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The Cochrane Database of Systematic Reviews logoLink to The Cochrane Database of Systematic Reviews
. 2019 May 10;2019(5):CD013330. doi: 10.1002/14651858.CD013330

Non‐pharmacological interventions for preventing clotting of extracorporeal circuits during continuous renal replacement therapy

Sho Miki 1,✉, Yasushi Tsujimoto 2, Hiroki Shimada 3, Hiraku Tsujimoto 4, Hideto Yasuda 5, Yuki Kataoka 6, Tomoko Fujii 7
PMCID: PMC6509356

Abstract

This is a protocol for a Cochrane Review (Intervention). The objectives are as follows:

This review will aim to assess the efficacy, safety, and effectiveness of non‐pharmacological measures to maintain circuit patency in CRRT.

Background

Description of the condition

Acute kidney injury (AKI) is an abrupt decline in kidney function defined by increased creatinine levels and oliguria or decreased output of urine (KDIGO 2012). AKI occurs in nearly half of patients admitted to the intensive care unit (ICU) and is related to increased death (Bouchard 2015; Fujii 2018; Hoste 2015; Nisula 2013). When patients have severe AKI, renal replacement therapy (RRT) is required to manage electrolytes, fluid balance, and waste products. The need for RRT accounts for 16% to 24% of patients with AKI admitted to the ICU (Fujii 2018; Nisula 2013).

There are several modalities to administer RRT intermittently or continuously. Although intermittent RRT removes fluids rapidly, it has been suggested to cause hypotension and further damage to kidney function (Manns 1997; Silversides 2014). Furthermore, deranged electrolyte levels, which are frequently observed in AKI, are normalised more successfully when RRT is administered continuously than when it is administered intermittently (Uchino 2003). Accordingly, continuous RRT (CRRT) is recommended for haemodynamically unstable patients and is used most frequently in the ICU (Bouchard 2015; Fujii 2018; KDIGO 2012). A multinational survey conducted in 33 countries showed that 75.2% of RRT sessions were conducted with CRRT (Hoste 2015).

The choice of modalities of CRRT varies worldwide. A large international observational study showed that critically ill patients are frequently treated with continuous venovenous haemofiltration (CVVH) (Uchino 2007). This practice pattern might imply that intensivists expect convection for the removal of larger molecules to be more efficient than a diffusion‐based modality, i.e. continuous venovenous haemodialysis (CVVHD). However, a small observational study showed comparable small and mid‐sized molecular solute removal between CVVH and CVVHD (Ricci 2006).

CRRT is typically provided through a double lumen venous catheter as a continuous 24‐hour therapy; however, it is known that CRRT operates 21 to 23 hours/day in actual clinical settings (Mehta 2001; Uchino 2003; Vesconi 2009). The reasons for the interruption of CRRT could be clotting of the circuit, clogging of the membrane, or transport to outside of the ICU, such as to the operation theatre or for radiological imaging tests. Such treatment interruptions decrease the delivered CRRT dose, leading to insufficient uraemic control (Fealy 2002; Mitchell 2003). A small single‐centre study indicated that circuit clotting was the primary reason for the shortened circuit life (Venkataraman 2002). Undoubtedly, exchanging the circuits due to circuit failure leads to increased medical costs and workloads of healthcare professionals (Fealy 2002; Mehta 2001).

Description of the intervention

A major intervention to maintain the patency of the CRRT circuit is anticoagulation. However, a multicentre clinical trial showed that half of the critically ill patients were treated with CRRT without any anticoagulant drugs (RENAL Replacement Therapy Study Investigators 2009). This might be because anticoagulation therapy increases the risk of bleeding, which frequently occurs in critically ill patients. Given the importance of circuit maintenance without anticoagulants and an ongoing systematic review of pharmacological interventions in CRRT (Tsujimoto 2016), this review will focus on non‐pharmacological strategies for circuit survival.

The clotting of CRRT circuits is attributed to stasis or turbulence of blood flow, haemoconcentration, or activation of the intrinsic coagulation system by blood–tube, blood–air, or blood–filter contact (RENAL Replacement Therapy Study Investigators 2000; RENAL Replacement Therapy Study Investigators 2009). Therefore, non‐pharmacological interventions to prevent clotting of the CRRT circuit include the strategic selection of a catheter or access site, optimising the blood flow rate, CRRT modalities, and methods of haemodilution.

How the intervention might work

The selection of a catheter and access site may play a significant role in determining the circuit life. Considering Poiseuille's law, a thick and short catheter may be theoretically preferable to avoid stasis of blood flow. To avoid kinking or curving of the catheter, which may cause impaired blood flow, the right jugular venous route may be preferable as it is straight and easily monitored by bedside nurses.

In CRRT, blood flow rates are typically set as 100 to 200 mL/min. In fact, the pump used in CRRT delivers blood with peristaltic revolutions, and the flow rate is the rate of the pump revolution. An observational study revealed that there is forward and backward blood flow between the pump and filter, which may cause stasis of the blood flow (Baldwin 2004). Considering the fluctuations of the blood flow due to the peristaltic roller pump, maintaining the blood flow at a high rate may be useful to prevent the filter from clotting.

Regarding choice of CRRT modalities, filtration may shorten the circuit lifetime compared to dialysis by haemoconcentrations due to its ultrafiltration process (Ricci 2006). During filtration, haematocrit levels increase and raise the risk of coagulation in the filter. In CVVH and CVVHDF, substitution fluids can be administered before (predilution) or after (postdilution) filtration. Predilution CRRT aims to decrease haemoconcentrations and improve the blood flow rheologically. However, predilution possibly reduces the molecular clearance, while the clinical impact is not evident in critically ill patients.

Why it is important to do this review

Circuit failure during CRRT affects the actual operation time of CRRT, which leads to the decreased efficiency of the treatment. Moreover, it increases the medical cost and adds to workloads. Thus, maintaining the patency of the CRRT circuit is crucial in the ICU. This review will provide a clinically relevant body of evidence to assist healthcare professionals in their choice of methods to deliver CRRT.

Objectives

This review will aim to assess the efficacy, safety, and effectiveness of non‐pharmacological measures to maintain circuit patency in CRRT.

Methods

Criteria for considering studies for this review

Types of studies

We will include in this review all randomised controlled trials (RCTs) and quasi‐RCTs (RCTs in which allocation to treatment was obtained by alternation, use of alternate medical records, date of birth or other predictable methods) of non‐pharmacological interventions for preventing clotting of extracorporeal circuits during CRRT. We will include studies that provide anticoagulation or sedative agents to both intervention and control arms according to a predefined protocol.

Types of participants

Inclusion criteria

We will include all AKI patients receiving CRRT in the ICU regardless of age or sex. In this review, AKI is defined according to the KDIGO definition and staging system (KDIGO 2012).

Exclusion criteria

None.

Types of interventions

We will include the following comparisons of interventions for CRRT.

  1. Internal jugular access versus femoral access

  2. Left‐sided catheters versus right‐sided catheters

  3. Subclavian venous versus superior vena cava as the line tip portion in the same access catheter insertion site

  4. Subclavian venous versus right atrium as the line tip portion in the same access catheter insertion site

  5. Superior vena cava versus right atrium as the line tip portion in the same access catheter insertion site

  6. Long catheter (> 20 cm) versus short catheter (≤ 20 cm)

  7. Pre‐dilution versus post‐dilution as defined by study investigators

  8. Higher blood flow (≥ 250 mL/min) versus standard blood flow (< 250 mL/min)

  9. Saline flushing versus no saline flushing

  10. CVVHD versus CVVH or CVVHDF

  11. Polyethyleneimine treatment of the AN69 membrane (AN69ST) versus other membrane

  12. Heparin‐grafted membrane (HGM) versus other membrane

  13. Single‐site infusion anticoagulation versus double‐site infusion anticoagulation

  14. Infusion anticoagulation from access line versus pre‐filter single site.

Types of outcome measures

Primary outcomes

  • Circuit life span (commences on starting CRRT and concludes at the circuit cessation for any reason).

  • Death: death from any cause at day 28 of follow‐up.

Secondary outcomes

  • Recovery of kidney function: numbers of participants free of RRT at day 28, 90, and 180 of follow‐up

  • Vascular access complications: includes function (e.g. ability to use CRRT, uninterrupted use without the need for any intervention, percentage change in access blood flow), or infections requiring antibiotic therapy suspected to be catheter related

  • Cost to health care services

  • Types and number of dialysis filters, circuits, and catheters

  • Consumption of dialysate

All costs will be reported in international monetary units

Search methods for identification of studies

Electronic searches

We will search the Cochrane Kidney and Transplant Register of Studies with assistance from the Information Specialist using search terms relevant to this review. The Register contains studies identified from the following sources.

  1. Monthly searches of the Cochrane Central Register of Controlled Trials (CENTRAL)

  2. Weekly searches of MEDLINE OVID SP

  3. Handsearching of kidney‐related journals and the proceedings of major kidney conferences

  4. Searching of the current year of EMBASE OVID SP

  5. Weekly current awareness alerts for selected kidney and transplant journals

  6. Searches of the International Clinical Trials Register (ICTRP) Search Portal and ClinicalTrials.gov.

Studies contained in the Register are identified through searches of CENTRAL, MEDLINE, and EMBASE based on the scope of Cochrane Kidney and Transplant. Details of these strategies, as well as a list of handsearched journals, conference proceedings and current awareness alerts, are available on the Cochrane Kidney and Transplant website.

See Appendix 1 for search terms used in strategies for this review.

Searching other resources

  1. Reference lists of review articles, relevant studies and clinical practice guidelines.

  2. Contact experts/organisations in the field seeking information about unpublished or incomplete studies.

  3. Grey literature sources (e.g. abstracts, dissertations and theses), additional to those already included in the Cochrane Kidney and Transplant Register of Studies, will not be searched.

Data collection and analysis

Selection of studies

The search strategy described will be used to obtain titles and abstracts of studies that may be relevant to the review. The titles and abstracts will be screened independently by two authors, who will discard studies that are not applicable, however, studies and reviews that might include relevant data or information on studies will be retained initially. Two authors will independently assess retrieved abstracts and, if necessary, the full text of these studies to determine which studies satisfy the inclusion criteria. Any disagreement will be resolved by discussion with another author acting as an arbiter.

Data extraction and management

Data extraction will be carried out independently by two authors using standard data extraction forms. Any disagreement will be resolved by discussion with another author acting as an arbiter. Studies reported in non‐English language journals will be translated before assessment. Where more than one publication of one study exists, reports will be grouped together and the publication with the most complete data will be included. Any discrepancy between published protocols and final reports will be highlighted.

Assessment of risk of bias in included studies

The following items will be independently assessed by two authors using the risk of bias assessment tool (Higgins 2011) (see Appendix 2). Any disagreement will be resolved by discussion with another author acting as an arbiter. We assumed that the use of anticoagulation is an important co‐intervention in this review. We will judge how the imbalance of anticoagulation affects treatment estimates in other bias domain.

  • Was there adequate sequence generation (selection bias)?

  • Was allocation adequately concealed (selection bias)?

  • Was knowledge of the allocated interventions adequately prevented during the study?

    • Participants and personnel (performance bias)

    • Outcome assessors (detection bias)

  • Were incomplete outcome data adequately addressed (attrition bias)?

  • Are reports of the study free of suggestion of selective outcome reporting (reporting bias)?

  • Was the study apparently free of other problems that could put it at a risk of bias (e.g. co‐intervention of anticoagulation)?

Measures of treatment effect

For dichotomous outcomes (e.g. death or recovery of kidney function) results will be expressed as risk ratio (RR) with 95% confidence intervals (CI). Where continuous scales of measurement are used to assess the effects of treatment (e.g. circuit life span, cost or fatigue), the mean difference (MD) will be used, or the standardised mean difference (SMD) if different scales have been used.

Unit of analysis issues

We will assess unit of analysis issues in the included studies in three possible ways in which they may arise.

Clustering at the level of the enrolled units in cluster‐randomised studies

In dealing with cluster‐RCTs, for dichotomous data, we will apply the design effect and calculate effective sample size and number of events using the intracluster correlation coefficient (ICC) among each unit and the average cluster size, as described in Chapter 16.3.5 of the Cochrane Handbook (Higgins 2011). If the ICC has not been reported, we will use the ICC of a similar study as a substitute. For continuous data, only the sample size will be reduced; means and standard deviation will remain unchanged (Higgins 2011).

Randomised cross‐over studies

We will consider only data from the first period.

Multiple comparisons

All intervention groups that are relevant to this review will be included.

Dealing with missing data

Any further information required from the original author will be requested by written correspondence (e.g. emailing and/or writing to corresponding author/s) and any relevant information obtained in this manner will be included in the review. Evaluation of important numerical data, such as screened, randomised patients as well as intention‐to‐treat, as‐treated and per‐protocol populations, will be carefully performed. Attrition rates, for example drop‐outs, losses to follow‐up and withdrawals, will be investigated. Issues of missing data and imputation methods (for example, last‐observation‐carried‐forward) will be critically appraised (Higgins 2011).

Assessment of heterogeneity

We will first assess the heterogeneity by visual inspection of the forest plot. We will quantify statistical heterogeneity using the I2 statistic, which describes the percentage of total variation across studies that is due to heterogeneity rather than sampling error (Higgins 2003). A guide to the interpretation of I2 values will be as follows.

  • 0% to 40%: might not be important

  • 30% to 60%: may represent moderate heterogeneity

  • 50% to 90%: may represent substantial heterogeneity

  • 75% to 100%: considerable heterogeneity.


The importance of the observed value of I2 depends on the magnitude and direction of treatment effects and the strength of evidence for heterogeneity (e.g. P‐value from the Chi2 test, or a confidence interval for I2) (Higgins 2011).

Assessment of reporting biases

We will create and examine a funnel plot. If we are able to pool more than 10 studies, we will use Egger's test to explore possible small study and publication biases (Egger 1997).

Data synthesis

Data will be pooled using a random effects model but a fixed‐effect model will also be used to ensure robustness of the model chosen and susceptibility to outliers.

Subgroup analysis and investigation of heterogeneity

Subgroup analysis will be used to explore possible sources of heterogeneity. Heterogeneity among participants could be related to age (<18 years, ≥18 years), prior condition (presence or absence of sepsis) (Levi 2013), or pharmacological intervention (citrate, unfractionated heparin, other anticoagulation, no anticoagulation). Adverse effects will be tabulated and assessed with descriptive techniques, as they are likely to be different for the various agents used. Where possible, the risk difference with 95% CI will be calculated for each adverse effect, either compared to no treatment or to another agent.

Sensitivity analysis

We will perform sensitivity analyses in order to explore the influence of the following factors on effect size.

  • Repeating the analysis excluding unpublished studies

  • Repeating the analysis taking account of risk of bias, as specified

  • Repeating the analysis excluding any very long or large studies to establish how much they dominate the results

  • Repeating the analysis excluding studies using the following filters: diagnostic criteria, language of publication, source of funding (industry versus other), and country

  • Repeating the analysis restricting studies using same dosage of anticoagulation in both intervention and control arms.

'Summary of findings' tables

We will present the main results of the review in 'Summary of findings' tables. These tables present key information concerning the quality of the evidence, the magnitude of the effects of the interventions examined, and the sum of the available data for the main outcomes (Schünemann 2011a). The 'Summary of findings' tables also include an overall grading of the evidence related to each of the main outcomes using the GRADE (Grades of Recommendation, Assessment, Development and Evaluation) approach (GRADE 2008; GRADE 2011). The GRADE approach defines the quality of a body of evidence as the extent to which one can be confident that an estimate of effect or association is close to the true quantity of specific interest. The quality of a body of evidence involves consideration of within‐trial risk of bias (methodological quality), directness of evidence, heterogeneity, precision of effect estimates and risk of publication bias (Schünemann 2011b). We plan to present the following outcomes in the 'Summary of findings' tables.

  • Circuit life span

  • Death from any cause at day 28

  • Recovery of kidney function

  • Vascular access complications.

Acknowledgements

We wish to thank the Cochrane Kidney and Transplant Group for their support, especially Fiona Russell and Gail Higgins. We wish to thank Emma Barber and the Cochrane Japan Centre for English editing.

Appendices

Appendix 1. Electronic search strategies

Database Search terms
CENTRAL

  1. "continuous venovenous h$emodialysis" or CVVHD:ti,ab,kw (Word variations have been searched)

  2. "continuous venovenous h$emodiafiltration" or CVVHDF:ti,ab,kw (Word variations have been searched)

  3. pre‐dilution or post dilution:ti,ab,kw (Word variations have been searched)

  4. (femoral or jugular) and catheter*:ti,ab,kw (Word variations have been searched)

  5. blood flow*:ti,ab,kw (Word variations have been searched)

  6. saline flush*:ti,ab,kw (Word variations have been searched)

  7. blood air contact*:ti,ab,kw (Word variations have been searched)

  8. membrane*:ti,ab,kw (Word variations have been searched)

  9. length and catheter*:ti,ab,kw (Word variations have been searched)

  10. {or #1‐#9}

  11. circuit*:ti,ab,kw (Word variations have been searched)

  12. prevent* and (clotting or clot*):ti,ab,kw (Word variations have been searched)

  13. {or #11‐#12}

  14. {and #10, #13}
MEDLINE

  1. Renal Replacement Therapy/

  2. Renal Dialysis/

  3. exp Hemofiltration/

  4. Ultrafiltration/

  5. (continuous venovenous h$emofiltration or CVVH).tw.

  6. (continuous venovenous h$emodialysis or CVVHD).tw.

  7. (continuous venovenous h$emodiafiltration or CVVHDF).tw.

  8. continuous renal replacement.tw.

  9. crrt.tw.

  10. (slow continuous ultrafiltration or SCUF).tw.

  11. exp Acute Kidney Injury/

  12. (acute kidney failure or acute renal failure).tw.

  13. (acute kidney injur$ or acute renal injur$).tw.

  14. (acute kidney insufficie$ or acute renal insufficie$).tw.

  15. acute tubular necrosis.tw.

  16. (ARI or AKI or ARF or AKF or ATN).tw.

  17. or/1‐16

  18. pre‐dilution.tw.

  19. post‐dilution.tw.

  20. flush$.tw.

  21. blood air contact.tw.

  22. venous bubble$.tw.

  23. air‐trap.tw.

  24. Catheters/

  25. Membranes, Artificial/

  26. membrane$.tw.

  27. blood flow$.tw.

  28. Equipment Failure/

  29. Equipment Design/

  30. Blood Flow Velocity/

  31. (femoral or jugular).tw.

  32. saline flush$.tw.

  33. or/18‐32

  34. and/17,33
EMBASE

  1. exp continuous renal replacement therapy/

  2. (continuous venovenous h$emofiltration or CVVH).tw.

  3. (continuous venovenous h$emodialysis or CVVHD).tw.

  4. (continuous venovenous h$emodiafiltration or CVVHDF).tw.

  5. (slow continuous ultrafiltration or SCUF).tw.

  6. acute kidney failure/

  7. acute kidney tubule necrosis/

  8. (acute kidney failure or acute renal failure).tw.

  9. (acute kidney injur$ or acute renal injur$).tw.

  10. (acute kidney insufficie$ or acute renal insufficie$).tw.

  11. acute tubular necrosis.tw.

  12. (ARI or AKI or ARF or AKF or ATN).tw.

  13. or/6‐12

  14. pre dilution.tw.

  15. post dilution.tw.

  16. exp catheter/

  17. (jugular$ and access).tw.

  18. (femoral$ and access).tw.

  19. length.tw.

  20. or/17‐19

  21. and/16,20

  22. blood flow velocity/

  23. saline flush$.tw.

  24. (continuous venovenous h$emodiafiltration or CVVHDF).tw.

  25. (continuous venovenous h$emodialysis or CVVHD).tw.

  26. blood air contact.tw.

  27. air‐trap.tw.

  28. dialysis membrane/ or "filters and membranes"/

  29. or/14‐15,21‐28

  30. and/13,29
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Appendix 2. Risk of bias assessment tool

Potential source of bias Assessment criteria
Random sequence generation
Selection bias (biased allocation to interventions) due to inadequate generation of a randomised sequence		 Low risk of bias: Random number table; computer random number generator; coin tossing; shuffling cards or envelopes; throwing dice; drawing of lots; minimisation (minimisation may be implemented without a random element, and this is considered to be equivalent to being random).
High risk of bias: Sequence generated by odd or even date of birth; date (or day) of admission; sequence generated by hospital or clinic record number; allocation by judgement of the clinician; by preference of the participant; based on the results of a laboratory test or a series of tests; by availability of the intervention.
Unclear: Insufficient information about the sequence generation process to permit judgement.
Allocation concealment
Selection bias (biased allocation to interventions) due to inadequate concealment of allocations prior to assignment		 Low risk of bias: Randomisation method described that would not allow investigator/participant to know or influence intervention group before eligible participant entered in the study (e.g. central allocation, including telephone, web‐based, and pharmacy‐controlled, randomisation; sequentially numbered drug containers of identical appearance; sequentially numbered, opaque, sealed envelopes).
High risk of bias: Using an open random allocation schedule (e.g. a list of random numbers); assignment envelopes were used without appropriate safeguards (e.g. if envelopes were unsealed or non‐opaque or not sequentially numbered); alternation or rotation; date of birth; case record number; any other explicitly unconcealed procedure.
Unclear: Randomisation stated but no information on method used is available.
Blinding of participants and personnel
Performance bias due to knowledge of the allocated interventions by participants and personnel during the study		 Low risk of bias: No blinding or incomplete blinding, but the review authors judge that the outcome is not likely to be influenced by lack of blinding; blinding of participants and key study personnel ensured, and unlikely that the blinding could have been broken.
High risk of bias: No blinding or incomplete blinding, and the outcome is likely to be influenced by lack of blinding; blinding of key study participants and personnel attempted, but likely that the blinding could have been broken, and the outcome is likely to be influenced by lack of blinding.
Unclear: Insufficient information to permit judgement
Blinding of outcome assessment
Detection bias due to knowledge of the allocated interventions by outcome assessors		 Low risk of bias: No blinding of outcome assessment, but the review authors judge that the outcome measurement is not likely to be influenced by lack of blinding; blinding of outcome assessment ensured, and unlikely that the blinding could have been broken.
High risk of bias: No blinding of outcome assessment, and the outcome measurement is likely to be influenced by lack of blinding; blinding of outcome assessment, but likely that the blinding could have been broken, and the outcome measurement is likely to be influenced by lack of blinding.
Unclear: Insufficient information to permit judgement
Incomplete outcome data
Attrition bias due to amount, nature or handling of incomplete outcome data.		 Low risk of bias: No missing outcome data; reasons for missing outcome data unlikely to be related to true outcome (for survival data, censoring unlikely to be introducing bias); missing outcome data balanced in numbers across intervention groups, with similar reasons for missing data across groups; for dichotomous outcome data, the proportion of missing outcomes compared with observed event risk not enough to have a clinically relevant impact on the intervention effect estimate; for continuous outcome data, plausible effect size (difference in means or standardised difference in means) among missing outcomes not enough to have a clinically relevant impact on observed effect size; missing data have been imputed using appropriate methods.
High risk of bias: Reason for missing outcome data likely to be related to true outcome, with either imbalance in numbers or reasons for missing data across intervention groups; for dichotomous outcome data, the proportion of missing outcomes compared with observed event risk enough to induce clinically relevant bias in intervention effect estimate; for continuous outcome data, plausible effect size (difference in means or standardized difference in means) among missing outcomes enough to induce clinically relevant bias in observed effect size; ‘as‐treated’ analysis done with substantial departure of the intervention received from that assigned at randomisation; potentially inappropriate application of simple imputation.
Unclear: Insufficient information to permit judgement
Selective reporting
Reporting bias due to selective outcome reporting		 Low risk of bias: The study protocol is available and all of the study’s pre‐specified (primary and secondary) outcomes that are of interest in the review have been reported in the pre‐specified way; the study protocol is not available but it is clear that the published reports include all expected outcomes, including those that were pre‐specified (convincing text of this nature may be uncommon).
High risk of bias: Not all of the study’s pre‐specified primary outcomes have been reported; one or more primary outcomes is reported using measurements, analysis methods or subsets of the data (e.g. sub‐scales) that were not pre‐specified; one or more reported primary outcomes were not pre‐specified (unless clear justification for their reporting is provided, such as an unexpected adverse effect); one or more outcomes of interest in the review are reported incompletely so that they cannot be entered in a meta‐analysis; the study report fails to include results for a key outcome that would be expected to have been reported for such a study.
Unclear: Insufficient information to permit judgement
Other bias
Bias due to problems not covered elsewhere in the table		 Low risk of bias: The study appears to be free of other sources of bias. (e.g. co‐intervention of anticoagulation)
High risk of bias: Had a potential source of bias related to the specific study design used; stopped early due to some data‐dependent process (including a formal‐stopping rule); had extreme baseline imbalance; has been claimed to have been fraudulent; had some other problem.
Unclear: Insufficient information to assess whether an important risk of bias exists; insufficient rationale or evidence that an identified problem will introduce bias.
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Contributions of authors

  1. Drafting the protocol: SM, HT, YT, HS, HY, YK, TF

  2. Study selection: SM, HT, YT, HS, HY, YK

  3. Extracting data from studies: SM, HS

  4. Entering data into RevMan: SM, YT, YK

  5. Carrying out the analysis: SM, YT, YK

  6. Interpreting the analysis: SM, HT, YT, HS, HY, YK, TF

  7. Drafting the final review: SM

  8. Disagreement resolution: YK

  9. Updating the review: SM, HT, YT, HS, HY, YK, TF

Declarations of interest

  • Sho Miki: none known

  • Hiraku Tsujimoto: none known

  • Yasushi Tsujimoto: none known

  • Hiroki Shimada: none known

  • Hideto Yasuda: none known

  • Yuki Kataoka: none known

  • Tomoko Fujii is supported by Japan Society for the Promotion of Science (JSPS) and has received a grant from JSPS. JSPS does not have contributed to the study design; collection, management, analysis and interpretation of data; writing of the report or the decision to submit the report for publication.

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References

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