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Ảnh hưởng của quá tải dịch lên các cơ quan

Ths.BS.Bùi Thị Hạnh Duyên

Trưởng Khoa Hồi sức tích cực-BV ĐHYD.TPHCM

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Nội dung

Thành phần và vận chuyển của nước trong cơ thể

Ảnh hưởng của quá tải dịch lên các cơ quan

Nhận diện quá tải dịch

Kiểm soát quá tải dịch

Tránh quá tải dịch

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Mở đầu

Dịch truyền:

Là điều trị nền tảng trong sốc và cung cấp nước điện giải cho cơ thể
Được sử dụng rất nhiều hàng ngày trên toàn thế giới, nhưng lại ít có sự chú ý về liều lượng và tác hại của BS lâm sàng khi sử dụng dịch truyền
Dịch truyền cần được xem như thuốc
Các tác hại của quá tải dịch lên các cơ quan cần được quan tâm và xử trí phù hợp

Rational Use of Intravenous Fluids in Critically Ill Patients. https://doi.org/10.1007/978-3-031-42205-8

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Thành phần và vận chuyển của nước trong cơ thể

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Thành phần của nước trong cơ thể

Rational Use of Intravenous Fluids in Critically Ill Patients. https://doi.org/10.1007/978-3-031-42205-8

Tổng lượng nước trong cơ thể (TBW) =60% Cân nặng
Nước trong nội bào (ICW) (66%)	Nước ngoại bào (ECW) (33%)
	Nước trong lòng mạch 20%	Nước mô kẽ 75%	Nước xuyên tế bào (transcellular water) 2.5%	Hệ bạch huyết 2.5%

Body water composition for an adult 80 kg male. ECW extracellular water, ICW intracellular water, ISF interstitial fluid, IVF intravascular fluid, TBW total body water, TCF transcellular fluid. These fluids are contained within epithelial lined spaces. Examples of this fluid are cerebrospinal fluid, pleural fluid, pericardial fluid, peritoneal fluid, bladder urine, eye fluid, joint fluid, etc.

4 compartments: This can be dealt with in different ways, classically you have fat–water–protein–and minerals while water on its own is also distributed into four compartments: intracellular water (ICW), interstitial water, intravascular water and transcellular, with extracellular water (ECW) calculated as the sum of interstitial + intravascular + transcellular water content.

4 D’s: Fluids are medications in which one should take into account the 4D’s in analogy to antimicrobial stewardship: Drug–Dose–Duration–De-escalation.

4 hits: The four hits are:

first hit = initial insult,

second hit = ischemia reperfusion,

third hit = global increased permeability syndrome (GIPS).

fourth hit = potential risk of hypoperfusion during de-resuscitation.

4 indications: Fluids can be given for four reasons: resuscitation, maintenance, replacement and nutrition.

4 fluid losses: Traditionally four ways can be taken into account with regard to fluid losses: insensible loss, urine output, gastrointestinal losses and third space. Additional losses can occur in trauma with overt bleeding or in severely burned patients.

4 phases: The four dynamic fluid phases are: resuscitation, optimization, stabilization and evacuation.

4 questions: The four main questions surrounding fluid therapy that need to be solved are:

when to start IV fluids?

when to stop IV fluids?

when to start fluid removal?

when to stop fluid removal?

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Hấp thu nước từ lòng ruột vào lòng mạch

Nước được hấp thụ vào cơ thể từ lòng ruột qua màng TB biểu mô ruột
Sự hấp thụ nước bị ảnh hưởng bởi độ thẩm thấu ở lòng ruột, sự hấp thụ chất tan và cấu trúc giải phẫu của ruột
TB nội mô bơm natri nội bào qua kênh Na-K-ATPase gắn trên màng vào mô kẽ niêm mạc 🡪 khuếch tán đẳng tích của nước từ lòng ruột vào tế bào biểu mô và từ đó vào mô kẽ niêm mạc🡪 hấp thu dịch vào lòng mạch

Rational Use of Intravenous Fluids in Critically Ill Patients. https://doi.org/10.1007/978-3-031-42205-8

Water is absorbed into the body from the intestinal lumen across the intestinal epithelial membrane and absorption is influenced by luminal osmolality, solute absorption and the anatomical structures of the intestine [9].

Epithelial cells pump intracellular sodium via membrane-bound sodium potassium ATP-ase into the mucosal interstitium, enabling an isosmotic diffusion of water from the lumen into the epithelial cell and thence into the mucosal interstitial fluid.

For as long as the epithelium is secreting salt and water to the interstitium, the mucosal capillaries and venules can continue in a steady state of fluid absorption to the plasma.

These are diaphragm-fenestrated capillaries, specialised to permit high transendothelial absorption rates. The fenestrations are 10–30 nm wide and formed by the condensation of the luminal and abluminal endothelial cell membranes. They support a diaphragm that functions as a low-resistance filtration/absorption barrier.

Figure 2.2 illustrates the absorption pathway from the intestinal lumen to the plasma. Some interstitial fluid is also removed by lymphatic pumping. Should intestinal water absorption dry up, the epithelial secretion of solvent and small solutes that provides exception to the Michel–Weinbaum model of steady-state fluid filtration also ceases, so that microvascular steady-state filtration of plasma solvent to the tissues without reabsorption is restored and gastro-intestinal fluid loss is prevented.

The other tissue microvascular beds in which we find diaphragm-fenestrated capillaries for the absorption of interstitial fluid include exocrine glands, renal peritubular, endocrine glands, peripheral ganglia, nerve epineurium, circumventricular organs, choroid plexus and the ciliary process of the eye.

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Dịch thoát khỏi lòng mạch qua lọc vi mạch xuyên nội mô đến dịch ngoại bào của mô hoặc cơ quan được tưới máu
Dịch từ mô kẽ được tái hấp thu vào lòng mạch qua hệ bạch huyết

Rational Use of Intravenous Fluids in Critically Ill Patients. https://doi.org/10.1007/978-3-031-42205-8

The paracellular (inter endothelial cleft) fluid filtration pathway of continuous capillaries

Plasma Volume

Plasma volume is a critical care concept rather than an anatomic entity. It is often measured as the volume of distribution of an indicator dye such as Evans Blue or radio-labelled albumin, spaces which are substantially larger than the calculated intravascular erythrocyte dilution volume. When reading clinical studies that report plasma volume, it is helpful to bear in mind what has actually been measured or calculated. Broadly, the normal circulating plasma volume is around 2.5–3.0 L at sea level in men and falls by 15–20% with a sojourn to high-altitude living. The circulating plasma contains around 2 L of blood cells (mostly erythrocytes), giving a circulating blood volume at sea level of about 4.5 L [10]. The third contributor to the total intravascular volume is the slower-moving fluid within the endothelial glycocalyx layer, which has been estimated to be as much as 1.5 L in healthy adults or as little as a few hundred milli litres in a variety of cardiovascular disease states [11, 12]. For our approximation we can call it 0.5 L, giving a total intravascular volume of about 5 L at sea level.

The circulatory flow rate of blood (Qt) is supported by the elastic recoil of venules and small veins on the post-capillary blood volume. The venular filling pressure of around 18 mmHg provides a gradient down to the central venous pressure, which is kept close to zero by the healthy heart. The ventricles fill during diastole from the venous excess volume, and the flow to the ventricle is kept nearly constant by the contraction of the atrium. The ventricles eject blood against an afterload that raises the pressure of blood within pulmonary and systemic arteries for distribution to the tissues [13].

Critical care practitioners fear reduced plasma volume with consequent reduced Qt. They place wide-bore catheters within large veins for ‘access’ by which to administer vital medicines, and to allow the infusion of ‘resuscitation’ fluids. In most critical care patients, the intravenous route is the predominant source of fluid input.

The fluid leaves the circulating plasma volume by transendothelial microvascular filtration to the extravascular extracellular fluid of the perfused tissue or organ [14]. Figure 2.3 illustrates the paracellular (inter endothelial cleft) fluid filtration pathway of continuous capillaries.

Traditional clinical teaching has too often ignored the Starling principle and the heterogeneity of the permeability barriers in tissues and organs, which we consider next

The Starling Principle and Microvessel Heterogeneity

The idea that a single capillary could simultaneously filter fluid from plasma to the interstitial fluid and absorb it back again was always difficult to believe and had never been seen in laboratory experiments. The diagram showing a declining sum of hydrostatic and osmotic pressure differences from the arteriolar entry to the venular exit of a capillary, with flow reversal as the osmotic pressure difference exceeds the hydrostatic pressure difference, has been called The Diagram to Forget. The capillaries of sinusoidal organs such as liver, spleen and bone marrow receive 25–30% of the left ventricular output via the hepatic artery and portal vein. The splanchnic microvessels are very ‘leaky’ indeed. They have a discontinuous endothelial surface layer that allows proteins to pass freely in either direction through transendothelial fenestrae and through interendothelial junction gaps so that no osmotic pressure gradient can occur. In such tissues, the unopposed hydrostatic pressure difference ensures that only transendothelial fluid filtration occurs.

In non-sinusoidal tissues, the endothelial surface layer is continuous and largely impermeable to proteins. The paracellular endothelial barrier here presents a layered structure that depends on a continuous activation of signalling pathways regulated by sphingosine-1- phosphate (S1P) and intracellular cAMP. The layers are

The glycocalyx and its endothelial surface layer

The junction breaks (or gaps) of the tight junction strand

The adherens junction

�

Solvent and small solutes first pass through the resistance of the endothelial surface layer. The greater resistance occurs where fluid is jetted though infrequent slit-like interendothelial tight junction breaks to the interendothelial cleft. The adherens junction provides a third, variable resistance to the paracellular flow of filtrate [15].

Plasma proteins are concentrated on the intravascular aspect of the endothelial surface layer and the filtrate entering the interendothelial cleft is almost protein-free. Soluble interstitial proteins diffuse into the post-glycocalyx solvent filtrate, and the protein concentration in the fluid of the interendothelial clefts will therefore depend on the rates at which the solvent from the plasma filtrate and protein from the interstitium enter the cleft. At high filtration rates, the protein concentration (and colloid osmotic pressure) in the cleft is low, but as the transendothelial filtration rate falls the protein concentration (and colloid osmotic pressure) in the interendothelial cleft rises. The dependence of the colloid osmotic pressure Starling force on the solvent filtration rate within a subglycocalyx ‘protected region’ of the general interstitial fluid thus ensures that the osmotic forces oppose but, at steady state, do not reverse the flow of the filtrate. This is the Michel–Weinbaum Model, confirmed by experiments published in 2004.

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Starling Force

Rational Use of Intravenous Fluids in Critically Ill Patients. https://doi.org/10.1007/978-3-031-42205-8

Vai trò tích cực của lớp glycocalyx nội mô trong việc hình thành trạng thái cân bằng dịch xuyên mao mạch🡪 phương trình Starling cần phải được xem lại

The Starling Equation

Fluid exchange across the capillary membrane was investigated by the English physiologist Ernest Starling (1866–1927) who, in 1896, formulated his Starling Equation, which is still considered to be valid. The “traditional” equation summarizes the factors that determine the transcapillary exchange in the following way:Fluid exchangefcipi=−()−−()KPP

where Kf is a proportionality constant, Pc and Pi are the hydrostatic fluid pressure in the capillary and interstitium, respectively, and πp and πi are the colloid osmotic pressure in the plasma and interstitial fluid, respectively. The symbol σ is the reflection coefficient, which explains how easily macromolecules pass through the capillary wall. A reflection coefficient of 1.0 means that the membrane is impermeable, and 0 means that the molecule passes without any difficulty. The value of σ greatly varies between vascular beds.

Recent microcirculatory research suggests that the principles behind the Starling equation need to be revised due to the active role played by the endothelial glycocalyx layer in forming the transcapillary fluid equilibrium. These alternations are discussed in detail by Tom Woodcock in the first chapter of this book.

Plasma Volume

Plasma volume is a critical care concept rather than an anatomic entity. It is often measured as the volume of distribution of an indicator dye such as Evans Blue or radio-labelled albumin, spaces which are substantially larger than the calculated intravascular erythrocyte dilution volume. When reading clinical studies that report plasma volume, it is helpful to bear in mind what has actually been measured or calculated. Broadly, the normal circulating plasma volume is around 2.5–3.0 L at sea level in men and falls by 15–20% with a sojourn to high-altitude living. The circulating plasma contains around 2 L of blood cells (mostly erythrocytes), giving a circulating blood volume at sea level of about 4.5 L [10].

The third contributor to the total intravascular volume is the slower-moving fluid within the endothelial glycocalyx layer, which has been estimated to be as much as 1.5 L in healthy adults or as little as a few hundred milli litres in a variety of cardiovascular disease states [11, 12]. For our approximation we can call it 0.5 L, giving a total intravascular volume of about 5 L at sea level.

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Sự thanh thải dịch phế nang

Cả tế bào biểu mô phế nang loại I và loại II đều tham gia vận chuyển ion xuyên biểu mô.
Na được vận chuyển kênh natri biểu mô (ENaC) và các kênh natri khác, và sau đó qua kênh Na/K-ATPase.
Clor được vận chuyển bằng con đường xuyên tế bào thông qua chất điều hòa dẫn truyền màng xơ nang (CFTR) hoặc bằng con đường cạnh tế bào.
Sự vận chuyển ion theo vectơ này tạo ra một gradient thẩm thấu thúc đẩy sự thanh thải của dịch phù phế nang.
Nước di chuyển qua con đường xuyên tế bào thông qua kênh aquaporin 5 (AQP5) hoặc bằng con đường cạnh tế bào

Taenaka and Matthay, Anat Rec. 2023;1–14. wileyonlinelibrary.com/journal/ar

FIGURE 1 Normal alveolar fluid clearance pathways. The interstitial, capillary, and alveolar compartments are shown with pulmonary edema fluid in the alveolus. Both Type I and II alveolar epithelial cells are involved in transepithelial ion transport. Sodium (Na+) is transported across the apical side of the epithelial cells through the epithelial sodium channel (ENaC) and other apical sodium channels, including nonselective cation channels (NCC), cyclic nucleotide-gated channels (CNG), and other selective cation channels (SCC), and then across the basolateral side via the sodium/potassium ATPase (Na/K-ATPase). Chloride (Cl ) is transported by transcellular route through the cystic fibrosis transmembrane conductance regulator (CFTR) or by a paracellular route. This vectorial ion transport creates an osmotic gradient that drives the clearance of alveolar edema fluid. Water (H2O) is crossing by transcellular route through an aquaporin 5 (AQP5) channel or by a paracellular route. Figure prepared by Diana Lim

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Ảnh hưởng của quá tải dịch lên các cơ quan

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Quá tải dịch: tăng nguy cơ rối loạn chức năng đa cơ quan (MOD) và tử vong ở BN sốc NK

NC hồi cứu 104 BN sốc NK tại ICU: 55,8% BN sống ngày 28
70% BN có suy đa cơ quan ngày thứ 3
Cân bằng dịch tích lũy (CFB) 72h là yếu tố nguy cơ tiên đoán MOD và tử vong ở BN sốc NK

Huang AC et al. Fluid balance correlates with clinical course of multiple organ dysfunction syndrome and mortality in patients with septic shock. PLoS One. 2019 Dec 2;14(12):e0225423.

Huang AC, Lee TY, Ko MC, Huang CH, Wang TY, Lin TY, Lin SM. Fluid balance correlates with clinical course of multiple organ dysfunction syndrome and mortality in patients with septic shock. PLoS One. 2019 Dec 2;14(12):e0225423. doi: 10.1371/journal.pone.0225423. PMID: 31790451; PMCID: PMC6886786

Abstract

Introduction

Positive fluid balance is a prognostic factor for mortality in patients with sepsis; however, the association between cumulated fluid balance (CFB) and sepsis-induced multi-organ dysfunction syndrome (MODS) has yet to be elucidated. In this study, we sought to determine whether CFB is correlated with MODS and mortality in cases of septic shock.

Methods

The study retrospectively recruited patients with septic shock from the intensive care unit of a tertiary care hospital. Multiple organ dysfunction syndrome (MODS) was identified as sequential organ failure assessment (SOFA) score � 2 in more than one organ system. The CFB is the sum of all daily intake and output. An independent t-test, single and multivariate logistic regression, the receiver operating characteristic (ROC) curves, and the Pearson correlation coefficient were used to determine whether a relationship exists between CFB and the development of MODS and mortality.

Results

Among the 104 patients enrolled in the study, 58 (55.8%) survived more than 28 days, and 73 (70.2%) developed MODS on day 3. The values of CFB in the first 24 hours and 72 hours after diagnosis of septic shock in patients with MODS were higher than these in patients without MODS (1086.6 ± 176.3 vs. 325.5 ± 205.7 ml, p = 0.013 and 2408 ± 361 vs. 873.1 ± 489 ml, p < 0.0001). In a multivariate logistic regression, the independent factors associated with the development of MODS on day 3 were APACHE II score at ICU admission (27.6 ± 7.6 in patients with MODS vs. 20.5 ± 6.4 in those without; O.R. 1.18; 95% C.1 I. 1.08–1.30; p < 0.001), disseminated intravascular coagulopathy (DIC) (n = 28; 38.4% vs. n = 2; 6.5%; O. R. 23.67; 95% C.I. 3.58–156.5; p = 0.001), and CFB in the first 72 hours (72-hr CFB) > median (1767.50ml) (n = 41; 56.2% vs. n = 11; 35.5%; O.R. 3.67; 95% C.I., 1.18–11.40; p =0.024). Moreover, a multivariate logistic regression also identified neoplasm (n = 25; 54.3% vs. n = 17; 29.3%; O.R. 3.45; 95% C.I. 1.23–10.0; p = 0.019) and 72-hr CFB > median (n = 30; 65.2% vs. n = 21; 36.2%; O.R. 4.13; 95% C.I. 1.34–12.66; p = 0.013) as independent factors associated with 28-day mortality. 72-hr CFB values were strongly correlated with the SOFA score (r = 0.445, p < 0.0001). The area under the ROC curve revealed that 72-hr CFB has good discriminative power in associating the development of MODS (0.644, p = 0.002) and predicting subsequent 28-day mortality (0.704, p < 0.0001).

Conclusions

72-hr CFB appears to be correlated with the likelihood of developing MODS and mortality in patients with septic shock. Thus, it appears that 72-hr CFB could perhaps be used as an indicator for MODS and a predictor for mortality in those patients

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Quá tải dịch tăng nguy cơ tử vong ở BN nặng có suy thận cấp

NC hồi cứu 1120 BN AKI trong ICU
Phân nhóm (cluster) dựa vào mức độ cân bằng dịch
Nhóm có % cân bằng dịch âm ở 72h có tỷ lệ tử vong thấp (nhóm 1 và 2)
Nhóm có cân bằng dịch > 10% ở 72h có tỷ lệ tử vong cao (nhóm 5–8).

Yosuke Hayashi et al, https://doi.org/10.1038/s41598-023-44778-0

https://doi.org/10.1038/s41598-023-44778-0

Clustering based on fluid accumulation

The patients were divided into eight groups based on %FO transition (Fig. 3). We found that the clusters with

negative %FO at 72 h had low mortality rates (clusters 1 and 2), whereas the cluster with > 10% of %FO at 72 h

had high mortality rates (clusters 5–8). The greater the increase in %FO during hours 0 to 24, the more mortality

was worsened, with the exception of cluster 6. Cluster 6 had the 2nd highest mortality among clusters, but the

%FO during hours 0–24 was lower than that in clusters 5 and 7, which had lower mortalities than did this cluster.

While the association between %FO during hours 0–24 and mortality was inconsistent in cluster 6, a relatively

higher %FO during hours 24 to 48 and 48 to 72 was observed in this cluster.

Phân cụm dựa trên sự tích lũy dịch

Các bệnh nhân được chia thành tám nhóm dựa trên quá trình chuyển đổi %FO (Hình 3). Chúng tôi nhận thấy rằng các cụm có %FO âm ở 72 giờ có tỷ lệ tử vong thấp (cụm 1 và 2), trong khi cụm có > 10% %FO ở 72 giờ có tỷ lệ tử vong cao (cụm 5–8). %FO càng tăng trong các giờ từ 0 đến 24 thì tỷ lệ tử vong càng trở nên trầm trọng hơn, ngoại trừ cụm 6. Cụm 6 có tỷ lệ tử vong cao thứ 2 trong số các cụm, nhưng %FO trong các giờ 0–24 thấp hơn so với ở cụm 5 và 7 có tỷ lệ tử vong thấp hơn cụm này.

Mặc dù mối liên quan giữa %FO trong giờ 0–24 và tỷ lệ tử vong không nhất quán trong cụm 6, nhưng

%FO cao hơn trong các giờ từ 24 đến 48 và 48 đến 72 được quan sát thấy trong cụm này

Increased fluid overload (FO) is associated with poor outcomes in critically ill patients, especially in

acute kidney injury (AKI). However, the exact timing from when FO influences outcomes remains

unclear.

We retrospectively screened intensive care unit (ICU) admitted patients with AKI between

January 2011 and December 2015. Logistic or linear regression analyses were performed to determine

when hourly %FO was significant on 90-day in-hospital mortality (primary outcome) or ventilator free

days (VFDs). In total, 1120 patients were enrolled in this study. Univariate analysis showed that

a higher %FO was significantly associated with higher mortality from the first hour of ICU admission

(odds ratio 1.34, 95% confidence interval 1.15–1.56, P < 0.001), whereas multivariate analysis adjusted

with age, sex, APACHE II score, and sepsis etiology showed the association was significant from the

27th hour. Both univariate and multivariate analyses showed that a higher %FO was significantly

associated with shorter VFDs from the 1st hour. The significant associations were retained during

all following observation periods after they showed significance. In patients with AKI, a higher %FO

was associated with higher mortality and shorter VFDs from the early phase after ICU admission. FO

should be administered with a physiological target or goal in place from the initial phase of critical

illness.

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Yếu tố ảnh hưởng lên tưới máu thận (RBF)

European Heart Journal: Acute Cardiovascular Care (2022) 11, 786–793 https://doi.org/10.1093/ehjacc/zuac104

Determinants of renal perfusion

Mean arterial pressure (MAP) is not the only determinant of renal perfusion. Renal blood flow (RBF) is determined by the pressure gradient between the inflow and the outflow pressures of the kidneys and by the vascular resistance to flow (RBF=ΔP/R).10 The inflow pressure of the kidney is closely related to MAP, while the outflow pressure is determined by the renal venous pressure or intra-abdominal pressure (IAP), depending on which one is higher.11 Resistance is mainly determined by the radius of both the afferent and efferent arterioles.10 While vasoconstriction of both arteriolar beds results in decreased RBF, efferent arteriolar vasoconstriction has less of an impact on the GFR because it increases the glomerular capillary pressure and filtration fraction.7,12 Hypotension (i.e. reduced MAP) markedly reduces RBF by decreasing inflow pressure. On the other hand, increased outflow pressure may become the limiting factor for kidney perfusion in the setting of abdominal compartment syndrome13 or systemic venous congestion secondary to right-sided heart failure or cirrhosis.14 In this setting, interstitial oedema within the encapsulated kidneys leads to compressive forces upon the intra-renal vessels and further increases impedance to RBF

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Salahuddin et al. BMC Nephrology (2017) 18:45 DOI 10.1186/s12882-017-0460-6

NC tiến cứu 339 BN nhập ICU được theo dõi suy thận và cân bằng dịch
AKI 41.6%; RISK 8%, NJURY 7%; FAILURE 26% theo tiêu chuẩn RIFLE
Cân bằng dịch cao hơn đáng kể trong

So với BN không AKI, BN bị AKI; cân bằng dịch cao hơn vào N1 và N3

1755 ± 2189 vs 924 ± 1846 ml, p < 0,001 vào N1 ICU.
665 ± 1686 vs 167 ± 1658 ml, p = 0.007 vào N3 ICU

Trên phân tích hồi quy đa biến, cân bằng dịch trong 24 h ICU có ý nghĩa tiên đoán AKI OR 1,02 (KTC 95% 1,01,1,03 p = 0,003),

Salahuddin et al. BMC Nephrology (2017) 18:45 DOI 10.1186/s12882-017-0460-6

NC tiến cứu 339 BN nhập ICU được theo dẫn suy thận và cân bằng dịch

AKI 41.6%; RISK 8%, NJURY 7%; FAILURE 26% theo tiêu chuẩn RIFLE

Cân bằng chất dịch cao hơn đáng kể trong

BN bị AKI; 1755 ± 2189 v/s 924 ± 1846 ml, p < 0,001 vào ngày 1 ICU.

Trên phân tích hồi quy đa biến, cân bằng dịch thực trong 24 giờ đầu nhập ICU, OR 1,02 (KTC 95% 1,01,1,03 p = 0,003),

tỷ lệ tích lũy dịch được điều chỉnh theo trọng lượng cơ thể OR1,009 (KTC 95% 1,001,1,017, p = 0,02), cân bằng dịch trong 24 giờ đầu nhập ICU với creatinine huyết thanh được điều chỉnh theo cân bằng dịch, OR 1,024 (KTC 95% 1,012,1,035 , p = 0,005),

Fluid balance was significantly higher in patients with AKI; 1755 ± 2189 v/s 924 ± 1846 ml, p < 0.001 on ICU day 1 and 665 ± 1686 v/s 167 ± 1658 ml, p = 0.007 on day 3

Abstract

Background: Acute Kidney injury (AKI) is common and increases mortality in the intensive care unit (ICU). We

carried out this study to explore whether fluid overload is an independent risk factor for AKI.

Methods: Single-center prospective, observational study. Consecutively admitted, ICU patients were followed for

development of AKI. Intravenous fluid volumes, daily fluid balances were measured, hourly urine volumes, daily

creatinine levels were recorded.

Results: Three hundred thirty nine patients were included; AKI developed in 141 (41.6%) patients; RISK in 27 (8%)

patients; INJURY in 25 (7%); FAILURE in 89 (26%) by the RIFLE criteria. Fluid balance was significantly higher in

patients with AKI; 1755 ± 2189 v/s 924 ± 1846 ml, p < 0.001 on ICU day 1. On multivariate regression analysis, a net

fluid balance in first 24 h of ICU admission, OR 1.02 (95% CI 1.01,1.03 p = 0.003), percentage of fluid accumulation

adjusted for body weight OR1.009 (95% CI 1.001,1.017, p = 0.02), fluid balance in first 24 h of ICU admission with

serum creatinine adjusted for fluid balance, OR 1.024 (95% CI 1.012,1,035, p = 0.005), Age, OR 1.02 95% CI 1.01,1.03,

p < 0.001, CHF, OR 3.1 (95% CI 1.16,8.32, p = 0.023), vasopressor requirement on ICU day one, OR 1.9 (95% CI 1.13,3.

19, p = 0.014) and Colistin OR 2.3 (95% CI 1.3, 4.02, p < 0.001) were significant predictors of AKI. There was no

significant association between fluid type; Chloride-liberal, Chloride-restrictive, and AKI.

Conclusions: Fluid overload is an independent risk factor for AKI.

Keywords: Acute kidney injury, Fluid overload, Renal congestion, Chloride-liberal fluids, Critical illness

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CVP cao tăng nguy cơ suy giảm chức năng thận/BN suy tim mất bù

Mullens et al. JACC Vol. 53, No. 7, 2009, Venous Congestion and Worsening Renal Function February 17, 2009:589–96

So với BN không có chức năng thận xấu hơn, BN có chức năng thận xấu hơn (cre/máu >= 0.3 mg/dl trong thời gian nằm viện) ở nhóm BN:

CVP cao hơn lúc NV (18 +/- 7 mm Hg vs 12 +/- 6 mmHg, p = 0,001)
CVP cao hơn sau khi điều trị nội khoa tích cực (11 +/- 8 mm Hg vs 8 +/- 5 mm Hg, p = 0,04).
Xảy ra ít hơn hơn ở những BN có CVP < 8 mm Hg (p=0,01).
AUC-ROC CVP=0.734, p= 0.0001 ; CI 0.552, p=0.6, khác biệt p=0.012)

CVP

CI

HATT

PCWP

CI cardiac index; Cr serum creatinine; CVP central venous pressure; PCWP pulmonary capillary wedge pressure; SBP systolic blood pressure.

Objectives

To determine whether venous congestion, rather than impairment of cardiac output, is primarily associated with the development of worsening renal function (WRF) in patients with advanced decompensated heart failure (ADHF).

Mullens et al. JACC Vol. 53, No. 7, 2009, Venous Congestion and Worsening Renal Function February 17, 2009:589–96

In addition, using ROC curve analysis, we observed that baseline CVP (0.734, p= 0.0001) but not baseline CI (0.552, p 0.6) predicted the development of WRF (difference p=0.012)

Background

Reduced cardiac output is traditionally believed to be the main determinant of WRF in patients with ADHF.

Methods

A total of 145 consecutive patients admitted with ADHF treated with intensive medical therapy guided by pulmonary artery catheter were studied. We defined WRF as an increase of serum creatinine >= 0.3 mg/dl during hospitalization.

Results

In the study cohort (age 57 +/-14 years, cardiac index 1.9 +/- 0.6 l/min/m2, left ventricular ejection fraction 20 +/- 8%, serum creatinine 1.7 +/-0.9 mg/dl), 58 patients (40%) developed WRF. Patients who developed WRF had a greater central venous pressure (CVP) on admission (18 +/- 7 mm Hg vs. 12 +/- 6 mm Hg, p = 0.001) and after intensive medical therapy (11 +/- 8 mm Hg vs. 8 +/- 5 mm Hg, p =0.04). The development of WRF occurred less frequently in patients who achieved a CVP < 8 mm Hg (p=0.01). Furthermore, the ability of CVP to stratify risk for development of WRF was apparent across the spectrum of systemic blood pressure, pulmonary capillary wedge pressure, cardiac index, and estimated glomerular filtration rates.

Conclusions

Venous congestion is the most important hemodynamic factor driving WRF in decompensated patients with advanced heart failure. (J Am Coll Cardiol 2009;53:589–96) © 2009 by the American College of Cardiology Foundation

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Quá tải dịch và nguy cơ tổn thương thận cấp ở BN sau ghép gan

NC hồi cứu 121 BN ghép gan
Cân bằng dịch tích lũy 12h và 4 ngày sau PT với kết cục xấu
Cân bằng dịch tích lũy trong 4 ngày có liên quan độc lập với AKI (OR = 2,3; 95%CI: 1,37-3,86, P = 0,02) và điều trị thay thế thận (OR = 2,89; 95%CI: 1,52-5,49 , P =0,001).

🡪 BN ghép gan, cân bằng dịch tích lũy dương 4 ngày sau ghép gan tăng nguy cơ AKI và điều trị thay thế thận

Codes L et al. Cumulative positive fluid balance is a risk factor for acute kidney injury and requirement for renal replacement therapy after liver transplantation. World J Transplant. 2018 Apr 24;8(2):44-51. doi: 10.5500/wjt.v8.i2.44.

Codes L, de Souza YG, D'Oliveira RAC, Bastos JLA, Bittencourt PL. Cumulative positive fluid balance is a risk factor for acute kidney injury and requirement for renal replacement therapy after liver transplantation. World J Transplant. 2018 Apr 24;8(2):44-51. doi: 10.5500/wjt.v8.i2.44. PMID: 29696105; PMCID: PMC5915376.

AIM

To analyze whether fluid overload is an independent risk factor of adverse outcomes after liver transplantation (LT).

METHODS

One hundred and twenty-one patients submitted to LT were retrospectively evaluated. Data regarding perioperative and postoperative variables previously associated with adverse outcomes after LT were reviewed. Cumulative fluid balance (FB) in the first 12 h and 4 d after surgery were compared with major adverse outcomes after LT.

RESULTS

Most of the patients were submitted to a liberal approach of fluid administration with a mean cumulative FB over 5 L and 10 L, respectively, in the first 12 h and 4 d after LT. Cumulative FB in 4 d was independently associated with occurrence of both AKI and requirement for renal replacement therapy (RRT) (OR = 2.3; 95%CI: 1.37-3.86, P = 0.02 and OR = 2.89; 95%CI: 1.52-5.49, P = 0.001 respectively). Other variables on multivariate analysis associated with AKI and RRT were, respectively, male sex and Acute Physiology and Chronic Health Disease Classification System (APACHE II) levels and sepsis or septic shock. Mortality was shown to be independently related to AST and APACHE II levels (OR = 2.35; 95%CI: 1.1-5.05, P = 0.02 and 2.63; 95%CI: 1.0-6.87, P = 0.04 respectively), probably reflecting the degree of graft dysfunction and severity of early postoperative course of LT. No effect of FB on mortality after LT was disclosed.

CONCLUSION

Cumulative positive FB over 4 d after LT is independently associated with the development of AKI and the requirement of RRT. Survival was not independently related to FB, but to surrogate markers of graft dysfunction and severity of postoperative course of LT.

Keywords: Liver transplantation, Fluid balance, Acute kidney injury

Core tip: Whether fluid overload is an independent mediator of adverse outcomes on early postoperative liver transplantation (LT). The influence of fluid accumulation on morbidity and mortality after LT has not been well evaluated up to now. This study aims to analyze whether fluid management influences the early postoperative outcome after LT. Cumulative positive fluid balance (FB) over 4 d after LT influence the development of acute kidney injury and it is a risk factor for the requirement for renal replacement therapy. Survival is not independently related to FB but to surrogate markers of graft dysfunction.

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Quá tải dịch và tăng áp lực ổ bụng

Jacobs R, Fluid Management, Intra-Abdominal Hypertension and the Abdominal Compartment Syndrome: A Narrative Review. Life (Basel). 2022 Sep 6;12(9):1390. doi: 10.3390/life12091390.

Áp lực tưới máu các cơ quan =MAP-IAP

Jacobs R, Wise RD, Myatchin I, Vanhonacker D, Minini A, Mekeirele M, Kirkpatrick AW, Pereira BM, Sugrue M, De Keulenaer B, Bodnar Z, Acosta S, Ejike J, Tayebi S, Stiens J, Cordemans C, Van Regenmortel N, Elbers PWG, Monnet X, Wong A, Dabrowski W, Jorens PG, De Waele JJ, Roberts DJ, Kimball E, Reintam Blaser A, Malbrain MLNG. Fluid Management, Intra-Abdominal Hypertension and the Abdominal Compartment Syndrome: A Narrative Review. Life (Basel). 2022 Sep 6;12(9):1390. doi: 10.3390/life12091390. PMID: 36143427; PMCID: PMC9502789.

Figure 3

The vicious cycle of fluid resuscitation, abdominal hypertension and kidney injury. Adapted according to the Open Access CC BY License 4.0 from Malbrain et al., with permission [17]. AKI: acute kidney injury; IAH: intra-abdominal hypertension

Animal data

We found eleven animal studies, of which three were suitable, reporting on resuscitation and secondary IAH (Table 5). Fluid resuscitation leads to IAH and venous congestion (or venous hypertension), resulting in gut edema and diminished gut contractility [117]. Melatonin may prevent deleterious effects related to fluid overload [118]. Extensive fluid resuscitation preserves cardiac output, urine output, and serum parameters (e.g., ALT, lipase, AP, lactate, creatinine) in pigs with ACS, but organ damage occurs (vicious cycle) [119]. Previous animal studies showed that IAH provokes the release of pro-inflammatory cytokines which may serve as a second insult for the induction of MOF [121]. This is illustrated in Figure 3.

Áp lực tưới máu các cơ quan=MAP-IAP

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Quá tải dịch và phù phổi

Maria Barile, European Journal of Radiology Open 7 (2020) 100274

Các bạch mạch chạy dọc theo bó mạch phế quản và vách liên tiểu thùy dọc theo ngoại vi của tiểu thùy phổi.
Lưu lượng bạch mạch có thể tăng 3-10 lần trong trường hợp phù phổi thủy tĩnh

Maria Barile, European Journal of Radiology Open 7 (2020) 100274

Fig. 1. Schematic representation of the hydrostatic and oncotic pressure gradients which influence fluid movement across the pulmonary blood vessel walls (capillary endothelium). Pintravascular : hydrostatic pressure in the vessel. Pinterstitial : hydrostatic pressure in the interstitium. Πintravascular : protein oncotic pressure in the vessel. Πinterstitial : protein oncotic pressure in the interstitium.

Fig. 2. Drawing of the secondary pulmonary lobule of the lung. The interlobular septa runs along the periphery of the lobule, containing lymphatics. The pulmonary artery, bronchus, and central lymphatics run along the center of the secondary pulmonary lobule

The physiologic determinates of edema include 1) hydrostatic pres- sure, defined as the pressure within the capillaries driving fluid out of the vessels, 2) oncotic pressure, described as pressure related to the macromolecules in the blood which help to retain fluid in the vessels, and 3) membrane permeability, the ease with which fluid passes through the capillary or alveolar walls (Fig. 1). The relative balance of the hy- drostatic and oncotic pressures in addition to the membrane perme- ability determine the net fluid movement between the vasculature and the pulmonary interstitium and alveolar air spaces. The lymphatic channels are also important in maintaining fluid balance as they allow for return of the extravascular fluid back into the central vasculature. The lymphatic channels run along the bronchovascular bundles and interlobular septa along the periphery of the pulmonary lobule (Fig. 2). The lymphatic flow can increase 3-10x in the setting of hydrostatic pulmonary edema [1], thereby providing an opportunity to re-establish euvolemia.

Rational Use of Intravenous Fluids in Critically Ill Patients. https://doi.org/10.1007/978-3-031-42205-8

Pulmonary Starling Forces and the Extravascular Lung Water

The pulmonary circulation operates at much lower hydrostatic capillary pressure than the various systemic loops but sustains steady-state solvent filtration to the pulmonary interstitium. As the lungs reside in a sub-atmospheric pressured body space, the interstitial fluid pressure there is lower than that in subcutaneous tissue and fluid from pulmonary capillaries is primarily drawn into the perivascular interstitial space by virtue of the subpleural pressure there. Fluids and solutes are largely excluded from the alveoli by the tight junctions of the alveolar epithelium.

In the progression of pulmonary oedema, fluid accumulates first in the interstitial space around the airways forming ‘peribronchial cuffs’. The Staverman reflection co-efficient sigma for albumin in pulmonary capillaries is, on average, around 0.7. There is thus more interstitial protein in the lung than in other tissues with continuous capillaries, and the colloid osmotic pressure difference only weakly opposes steady-state filtration at low capillary pressure. Bronchial artery-supplied capillaries also filter fluid to the pulmonary interstitium and so contribute to the interstitial fluid volume and pulmonary lymph flow.

The volume of pulmonary interstitial fluid is strictly controlled by the lymphatic system. Extravascular lung water can be measured at the bedside by double indicator dilution or by thermodilution alone but includes intracellular fluid. The normal value is about 0.5 L. In severe pulmonary oedema values of more than 1.5 L are recorded, almost all of the excess being extracellular fluid in the interstitium or alveoli.

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Quá tải dịch tăng nguy cơ tăng áp lực nội sọ ở BN chấn thương đầu

Moore et al. Intensive Care Medicine Experimental 2015, 3(Suppl 1):A439 http://www.icm-experimental.com/content/3/S1/A439

NC hồi cứu 100 BN chấn thuơng đầu
So với BN có cân bằng dịch âm, BN có cân bằng dịch dương N3 đến N7 có ICP TB cao hơn (13,9 vs 12,6 mmHg, p = 0,05).
Cân bằng dịch dương dương N3 -N7 có liên quan đáng kể đến sự gia tăng ICP TB từ N 3 đến N7 (p = 0,04)

Moore et al. Intensive Care Medicine Experimental 2015, 3(Suppl 1):A439

http://www.icm-experimental.com/content/3/S1/A439

NC hồi cứu 100 BN chấn thương đầu có theo dõi ICP

Cân bằng dịch tích lũy N3-N7 sau chấn thương

Introduction

Traumatic brain injury (TBI) is a huge public health problem

leading to great personal suffering to victims and

relatives and huge costs to society. Patients with TBI

typically require substantial fluid replacement and resuscitation.

However, evidence suggests that fluid accumulation,

which could potentially increase cerebral swelling,

may be associated with an increase in the incidence of

elevated intracranial pressure (ICP) in patients with TBI1.

We hypothesized that fluid balance (FB) after the first

48 hours following injury would be an independent predictor

of ICP over the next five days.

Objectives

To assess the relationship between FB and ICP in

patients with severe TBI from day 3 to 7 after injury.

Methods

We conducted a retrospective analysis of 100 adult

trauma patients admitted to the ICU of a tertiary major

trauma centre from Oct 2010 to Jun 2013 with head

injury +/- multitrauma, who had an ICP monitor

inserted for ≥ 7 days. FB for day 3 to 7 was calculated

from the daily ICU charts (all fluid input minus all fluid

output for this period). Mean ICP for day 3 to 7 was

calculated from all end-hourly measurements taken on

patients for this period. Further demographic, pre-hospital,

clinical and biochemical data were collected from

pathology, ICU and trauma registry databases. All

repeated measures were averaged from day 3 to 7. We

compared mean ICP for day 3 to 7 between patients

with a positive versus negative FB for day 3 to 7. FB for

day 3 to 7 and potential confounders were used in univariable

and multivariable linear regression analyses

with mean ICP for day 3 to 7 (Table 1).

Results

Median age of the patients was 30 years, 83% were male

and mean injury severity score (1998 version) was 37.

Fifteen patients died in hospital, and median ICU length

of stay was 16 days. Fifty three percent of patients had a

positive FB and 47% had a negative FB for day 3 to 7.

Patients with a positive versus negative FB for day 3 to 7

had a higher mean ICP (13.9 v 12.6 mmHg, p = 0.05).

After adjustment for confounders, a more positive FB

for day 3 to 7 was significantly associated with an increase

in mean ICP for day 3 to 7 (p = 0.04, R2 for model = 0.46).

Conclusions

A more positive FB for day 3 to 7 post TBI was independently

associated with an increased risk for a higher ICP.

Further interventional studies aimed at testing the value of

controlling FB in TBI patients after the ‘critical’ resuscitation

period are warranted

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Quá tải dịch truyền ảnh hưởng xấu lên chức năng các cơ quan

Abhilash Koratala et al, Cardiorenal Med 2022;12:141–154. DOI: 10.1159/000526902

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Nhận diện quá tải dịch

22 of 49

Đánh giá tình trạng dịch của BN

Theo dõi cân nặng:

Có thể giúp đánh giá theo dõi cân bằng dịch nhưng cần loại cân đặc biệt để cân BN nằm ICU
Có nhiều vấn đề trong cân BN: tã, quần áo, dịch dẫn lưu, định chuẩn cân…

Theo dõi cân bằng dịch xuất nhập:

Cần chi tiết và phương pháp đo lường chính xác
Nước mất không nhận biết

Cần phối hợp nhiều phương pháp để đánh giá

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Đánh giá tình trạng dịch của BN

Lâm sàng:

Dấu véo da, phù, dấu ấn lõm, ran ở phôỉ
Dịch màng phổi, màng bụng, màng tim

Biomarker:

BNP, NT-proBNP

CLS:

Xquang phổi
Siêu âm POCUS, siêu âm phổi, siêu âm tim
IVC, siêu âm doppler đánh giá xung huyết tĩnh mạch (VExUS)

Các thông số huyết động

CVP, PCWP
Thể tích nước ngoại mạch phổi (EVLW)
Chỉ số tính thấm mao mạch phổi PVPI
Chỉ số thể tích cuối tâm trương toàn bộ GEDVI

Đo trở kháng sinh học thành phần cơ thể Bioimpedance analysis (BIA)

Abhilash Koratala et al, Cardiorenal Med 2022;12:141–154. DOI: 10.1159/000526902

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Siêu âm doppler đánh giá xung huyết tĩnh mạch (VExUS)

Abhilash Koratala et al, Cardiorenal Med 2022;12:141–154. DOI: 10.1159/000526902

https://www.pocus101.com/vexus-calculator/

Venous excess ultrasound (VExUS) grading: when the diameter

of IVC is >2 cm, three grades of congestion are defined

based on the severity of abnormalities on hepatic, portal, and renal

parenchymal venous Doppler. Hepatic vein Doppler is considered

mildly abnormal when the systolic (S) wave is smaller than the

diastolic (D) wave, but still below the baseline; it is considered severely

abnormal when the S-wave is reversed. Portal vein Doppler is considered mildly abnormal when the pulsatility is 30–50%, and severely abnormal when it is ≥50%. Asterisks represent points of

pulsatility measurement. Renal parenchymal vein Doppler is mildly

abnormal when it is pulsatile with distinct S, D components, and

severely abnormal when it is monophasic with D-only pattern. Figure

adapted from NephroPOCUS.com with permission

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Siêu âm doppler đánh giá xung huyết tĩnh mạch (VExUS)

Abhilash Koratala et al, Cardiorenal Med 2022;12:141–154. DOI: 10.1159/000526902

Left panel: Plethoric IVC (arrowhead), diastolic (D)-only pattern on hepatic vein Doppler, pulsatile portal

vein Doppler, and D-only or monophasic renal parenchymal vein Doppler obtained from a patient with fluid

overload and severe venous congestion; right panel: normal-appearing IVC with <2 cm diameter (arrowhead)

and normal venous waveforms.