of SEA cases in children [ 10 ]. While plasma K > 7 mmol/L is found in severe hyperkalemia, children with moderate hyperkalemia have plasma potassium within a range of 6–7 mmol/L [ 32 ]. Notably, normal potassium levels are higher in newborns and infants due to their lower glomerular filtration rates and partial aldosterone resistance [ 37 ]. Pseudohyperkalemia arises from hemolysis and potassium leakage during or after capillary or venous blood collection. This phenomenon is more prevalent in small children, where the use of smaller needles and surrounding tissue squeezing during blood sample collection can contribute to its occurrence. Pseudohyperkalemia also occurs in patients with leukocytosis or blood clotting or may be a consequence of preanalytical errors including improper blood sample storage, delayed analysis, and specimen contamination [ 38 ]. It is recommended to repeat hemolyzed hyperkalemia samples to ensure accurate results [ 39 ].
Hyperkalemia most commonly occurs in children with acute kidney injury or ESKD. It can be attributed to various factors including excessive potassium intake, potassium redistribution, tissue injury (mainly skeletal and cardiac muscle), and massive cell lysis (as seen in tumor lysis syndrome). Additionally, it can be caused by decreased potassium excretion due to kidney dysfunction, mineralocorticoid deficiency, aldosterone resistance (such as in renal tubular acidosis type 4), or hyporeninemic hypoaldosteronism. The various etiologies of hyperkalemia are demonstrated in Table 4 . Differential diagnosis of hyperkalemia is shown in Fig. 4 using a TTGK threshold of greater or less than 6, as evidenced by Choi et al. [ 40 ] While hyperkalemia is often asymptomatic, individuals may manifest symptoms such as weakness, muscular paralysis, and respiratory failure. Additional symptoms may be associated with the underlying disease, such as polydipsia and polyuria in diabetic ketoacidosis or failure to thrive in tubular disorders [ 32 , 41 ]. Early ECG signs of hyperkalemia include peaked T waves, progressing to flattened broad P waves, and QRS complex prolongation with increasing potassium concentrations. In severe cases, hyperkalemia may lead to heart block, asystole, and ventricular tachycardia/fibrillation [ 42 ].
Algorithm for differential diagnosis of hyperkalemia, modified according to Yang et al. [ 43 ]. After excluding pseudohyperkalemia, urinary potassium wasting using TTKG and urine output volume are assessed to divide hyperkalemic children into three groups. Plasma aldosterone level is used to further discriminate individuals with reduced potassium wasting and adequate urine output. K- potassium, AKI- acute kidney injury, CKD- chronic kidney disease, PHA- pseudohypoaldosteronism, RTA- renal tubular acidosis, COX- cyclooxygenase, RAAS- renin–angiotensin–aldosterone-system, RBC- red blood cells, IV-intravenous, Osm-osmolality, TTGK- trans-tubular potassium gradient
The treatment of hyperkalemia involves a stepwise approach to stabilize the myocardium, drive potassium into cells, and remove excess potassium from the patient. Initially, to stabilize the myocardium, calcium chloride or gluconate is administered slowly as an intravenous push in severe hyperkalemia. Monitoring serum calcium levels after each dose is crucial to avoid potential hypercalcemia, with preference given to assessing serum ionized calcium levels alongside cardiac monitoring. Due to the short-lived effect, repeated doses may be necessary. To drive potassium into cells, a combination of dextrose plus insulin infusion is utilized and is considered one of the most potent treatments for hyperkalemia short of hemodialysis. This approach facilitates the intracellular shift of potassium in exchange for sodium, and careful insulin dosing is essential to prevent hypoglycemia [ 44 ]. In the presence of acidosis, the pH is increased through methods such as hyperventilation, NaHCO3 administration, or a combination of both. However, caution is exercised and bicarbonate should not be administered to patients with a pH exceeding 7.4. Repeated sodium bicarbonate administration may be complicated by hypernatremia, volume overload, and hypocalcemia [ 41 ]. Additionally, beta-2 agonists (salbutamol, albuterol) and sodium bicarbonate contribute to decreasing potassium levels by promoting the movement of potassium into cells [ 45 , 46 ].
To reduce the potassium load within the patient, it is advised to discontinue all dietary sources of exogenous potassium in meals, drinks, formulas, and potassium-raising medications. For the elimination of excess potassium, diuretics can increase potassium urinary excretion in children with preserved diuresis. Loop diuretics have the highest kaliuretic effect. The utilization of sodium polystyrene sulfonate (SPS), a sodium/potassium exchange resin, is also recommended. This can be administered either as an enema in 20% sorbitol or orally as a powder mixed with liquid. Enema administration is preferred for its higher effectiveness in inducing potassium losses through diarrhea. The typical dose of SPS is approximately 1 g/kg, resulting in a reduction of serum potassium by around 0.8 meq/L. To ensure efficacy, it is essential to retain the resin in place for at least half an hour. Potential complications of SPS administration include hypocalcemia, hypomagnesemia, sodium overload, and hypokalemia [ 47 ]. Therefore, when administering SPS orally, it is important to avoid concurrent use of laxatives and antacids. An additional cation exchange resin that can be used to eliminate potassium includes sodium polystyrene sulfonate and calcium polystyrene sulfonate. These exchange sodium or calcium for potassium within the large intestine. These resins are administered orally or rectally and can be used preferentially for patients with chronic hyperkalemia. Although they can bind up to 1 mmol of potassium per 1 g of resin, their administration may lead to electrolyte abnormalities and gastrointestinal disturbances as side effects. Currently, their use in acute hyperkalemia cases is not supported by high-quality evidence [ 48 ]. Various medical therapies for acute hyperkalemia are shown in Table 5 . In cases of persistent hyperkalemia despite conservative measures, renal replacement therapy is utilized, with hemodialysis being the preferred modality due to its rapid and immediate effectiveness.
Magnesium (Mg) is the second most prevalent intracellular cation within the human body. Nearly 60% of total magnesium is found in bones predominantly as surface substituents of hydroxyapatite. The majority of the remaining magnesium is distributed in skeletal muscle and soft tissue, with only about 1% residing in the extracellular compartment. Magnesium is an essential cofactor for more than 300 enzymatic reactions, especially those involving energy metabolism (ATP generation), DNA, and protein synthesis. Additionally, magnesium also maintains neuromuscular excitability, cardiac function, and regulates potassium and calcium homeostasis While most of the magnesium (55–70%) is in ionized form, 20–30% of magnesium is protein bound and the remaining magnesium (5–15%) is complexed with anions [ 49 ]. Gut absorption and kidney reabsorption/excretion are the main determinants of serum magnesium levels. Due to the binding of extracellular magnesium to serum albumin, measuring magnesium levels does not accurately represent the total magnesium stores in the body. Magnesium is vital for facilitating the movement of potassium, sodium, and calcium in and out of cells. The normal range of plasma magnesium concentration is around 0.62 to 1.1 mmol/L. The interplay between these ions is significant and abnormalities in the levels of these ions, such as low potassium and magnesium, can cause severe arrhythmias. Maintaining a balance of magnesium is intricately linked to achieving a balance in levels of sodium, calcium, and potassium [ 50 ].
Hypomagnesemia is characterized by a serum magnesium concentration below 0.62 mmol/L and is typically more common than hypermagnesemia. The condition typically arises from diminished magnesium absorption or heightened loss via the kidneys or diarrhea. Changes in thyroid hormone activity and the use of specific medications such as pentamidine, diuretics, and alcohol can also contribute to the development of hypomagnesemia. Table 6 shows the etiology of hypomagnesemia. Notably, hypomagnesemia can disrupt the impact of PTH and lead to hypocalcemia and hypokalemia. The manifestations of hypomagnesemia include muscle tremors, tetany, changes in mental state, ocular nystagmus, and cardiac arrhythmias like torsades de pointes. Additional symptoms may encompass seizures, dysphagia, vertigo, and ataxia [ 51 ]. A very useful tool to aid in the differential diagnosis of hypomagnesemia is a calculation of the fraction excretion of magnesium (FEMg). The formula for FEMg is (urine Mg x serum creatinine)/(serum Mg x urine creatinine) × 100 [ 52 ]. While values of < 2% indicate extrarenal losses, FEMg of > 2% points to the renal cause of Mg wasting [ 53 ]. The interpretation of magnesium levels and corresponding clinical symptoms is demonstrated in Table 7 . The management approach for hypomagnesemia depends on the severity and the patient’s clinical condition. Mild cases can be treated with oral replacement therapy, starting with doses of 400–800 mg of elemental magnesium daily, divided into multiple doses to reduce adverse effects and improve tolerance. However, in instances of severe or symptomatic hypomagnesemia, or if malabsorption is suspected as the underlying cause, parenteral therapy or intravenous magnesium replacement can be indicated. Intravenous administration of magnesium sulfate is typically employed with a dosage range of 25–50 mg/kg/dose (max. 2 g) every 4–6 h (or every 8 h in neonates) over a 2–4 h period, ensuring that the rate does not exceed 125 mg/kg/hr [ 54 ]. Notably, 10 ml of 10% magnesium sulfate solution contains 1 g of magnesium sulfate and 98.6 mg of elemental magnesium equivalent to 4.06 mmol. In patients with torsades de pointes and cardiac arrest, 50 mg/kg/dose (max. 2 g/dose) of IV push magnesium sulfate should be given over 10 min [ 55 ]. The maximum concentration of elementary magnesium should not exceed 60 mg/ml for peripheral line administration and 200 mg/ml overall. Dosing should be reduced in children with renal impairment to avoid magnesium accumulation. Additionally, calcium supplementation is often necessary because individuals with hypomagnesemia often exhibit hypocalcemia as well [ 51 , 53 , 54 ].
Hypermagnesemia is characterized by a serum magnesium concentration exceeding 1.1 mmol/L with renal failure being the most common cause. Other etiologies are associated with excessive oral or parenteral magnesium intake in cases of post-magnesium infusion for hypomagnesemia and parenteral nutrition. Additional causes can include tumor lysis syndrome and magnesium containing medication such as antacids and magnesium supplements. Neurological manifestations of hypermagnesemia encompass paralysis, drowsiness, ataxia, muscle weakness, and confusion. A moderate increase in magnesium levels can lead to vasodilation, however severe hypermagnesemia may result in hypotension. Excessively elevated serum magnesium levels can manifest as lowered levels of consciousness, hypoventilation, cardiac arrhythmias, bradycardia, and ultimately cardiopulmonary arrest [ 56 ]. Addressing hypermagnesemia involves using calcium administration to counteract elevated magnesium levels in the bloodstream as it can remove magnesium from serum. Additionally, it is crucial to identify and decrease the sources of magnesium intake. In severe cases, cardiorespiratory support may be required until magnesium levels are under control. The administration of intravenous calcium, such as calcium gluconate (100 mg/kg/dose, max. 3 g) or calcium chloride (20 mg/kg/dose, max. 1 g), is recommended [ 54 ]. This dosage can be repeated as necessary to correct life-threatening arrhythmias. For severe cases of hypermagnesemia, dialysis is the preferred treatment. In situations where renal and cardiovascular functions are normal, intravenous saline diuresis involving the administration of normal saline and furosemide can enhance renal magnesium excretion until dialysis is feasible. However, it is important to note that diuresis may enhance the excretion of calcium which can lead to hypocalcemia and exacerbation of the signs and symptoms of hypermagnesemia [ 50 ].
Calcium (Ca) is the most prevalent mineral in the body, playing crucial roles in various processes that rely on intracellular calcium concentration. These include enzymatic reactions, the contraction of muscles, cardiac function, aggregation of platelets, and receptor activation. The normal serum calcium levels vary with age and are depicted in Table 8 . Calcium is crucial for processes such as neuromuscular junction and bone strength. Most of the total calcium (99%) is in the bone tissue and the remaining less than 1% is in the extracellular fluid (ECF). Half of the ECF calcium is bound to albumin and the other half exists in its ionized, biologically active form. The regulation of calcium concentration is managed through vitamin D and PTH. A decrease in plasma calcium levels stimulates PTH secretion from the parathyroid glands, leading to increased bone resorption and subsequent release of calcium into the bloodstream. PTH additionally enhances calcium reabsorption in the kidneys by facilitating the production of 1,25-dihydroxyvitamin D. This active form of vitamin D enhances calcium and phosphate intestinal absorption and decreases renal excretion of these ions. Notably, 1,25-dihydroxyvitamin D also inhibits PTH synthesis. Calcitonin counteracts the action of vitamin D and PTH by inhibiting bone resorption and increasing renal calcium excretion, thus resulting in a reduction of calcium plasma levels. On the other hand, hypercalcemia causes decreased PTH secretion and inhibition of calcium release from bone tissue. Additionally, the total serum calcium level is directly linked to serum albumin concentration, with every 1 g/dL increase in serum albumin associated with a rise of 0.25 mmol/L in total serum calcium [ 57 ]. Conversely, with a decrease of 1 g/dL in serum albumin the total serum calcium will decrease by about 0.25 mmol/L. While total serum albumin is directly correlated to total serum calcium, there is an inverse relationship between ionized calcium and serum albumin. Clinically, a formula for adjusting total calcium for albumin is used: Adjusted Ca (mmol/L) = total Ca (mmol/L) + ({40—albumin (g/L)} × 0.02).
A decrease in serum albumin results in a higher proportion of total calcium existing in the ionized form. In instances of low albumin levels, despite a potential decrease in total calcium levels, the ionized calcium level may remain within the normal range. Additionally, calcium counteracts the actions of magnesium and potassium at the cell membrane. This ability allows it to be highly effective in addressing the consequences of both hypermagnesemia and hyperkalemia [ 50 ].
Hypocalcemia is caused by decreased gastrointestinal absorption, decreased bone resorption, or increased kidney Ca excretion. It can occur in various conditions such as disturbances in serum magnesium levels, toxic shock syndrome, tumor lysis syndrome, post-thyroid surgery, and fluoride poisoning. Hypocalcemia can be divided into four main categories: neonatal, with high PTH, with low PTH, and miscellaneous. These various categories are demonstrated in Table 9 . The main determinant of hypocalcemia is ionized calcium concentration. The onset of symptoms in hypocalcemia typically occurs when ionized levels drop to around a level of 0.63 mmol/L and present as tingling sensations in the extremities and face, carpopedal spasm, stridor, tetany, muscle cramps, and seizures. Patients may also exhibit hyperreflexia with positive Chvostek and Trousseau signs. Cardiac implications include reduced contractility and an increased risk of heart failure, while hypocalcemia can exacerbate digitalis toxicity. Prompt treatment of hypocalcemia involves administration of calcium, typically 10% calcium gluconate or calcium chloride. 1 ml of 10% calcium gluconate contains 100 mg of calcium gluconate, which is equivalent to 9.3 mg of elementary calcium [ 58 ]. Contrastingly, 1 ml of 10% calcium chloride contains 100 mg of calcium chloride which is equal to 27 mg of elementary calcium per milliliter. For acute symptomatic cases, give 20 mg/kg of elemental calcium IV over a 10–20 min period, which is approximately 2 ml/kg of 10% calcium gluconate or 0.7 ml/kg of 10% calcium chloride [ 58 ]. Follow this with an IV infusion of 200 mg/kg (or 500 mg/kg in neonates) of 10% calcium gluconate over 24 h [ 58 ]. Monitor serum calcium levels at intervals of 4 to 6 h to maintain a total serum calcium concentration within the range of 1.75 to 2.25 mmol/L. Any irregularities in magnesium, potassium, and pH should be addressed as well. One thing to note is that untreated hypomagnesemia can render hypocalcemia resistant to treatment. Hence, it is crucial to assess serum magnesium levels when dealing with hypocalcemia, especially if the condition does not respond adequately to the initial calcium therapy [ 50 ].
Hypercalcemia can be divided based on severity (serum total Ca levels) to mild (< 3 mmol/L), moderate (3—3.5 mmol/L) and severe (> 3.5 mmol/L) [ 59 ]. It may be caused by increased bone resorption, increased gastrointestinal Ca absorption, or decreased renal Ca excretion. Approximately 90% of reported cases stem from primary hyperparathyroidism and malignancy. In these instances, there is an increased release of calcium from the bones and intestines, typically accompanied by potential impairment in renal clearance [ 60 ]. Generally, the causes of hypercalcemia may be divided into two categories- PTH-mediated and non-PTH-mediated. The various causes of hypercalcemia are depicted in Table 10 . The onset of hypercalcemia related symptoms typically occurs when the total serum calcium concentration ranges from 3 to 3.75 mmol/L. At lower levels, individuals may experience neurologic symptoms such as depression, fatigue, and confusion. Higher levels can lead to more severe manifestations, including hallucinations, seizures, disorientation, and hypotonicity. Hypercalcemia also disrupts the kidney’s ability to concentrate urine, potentially resulting in diuresis and subsequent dehydration [ 61 ]. The cardiovascular symptoms associated with hypercalcemia can be variable. Initially, there may be an increase in myocardial contractility until the calcium levels reach around 3.75 mmol/L. Beyond this threshold, myocardial depression occurs which can lead to decreased automaticity and shortened ventricular systole. Arrhythmias may result from a shortened refractory period. Additionally, hypercalcemia has the potential to exacerbate digitalis toxicity and contribute to hypertension. A significant number of individuals with hypercalcemia experience hypokalemia, and these conditions can collectively cause cardiac arrhythmias [ 62 ]. As the serum calcium surpasses 3.25 mmol/L, there is a typical shortening of the QT interval, accompanied by prolonged QRS and PR intervals as well. The progression of these abnormalities may lead to the development of atrioventricular block, which can lead to complete heart block. In severe instances, cardiac arrest can occur when the total serum calcium reaches 3.75 to 5 mmol/L. Additionally, hypercalcemia manifests gastrointestinal symptoms such as pancreatitis, constipation, dysphagia, and peptic ulcers. Renal effects involve a reduced capacity to concentrate urine which can result in diuresis and subsequent loss of crucial ions [ 60 ]. The clinical manifestations and interpretation of hypercalcemia levels are summarized in Table 11 .
For symptomatic hypercalcemia, typically when the total serum concentration is around 3 mmol/L or when the calcium level exceeds 3.74 mmol/L, immediate treatment is necessary. The primary focus is on restoring intravascular volume and facilitating calcium urine excretion. In patients with sufficient renal and cardiovascular function, this is achieved by administering 0.9% saline allowing for serum calcium dilution and urinary calcium excretion [ 63 ]. The infusion continues until any fluid deficit is addressed and adequate diuresis is established. Throughout this treatment, closely monitor and sustain appropriate levels of potassium and magnesium due to the diuresis potentially causing deficiencies. Loop diuretics also increase calcium excretion, but should be used with caution because they may contribute to intravascular dehydration. Calcitonin may be used transiently (max. 48–72 h) due to the risk of tachyphylaxis [ 64 ]. Intravenous bisphosphonates are potent inhibitors of bone resorption, effectively lowering serum calcium levels. Denosumab can be used in patients with contraindications for bisphosphonates (e.g. chronic kidney disease). Glucocorticoids are also effective in reducing calcium levels, particularly in granulomatous disease [ 63 ]. In cases where there is a need for a rapid reduction in serum calcium, especially in patients with renal or cardiac dysfunction, hemodialysis is the preferred treatment. For severe conditions, chelating agents like 50 mmol of phosphate administered orally over 8 to 12 h or EDTA at a dose of 10 to 50 mg/kg over 4 h may be employed [ 63 ].
Following calcium, phosphorous is the most abundant essential mineral in the human body. Phosphate has various functions for the body including endochondral ossification, teeth, cellular functions, and bone mineralization. Nearly 80 to 90% of phosphorous is found in bones and teeth as hydroxyapatite and the rest is distributed across the extracellular fluid (ECF), soft tissues, and red blood cells [ 65 ]. Phosphate is freely filtered by the glomerulus at a rate of about 13 mg/kg/day in a healthy individual and approximately 60% to 70% of the filtered phosphate is reabsorbed in the proximal tubule [ 65 ]. This reabsorption process relies on a sodium-gradient dependent mechanism and involves various cotransporters. Serum phosphate levels are influenced by various factors such as the release of phosphate from bones, excretion by kidneys, and dietary intake. Three key hormones regulate phosphate homeostasis within the body: Vitamin D (1,25- dihydroxycholecalciferol), PTH, and fibroblast growth factor 23 (FGF-23) [ 66 ]. In the intestines, 1,25-dihyroxy vitamin D boosts phosphate uptake by increasing the expression of sodium phosphate cotransporters. On the other hand, FGF-23 is secreted by osteoblasts and osteocytes in response to elevated serum phosphate levels, ultimately reducing intestinal phosphate absorption by inhibiting the production of active vitamin D. In states of high serum phosphate levels, PTH is released to promote phosphate excretion by causing the internalization of various sodium phosphate cotransporters. Additionally, FGF-23 can reduce phosphate reabsorption within the proximal tubules by inhibiting transport proteins [ 66 ]. Hyperphosphatemia is defined as serum phosphate levels exceeding 1.45 mmol/L and can have various etiologies including external sources such as laxatives containing phosphate, vitamin D toxicity, endogenous sources including rhabdomyolysis and tumor lysis syndrome. Reduced phosphate excretion, most commonly due to kidney failure, or other conditions such as hypoparathyroidism and pseudohypoparathyroidism can also contribute to elevated phosphate levels [ 65 ]. Hyperphosphatemia can lead to symptoms associated with hypocalcemia due to the excessive binding of phosphate ions with calcium which results in decreased serum calcium levels. This can manifest as tetany, neurological symptoms, and muscle cramps [ 66 ]. Management of hyperphosphatemia focuses on identifying and treating the underlying cause. For patients with kidney failure, decreasing phosphate intake through phosphate binders is important to reduce the absorption of phosphate within the gastrointestinal tract. In patients with normal renal function, enhancing phosphate excretion can be accomplished by administering saline along with loop diuretics [ 67 ]. Hypophosphatemia is characterized by serum phosphate levels below 0.81 mmol/L and can arise from various causes such as reduced dietary intake due to malabsorption, malnutrition, and vitamin D deficiency. Additionally, it can be caused by increased phosphate excretion in cases of hyperparathyroidism, forced saline diuresis or genetic disorders affecting the proximal tubules [ 66 ]. Refeeding syndrome is another cause of hypophosphatemia that can lead to symptoms such as arrhythmias, muscle weakness, and seizures. Managing hypophosphatemia requires treating the root cause of the condition and providing phosphate supplementation [ 66 ].
Electrolyte abnormalities in children can present diverse challenges in clinical management and various factors must be understood for effective management. Distinguishing between acute and chronic electrolyte abnormalities is important in the approach for treatment. Acute imbalances may require immediate correction to prevent complications whereas chronic imbalances may need a more gradual correction, especially in cases to prevent osmotic demyelination syndrome [ 68 ]. Additionally, when a SEA is detected, physicians must be aware for potential errors in sampling or processing by considering the clinical context. This can be achieved through repeating tests to confirm the imbalance and once detected, the treatment should depend on the severity of the SEA. To ensure the detection of SEAs, physicians should have a high index of suspicion in cases involving high risk groups such as critically ill patients or those receiving intravenous fluids. Addressing these various factors can help improve overall patient management and outcomes.
Electrolyte imbalances are common in children and may cause life-threatening emergencies. Early identification of SEA and understanding of their pathophysiology is essential for adequate treatment. Adhering to safe correction limits and appropriate electrolyte monitoring is vital to prevent damage to the patient. The diagnosis is based on the history, physical examination, and laboratory tests. Medications are often responsible for changes in serum electrolytes. Therapy algorithms and treatment protocols should be available for clinicians to avoid inappropriate therapeutic measures.
Not applicable
No datasets were generated or analysed during the current study.
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No conflicts of interest, financial or otherwise, are declared by the authors.
This work was supported by the Ministry of Health of the Czech Republic (Conceptual Development of Research Organization, Motol University Hospital, Prague, Czech Republic, 00064203).
Rupesh Raina
Present address: Northeast Ohio Medical University, Rootstown, OH, USA
Department of Pediatrics, Second Faculty of Medicine, Charles University and Motol University Hospital, Prague, Czech Republic
Northeast Ohio Medical University, Rootstown, OH, USA
Shaarav Ghose
Department of Pediatric Nephrology, Akron Children’s Hospital, Cleveland, OH, USA
Cleveland Clinic, Akron General Medical Center, Akron, OH, USA
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Zieg, J., Ghose, S. & Raina, R. Electrolyte disorders related emergencies in children. BMC Nephrol 25 , 282 (2024). https://doi.org/10.1186/s12882-024-03725-5
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The agricultural sector and farming households in less developed economies, particularly in Asia, are becoming more vulnerable to climate change. Climate-stimulated reduction of farming yields leads to less income, weakened food security, and, eventually, poverty. Thus, the adaptation strategies of Asian farming communities are critical to achieving various Sustainable Development Goals (SDGs), including but not limited to Goals 1 (No Poverty), 2 (Zero Hunger), 8 (Decent Work and Economic Growth), and 13 (Climate Action). This chapter reviews existing and potential adaptation strategies for risk-prone farming communities in Asia against climate change. Systematically, this study employs a PRISMA-guided approach to retrieve the most relevant documents from the Web of Science™ and Scopus® databases published between January 2015 and December 2021. This chapter restricts its criteria to review any adaptation strategy practiced by farmers and their communities in Asia against climate change and climate-induced hazards. Conducted in January 2022, the searches and selection gathered 63 documents as review materials. Applying content analysis to the selected articles reveals that adaptation strategies are the cushions of farming communities against the adverse effects of climate change in Asia, including floods, droughts, and riverbank erosions. There are five key areas for practicing adaptation strategies, i.e., livelihood diversification, agricultural diversification, risk management, land/crop management, and farm and income management. This study synthesizes the findings as transformative, systemic, and systematic adaptation strategies to showcase their applicability to the agricultural sector in Asia. Given adequate effort and support, the five key areas in three dimensions would strengthen the fundamental characteristics of Asian farming communities to meet the relevant SDGs.
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Md Nazirul I. Sarker and Corinthias P. M. Sianipar contributed equally to this work.
School of Political Science and Public Administration, Neijiang Normal University, Sichuan, China
Md Nazirul I. Sarker
Organization for the Strategic Coordination of Research and Intellectual Properties, Meiji University, Kanagawa, Japan
Md Lamiur Raihan
Graduate School of Global Environmental Studies, Kyoto University, Kyoto, Japan
Tahmina Chumky
Graduate School of Agriculture, Kyoto University, Kyoto, Japan
Md Habibur Rahman
Faculty of Agricultural Economics and Rural Development, Bangabandhu Sheikh Mujibur Rahman Agricultural University, Gazipur, Bangladesh
G. M. Monirul Alam
School of Commerce, University of Southern Queensland, Darling Heights, QLD, Australia
Department of Global Ecology, Kyoto University, Kyoto, Japan
Corinthias P. M. Sianipar
Division of Environmental Science and Technology, Kyoto University, Kyoto, Japan
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European School of Sustainability Science and Research, Hamburg University of Applied Sciences, Hamburg, Germany
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Centre for Global Sustainability Studies, Universiti Sains Malaysia, Minden, Malaysia
Theam Foo Ng
School of Property, Construction and Project Management, RMIT University, Melbourne, VIC, Australia
Usha Iyer-Raniga
Centre for Sustainable Business, International Business University, Toronto, ON, Canada
Network for Education and Research on Peace and Sustainability and Graduate School of Humanities and Social Sciences, Hiroshima University, Higashi, Hiroshima, Japan
Ayyoob Sharifi
School of Education and Social Work, University of Dundee, Dundee, United Kingdom
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Sarker, M.N.I., Raihan, M.L., Chumky, T., Rahman, M.H., Alam, G.M.M., Sianipar, C.P.M. (2024). Adaptation Strategies for Asian Farmers Against Climate Change. In: Leal Filho, W., Ng, T.F., Iyer-Raniga, U., Ng, A., Sharifi, A. (eds) SDGs in the Asia and Pacific Region. Implementing the UN Sustainable Development Goals – Regional Perspectives. Springer, Cham. https://doi.org/10.1007/978-3-031-17463-6_122
DOI : https://doi.org/10.1007/978-3-031-17463-6_122
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