Journal Reading

Perioperative Fluid and Volume Management: Physiological Basis, Tools and Strategies

Guide : dr. Agustinus Juhardi MSc, Sp.An

By : Debbie Cinthia Dewi 11-2014-194

Registrar of Anesthesia Clinical StudiesMardi Rahayu Kudus HospitalFaculty of Medicine Universitas Kristen Krida Wacana Kudus2015

Perioperative Fluid and Volume Management: Physiological Basis, Tools and StrategiesMike S Strunden1,2*, Kai Heckel1,2, Alwin E Goetz1,2, Daniel A Reuter1,2

AbstractFluid and volume therapy is an important cornerstone of treating critically ill patients in the intensive care unit and in the operating room. New findings concerning the vascular barrier, its physiological functions, and its role regarding vascular leakage have lead to a new view of fluid and volume administration. Avoiding hypervolemia, as well as hypovolemia, plays a pivotal role when treating patients both perioperatively and in the intensive care unit. The various studies comparing restrictive vs liberal fluid and volume management are not directly comparable, do not differ (in most instances) between colloid and crystalloid administration, and mostly do not refer to the vascular barriers physiologic basis. In addition, very few studies have analyzed the use of advanced hemodynamic monitoring for volume management.This article summarizes the current literature on the relevant physiology of the endothelial surface layer, discusses fluid shifting, reviews available research on fluid management strategies and the commonly used fluids, and identifies suitable variables for hemodynamic monitoring and their goal directed use.

IntroductionThere is increasing evidence that fluid management influences patients outcome as well in critical illness, as during and after major surgery. Hence, the numerous different aspects contributing to fluid management have been in the focus of both basic and clinical research during the past years. Basically three questions are intrinsically tied to fluid administration perioperatively and in critically ill patients: 1) What happens to intravascular fluid in health and disease? 2) How do different intravenous fluids behave after application? 3) What are the goals for volume administration and how can they be assessed and reached? Current basic research brought fascinating insights of the function of the endothelial vascular barrier and, in particular, regarding functional changes that lead to vascular leakage. Experimental and clinical trials investigating the effects of both crystalloid and colloid solutions and their natural and artificial representatives have shown quite conflicting results. The same accounts for the mainly clinical studies that primarily focussed on clinical goals to guide perioperative volume therapy. However, all of those three aspects cannot be separated from each other when defining rational strategies for fluid management. Thus, this review article summarizes the knowledge of the function and dysfunction of the endothelial vascular barrier, on the effect of different intravenous fluids and on the opportunities of hemodynamic monitoring to enable drawing conclusions for rational concepts of perioperative fluid and volume management.

The Underlying AspectsThe physiologic basis: why does fluid stay within the vasculature? Two thirds of human body fluid is located in the intracellular compartment. The remaining extracellular space is divided into blood plasma and interstitial space. Both compartments communicate across the vascular barrier to enable exchange of electrolytes and nutriments as the basis for cell metabolism. The positive intravascular pressure continuously forces blood toward the interstitial space. Under physiologic conditions, large molecules, such as proteins and colloids, cannot cross the barrier in relevant amounts, which is a necessity for the regular function of circulation. Otherwise, the intravascular hydrostatic pressure would lead to uncontrollable loss of fluid toward the interstitial space and disseminated tissue edema [1]. In 1896, Ernest Starling suggested an interstitial colloid osmotic pressure far below the intravascular pressure. The concentration gradient across the vascular barrier generates a flow, which is directed into the vasculature and opposes the hydrostatic pressure resulting in an only low filtration per unit of time. According to the Starling principle, only the endothelial cell line is responsible for the vascular barrier function [1]. In a rat microvessel model, it has been shown that the interstitial colloid osmotic pressure was nearly 70% to intravascular osmotic pressure without causing interstitial edema, which is in contrast to the Starlings concept, suggesting an only minor role for the interstitial protein concentration [2]. The endothelial glycocalyx plays a pivotal role in this context. Every healthy vascular endothelium is coated by transmembrane syndecans and membrane-bound glypicans containing heparan sulfate and chondroitin sulfate side chains, which together constitute the endothelial glycocalyx [3,4]. Bound plasma proteins, solubilized glycosaminoglycans, and hyaluronan are loading the glycocalyx to the endothelial surface layer (ESL), which is subject of a periodic constitution and degradation. Under physiologic conditions, the ESL has a thickness of approximately 1 m and binds approximately 800 ml of blood plasma, so plasma volume can be divided into a circulating and noncirculating part [4,5]. Accordingly, the glycocalyx seems to act as a molecular filter, retaining proteins and increasing the oncotic pressure within the endothelial surface layer. A small space between the anatomical vessel wall and the ESL remains nearly protein free [2]. Thus, fluid loss across the vascular barrier is limited by an oncotic pressure gradient within the ESL [6]! Starlings classic principle was therefore modified to the double-barrier- concept in which not only the endothelial cell line but primarily the endothelial surface layer constitutes the vascular barrier [6].

Vascular Barrier Dysfunction: Reasons and ConsequencesThe ESL constitutes the first contact surface between blood and tissue and is involved in many processes beside vascular barrier function, such as inflammation and the coagulation system. A number of studies identified various agents and pathologic states impairing the glycocalyx scaffolding and ESL thickness. In a genuine pig heart model, Chappell et al. demonstrated a 30-fold increased shedding of heparan sulphate after postischemic reperfusion [7]. These data were approved by a clinical investigation, which showed increased plasma levels of syndecan-1 and heparan sulphate in patients with global or regional ischemia who underwent major vascular surgery [8]. Beside ischemia/reperfusion injury, several circulating mediators are known to initiate glycocalyx degradation. Tumor necrosis factor (a), cytokines, proteases, and heparanase from activated mast cells are well-described actors in systemic inflammatory response syndrome leading to reduction of the ESL thickness, which triggers increased leucocyte adhesion and trans- endothelial permeability [7,9,10]. Interestingly, hypervolemia also may cause glycocalyx impairment mediated by liberation of atrial natriuretic peptide [11]. Hypervolemia resulting from inadequately high fluid administration therefore may cause iatrogenic glycocalyx damage. As shown in basic research, the dramatic consequence of a rudimentary glycocalyx, which loses much of its ability to act as a second barrier, is strongly increased transendothelial permeability and following formation of interstitial edema [7,11]. The relevance of these experimental data were impressively underlined by Nelson et al., who found increased plasma levels of glycosaminoglycans and syndecan-1 in septic patients, wheres median glycosaminoglycan levels were higher in patients who did not survive [12].

Fluid Balance: where does fluid get lost?Urine production and insensible perspiration are physiologically replaced by free water absorbed from the gastrointestinal system and primarily affect the extravascular space, if they are not pathologically increased. Because the physiologic replacement is limited in fasted patients, it has to be compensated artificially by infusing crystal loids. The composition of the used infusion should be similar to the physiologic conditions to avoid acid-base disorders, which mostly accounts for balanced crystalloid infusions. During surgery, trauma or septic shock additional fluid loss (blood loss, vascular leakage) affects mainly the intravascular compartment [13,14]. Consequently, the first type of fluid loss is attenuated by redistribution between intracellular, interstitial, and intravascular space slowly and causes dehydration, whereas the second type of loss leads to acute hypovolemia. Preoperative hypovolemia after an overnight fasting period, as described in anesthesia text books [15,16], cannot be explained by the considerations above and does not occur regularly in all patients [17]. Fluid reloading is unjustified, at least in cardiovascular healthy patients before low-invasive surgery [17]. Mediated by increased liberation of atrial natriuretic peptide, undifferentiated fluid loading can cause glycocalyx degradation, increase vascular permeability, promote tissue edema formation and therefore may constitute a starting point of the vicious circle of vascular leakage and organ failure [11,18]. Fluid loss from insensible perspiration also is obviously overestimated in many patients, although loss of only 1 ml/kg per hour occurs even when the abdominal cave is opened [19]. In theory, it should be adequate to substitute only the losses described earlier to maintain a normal blood volume in the critically ill patient. Based on the assumption that a generous fluid administration could prevent hypotension and postoperative renal failure, frequently much greater amounts are infused perioperatively [20], although there is no evidence that the incidence of renal failure is decreased by a liberal infusion regimen during surgery [21]. Furthermore, prophylactic crystalloid infusion does not influence the occurrence of hypotension caused by vessel dilatation [22]. Nevertheless, patients require much more intravenous fluids than suggested by physiologic considerations. Shown by blood volume measurements, major surgery causes a deficit of 3-6 liters in the perioperative fluid balance [23,24]. The peak even persists up to 72 hours after trauma or surgery [25]. The common explanation for this phenomenon is a fluid shift into the so-called third space. This third space can be divided into an anatomic and a nonanatomic part. Physiologic fluid shifting from the vessel toward the interstitial space across an intact vascular barrier contains only small amounts of proteins. It does not cause interstitial edema as long as it can be quantitatively managed by the lymphatic system. Losses into the anatomic third space are based on this mechanism but in a pathologic quantity [13,14], which transgresses the capacity of the lymphatic system. The nonanatomic third space, in contrast, is believed to be a compartment separated from the interstitial space [13,14]. Losses toward this compartment are assumed to be trapped and lost for extracellular exchange. Cited examples for nonanatomic third space losses are fluid accumulation in traumatized tissue, bowel, or peritoneal cavity [15,16], but despite intensive research, such a space has never been identified! Fluid is shifted from the intravascular to the interstitial space! This fluid shift can be classified into two types [13]:Type 1, occurring always and even if the vascular barrier is intact, represents the physiologic, almost protein free shift out of the vasculature. Occasionally it emerges at pathologic amounts.Type 2, the pathologic shift is caused by dysfunction of the vascular barrier. In contrast to type 1, fluid crossing the barrier contains proteins close to plasma concentration [13]. This shift has basically three reasons. First, surgical manipulation increases capillary protein permeability excessively [26]. Interstitial fluid raised approximately 10% during realization of an enteral anastomosis in a rabbit without any fluids being infused [27]. Concomitant administration of 5 ml/kg of crystalloid infusion even doubled this edema. Second, reperfusion injury and inflammatory mediators compromise the vascular barrier [7-10]. Third, iatrogenic hypervolemia can lead to glycocalyx degradation and cause an extensive shift of fluid and proteins toward the tissue [23,24]. The pathologic shift affects all intravenous fluids. Opposed to the common believe that, in contrast to crystalloids, colloids would stay within the vasculature, Rehm et al. described a volume-effect >90% only when a tetrastarch solution was infused titrated to the actual intravascular volume loss. Administered as a bolus in a normovolemic patient, two thirds of the infused volume left the vasculature immediately [23,24]. Volume resuscitation with colloids obviously requires careful titration to current losses to avoid a remarkable protein shift toward the interstitial space [14]. Based on the double-barrier concept, hypoproteinemia even intensifies a vascular barrier dysfunction and promotes tissue edema formation. Perioperative fluid shifting is reflected in clinical data published two decades ago. Lowell et al. showed a weight gain of more than 10% in >40% of patients admitted to the intensive care unit after major surgery. This increase of body weight, representing interstitial edema, correlated strongly with mortality [28].Dehydration or Hypovolemia?Dehydration, affecting primarily the extravascular compartment, and acute hypovolemia are two different diagnoses and deserve different therapeutic considerations. Urine production and insensible perspiration cause a loss of colloid free fluid, which, due to redistribution between intravascular and extravascular space, does normally not impair the intravascular compartment directly. Thus, the resulting dehydration has to be treated by refilling the extravascular space and replacing further losses by crystalloid administration [13]. In contrast, acute hypovolemia at first affects the intravascular compartment. Because crystalloids distribute freely between interstitial and intravascular space, they are not suitable for volume resuscitation in acute hypovolemia. Lost colloids and proteins cause a decreased intravascular oncotic pressure, which would be aggravated by administration of colloid-free intravenous fluid and would enforce the formation of interstitial edema. Thus, fluids that mainly remain within the vasculature and maintain oncotic pressure are needed to treat acute loss of plasma volume effectively: colloids.

Intravenous fluids: crystalloids and colloidsCrystalloidsCrystalloids freely distribute across the vascular barrier. Only one fifth of the intravenously infused amount remains intravascularly [15,16]. Proclaimed by text- books, a fourfold amount of crystalloid infusion is needed to reach comparable volume effects as achieved with colloid administration. Whereas this is true if the vascular barrier is intact, in patients suffering from capillary leakage ratios from only 1.6:1 to 1:1 (crystalloid to colloid infusion) were observed to reach equivalent effects [29,30]. Nevertheless, colloid treatment resulted in a greater linear increase in cardiac preload and output in septic and nonseptic hypovolemic patients compared with crystalloid administration [31], and its volume expansion lasted longer during acute hemorrhage experimentally [32]. Although currently discussed, regarding the double-barrier concept one could assume that colloids distribute nearly as freely as crystalloids across a seriously impaired vascular barrier. However, volume resuscitation with crystalloid infusions was associated with serious complications, such as respiratory distress syndrome, cerebral edema, and abdominal compartment syndrome in patients with major trauma [33-35] and promotes the development of hyperchloremic acidosis [36]. Even if there is ongoing discussion about the benefits and risks of balanced crystalloid solutions, their use is beneficial to avoid acid-base disorders [25].ColloidsThe only natural colloid used in clinical matters is albumin. The artificial colloids hydroxyethyl starch (HES) and gelatin are used prevalently in European countries, whereas albumin is applied less commonly [37].AlbuminUnder physiologic conditions, albumin is the molecule mainly accountable for intravascular osmotic pressure and should be an ideal colloid to restore protein loss from the vasculature. However, as a natural colloid, albumin may cause severe allergic reaction and immunologic complications. Current date concerning albumin use to treat hypovolemia mainly originate from critically ill patients. A Cochrane review of 30 randomized, con- trolled trials, including 1,419 patients with hypovolemia, showed no evidence for a reduced mortality comparing albumin to crystalloid volume resuscitation. Usage of albumin may contrariwise even increase mortality [38]. More recently, the SAFE Study, including 6,997 patients and comparing albumin to normal saline fluid resuscitation, found neither beneficial effects nor an increased mortality in the albumin group. Additionally, no differences in days of mechanical ventilation or need for renal-replacement therapy were observed [39]. In con- trast to isooncotic albumin, which does not influence the outcome of critically ill patients, treatment with hyperoncotic albumin increased mortality [40]. Therefore, administration of isooncotic albumin may be justifiable in particular cases but not as a routine strategy for volume resuscitation.GelatinsGelatins are polydispersed polypeptides from degraded bovine collagen. The average molecular weight of gelatin solutions is 30,000 to 35,000 Da and their volume- expanding power is comparable. Several studies have examined the pharmacological safety of gelatins. In brief, all preparations are said to be safe in regard to coagulation and organ integrity [15,16] except kidney function. Mahmood et al. demonstrated higher levels of serum urea and creatinine as a more distinct tubular damage in patients treated with 4% gelatin solution compared with hydroxyethyl starch (HES) solutions while undergoing aortic aneurysm surgery [41]. There- fore, use of gelatins is limited in renal-impaired patients.

Hydroxyethyl starchHydroxyethyl starch, an artificial polymer, is derived from amylopectin, which is a highly branched chain of glucose molecules obtained from waxy maize or potatoes. Conservation from degradation and water solubility are achieved by hydroxyethylation of the glucose units HES solutions are available in several preparations and vary in concentration, molecular weight, molar substitution, C2/C2 ratio, solvent, and pharmacologic profile. Although small HES molecules (< 50-60 kD) are eliminated rapidly by glomerular filtration, larger molecules are hydrolyzed to smaller fractions and are partially taken up in the reticuloendothelial system. Although this storage seems not to impair the mononuclear pha- gocytic system, it is remarkable that low molecular weight HES accumulates less compared with high molecular weight HES [42]. Negative effects of high molecular HES on the coagulation system are well described. Preparations >200 kD lead to a reduction of von Willebrand factor and factor VIII, causing a decreased platelet adhesion. Low molecular weight preparations, such as HES 130/0.4, have only minimal effects on coagulation. HES in balanced solution increases the expression of activated platelet GP IIb/IIIa, indicating an improved hemostasis [43,44]. Focusing on kidney function, an 80% rate of osmotic nephrosislike lesions and impaired renal function were reported in kidney transplant recipients after administration of HES 200/0.62 to brain-dead organ donors [45,46]. In septic patients, usage of 10% HES 200/0.5 correlated with a higher incidence of renal failure compared with crystalloids [47]. Admittedly, HES was administered without regard to exclusion criteria and dose limitations in this study. The most likely pathomechanism of renal impairment by colloids is the induction of urine hyperviscosity by infusing hyperoncotic agents in dehydrated patients. Glomerular filtration of hyperoncotic molecules causes a hyperviscous urine and results in stasis of the tubular flow [48]. Elevated plasma oncotic pressure, regardless of which genesis, is known to cause acute renal failure since more than 20 years [49]. Based on this pathogenesis, all hyperoncotic colloids may induce renal damage, whereas isooncotic tetra starch solutions, such as 6% HES 130/0.4, seem not to impair renal function [41,46]. After administration of extremely high application rates (up to 66 liters in 21 days) in patients with severe head injury, no impairment of renal function was observed [50]. In contrast to results of the VISEP study [47], the SOAP study, which included more than 3,000 critically ill septic patients treated with pentastarch and tetrastarch solutions, also showed no higher risk for renal failure [51]. Hydroxyethyl starch was administered in much lower amounts (13 vs. 70 ml/kg) and for a shorter period in the SOAP study. There is evidence that HES also modulates inflammation. Synthetic colloids inhibit neutrophil adhesion to the endothelium and neutrophil infiltration of the lung [52,53].Furthermore, HES attenuated inflammatory response in septic rats as well as in rats volume resuscitated with HES 130/0.4 during severe hemorrhagic shock by decreasing tumor necrosis factor-alpha, interleukins, and oxidative stress [53,54]. Although advantageous aspects of volume replacement with so-called modern isooncotic tetrastarch solutions, in particular in reaching early hemodynamic stability are comprehensible [31,32], data on focussed, adequately powered, prospective clinical trials proving their outcome-relevance are needed.

Goals and stategies for volume replacementBecause the primary goal of the cardiovascular system is to supply adequate amounts of oxygen to the body and to match its metabolic demands, the target of volume management is to maintain adequate tissue perfusion to ensure tissue oxygenation. Hypovolemia, as well as hypervolemia, decreases tissue perfusion and may result in organ failure [55-59]. Even supplemental oxygen does not improve oxygenation in hypoperfused tissue [60]. Because hypovolemia is a frequent cause for hemodynamic deterioration in critically ill patients, securing an adequate intravascular volume is a cornerstone of hemodynamic management. But how can we assess adequate intravascular volume? Because the relation between hemodynamic variables is complex in health already, it is even more complex in disease and their interpretation requires a solid understanding of cardiovascular regulation mechanism.In hemodynamic unstable patients, basically four functional questions need to be answered. Because the primary goal of resuscitation is to secure tissue oxygenation, the first question is already the most decisive, but also the most difficult one: Is tissue oxygenation adequate? Because representative tissue oxygenation is not measurable directly, primarily three variables are used as surrogates: mixed venous oxygen saturation; central venous oxygenation; and serum lactate. Use, interpretation, and significance of these parameters concerning assessment of tissue oxygenation are discussed elsewhere. In brief, none of them is able to detect tissue oxygen debt definitely, because every single one is influenced by various morbidities and drug interactions [61-64]. The second question is: How can cardiac output (CO), as the main determinate of oxygen delivery, be improved? Or, better representing clinical matters: Is the patient volume responsive? The third question regards the vasomotor tone: Is it increased, decreased, or normal in the hypotensive patient? Fourth, heart work: Is the heart able to sustain an adequate CO when arterial pressure is restored without going into failure [65]?Usually physicians address these questions by measuring mean arterial pressure (MAP), central venous pressure (CVP), and by observing diuresis [66]. All of these parameters are easy to measure, but actually do not allow to assess hemodynamic instability sufficiently or to differentiate its cause adequately. If disease leads to a decrease of CO, the physiologic reaction of the body, mediated by baroreceptors, is to restore the like wise decreased arterial pressure to maintain cerebral perfusion pressure [67]. This is frequently accompanied by tachycardia, caused by modulation of the sympathetic tone. Hence, hypotension reflects the failure of this compensating mechanism, whereas normotension does not automatically ensure hemodynamic stability [68]. In addition, tachycardia and hypotension can be absent during hypovolaemic shock until intravascular volume loss reaches 20% or more [69,70]. CVP shows a poor correlation to blood volume [71], is inadequate to detect hypovolemia reliably, and most notably cannot sense a decreased cardiac output and tissue oxygen debt in an early state. Furthermore, changes in CVP after volume administration do not allow any conclusions to changes in stroke volume (SV) or cardiac output (CO) [72]. Measuring CVP is therefore inadequate to assess the patients hemodynamics and to manage volume resuscitation. Because CO is the primary determinate by which oxygen donation to the tissue is varied to match metabolic requirements, the effectiveness of a resuscitation therapy can be evaluated best by continuous monitoring of cardiac output. Several different methods, ranging from the classical indicator dilution techniques to less invasive approaches, such as arterial pulse contour analysis and Doppler techniques, are clinically available. A detailed description and discussion of their individual advantages and disadvantages is beyond the scope of this article and can be found in recent reviews [73,74]. Suitable monitoring techniques for defining treatment strategies are able to assess cardiac output as well as cardiac preload and, first of all, to predict volume responsiveness of the patient, which mostly applies to volumetric and functional parameters utilizing the heart-lung interaction under mechanical ventilation [75-78]. In the past, various studies were published that favored individual concepts of perioperative volume management strategies. Most of them originated from perioperative care and focussed primarily on the treatment in the operating room. Of course, those strategies impact postoperative ICU treatment as well. Restrictive strategies were compared with permissive or liberal ones. However, commonly accepted definitions of restrictive or liberal fluid strategies do not exist, making those studies nearly incomparable. Investigators normally labelled their traditional standard fluid regimen the standard group and compared it with their own restrictive fluid administration model. Liberal in one study was already restrictive in the other trial and fluid administration followed rigid schemas or different goals. Additionally, endpoints of the given studies varied from postoperative vomiting, pain, or tissue oxygenation to bowel recovery time, which de facto rules out a comparison [79-82]. One of the most cited studies in this regard is the work of Brandstrup et al., who demonstrated that perioperative fluid restriction (2740 vs. 5388 ml) reduced the incidence of anastomotic leakage, pulmonary edema, pneumonia, and wound infection in 141 patients undergoing major colorectal surgery without increasing renal failure rate. Interestingly, a closer look at the infusion protocol reveals a comparison between crystalloid versus colloid fluid administration. The restrictive group received mainly colloids, whereas the liberal group was treated exclusively with crystalloids [79]. All of those studies have in common that no hemodynamic goals were set, which is in contrast to the goal-directed-therapy (GDT) approach known most prominently from the study by Rivers et al., in which the authors used central venous pressure, mean arterial pressure, serum lactate, and mixed venous oxygen saturation as goals to optimize the early treatment in septic patients [83]. Further peri and postoperative studies in surgical patients underline the importance of functional hemodynamic goals to improve patients outcome. In a meta-analysis encasing four prospective randomized trials, cardiac output guided fluid management reduced hospital stay and lessened complication rate [84]. Additionally, interleukin-6 response was attenuated in a colorectal surgery study using a Doppler-optimized goal-directed fluid management [85]. Gopfert et al. reported a reduced time of mechanical ventilation and intensive care unit stay in cardiac surgery patients using the global end-diastolic volume index and cardiac output to manage volume administration [86]. The extravascular lung water index may be a useful tool for GDT, too, and is subject of current discussion [87]. Furthermore, goal-directed fluid therapy reduces inflammation, morbidity, and mortality not only in severe sepsis and septic shock, but also in patients who undergo major surgery [88-90].

ConclusionsConsolidated findings regarding the endothelial surface layer led to a new comprehension of the vascular barrier. Starlings principle was adjusted to the double-barrier concept and the mechanisms of ESL alteration in critically ill patients seem to play a major role in tissue edema formation. Because glycocalyx diminution leads to an increased capillary permeability, fluid loss toward the interstitial space, commonly considered to be a loss toward the third space, is one major consequence of ESL degradation. Studies concerning fluid and volume therapy prove an adverse effect of tissue edema formation on organ function and mortality. Therefore, knowledge of the consequences of infusing different types of crystalloids and colloids during physiologic and pathologic states is necessary. Furthermore, fluid and volume administration are two different therapies for two different diagnoses. Dehydration resulting from urine loss, preoperative fasting, and insensible perspiration requires fluid administration primarily based on crystalloid infusions. Intravascular volume deficit, i.e., acute hypovolemia, resulting in a decreased cardiac output requires volume replacement, where colloid administration appears meaningful, although current clinical data are not finally consistent. The right amount of administered volume should be titrated goal directed using a strategy based on macro-hemodynamic parameters of flow and volume.

Bacaan Jurnal

Manajemen Cairan dan Volume Perioperatif : Berdasarkan Fisiologis, Pengaturan dan Strategi

Pembimbing : dr. Agustinus Juhardi MSc, Sp.An

Oleh : Debbie Cinthia Dewi 11-2014-194

Kepaniteraan Klinik Ilmu AnestesiRumah Sakit Mardi Rahayu Kudus Fakultas Kedokteran Universitas Kristen Krida Wacana Kudus2015

Manajemen Cairan dan Volume Perioperatif : Berdasarkan Fisiologis, Pengaturan dan StrategiMike S Strunden1,2*, Kai Heckel1,2, Alwin E Goetz1,2, Daniel A Reuter1,2

AbstrakTerapi cairan dan volume merupakan landasan penting dalam merawat pasien yang sakit kritis di unit perawatan intensif dan di ruang operasi. Temuan terbaru mengenai lapisan dinding pembuluh darah atau endothelium, serta fungsi fisiologis, dan peran mengenai kebocoran plasma telah memberikan pandangan baru tentang pemberian cairan dan volume. Dalam menghindari keadaan hypervolemia, serta hipovolemia, memainkan peranan yang sangat penting ketika merawat pasien selama operasi dan pasien di unit perawatan intensif. Berbagai studi membandingkan pemberian cairan dan volume secara restriktif atau dibatasi dengan pemberian yang banyak secara langsung tidak dapat disamakan, tidak begitu berbeda (dalam kebanyakan kasus) antara pemberian koloid dan pemberian kristaloid pada sebagian besar kasus tidak mengacu pada dasar fisiologis, dan pembuluh darah. Selain itu, sangat sedikit penelitian yang telah menganalisis penggunaan serta pemantauan hemodinamik canggih untuk manajemen cairan dan volume.Artikel ini merangkum literatur tentang fungsi fisiologi secara nyata berdasarkan lapisan permukaan endotel, membahas distribusi cairan, ulasan penelitian tentang strategi manajemen cairan dan cairan yang umum digunakan, dan mengidentifikasi variabel yang sesuai untuk pemantauan hemodinamik dan tujuan penggunaan yang diarahkan berdasarkan kebutuhan.

PendahuluanBanyak sumber yang mengatakan bahwa manajemen cairan mempengaruhi perbaikan keadaan pasien pada keadaan kritis saat selama dan setelah operasi besar. Oleh karena perbedaan jumlah aspek yang berkontribusi tentang manajemen cairan akhirnya penelitian terfokus kepada hal dasar dan klinis yang telah diteliti selama beberapa tahun terakhir. Pada dasarnya ada tiga hal secara intrinsik terkait dengan pemberian cairan pada pasien perioperatif dan pasien sakit kritis: 1) Apa yang terjadi pada cairan intravaskular pada keadaan sehat dan sakit? 2) Bagaimana perbedaan efek pada saat pemeberian cairan infus? 3) Apa tujuan pemberian cairan, apa saja yang dinilai dan apa telah mencapai kadarnya? Penelitian berdasarkan fungsi dinding pembuluh endotel dan khususnya mengenai perubahan fungsional yang menyebabkan kebocoran pembuluh darah memberikan pengetahuan yang menarik. Hasil dari uji penelitian dan hasil klinis dasar, memberikan perbedaan efek dari kedua larutan kristaloid dan koloid yang alami dan buatan menunjukkan hasil yang cukup bertentangan. Hal yang sama ditujukan berdasarkan hasil studi terutama klinis yang difokuskan pada tujuan untuk memandu terapi cairan dan volume pasien perioperatif. Namun, semua dari ketiga aspek tersebut tidak dapat dipisahkan satu sama lain ketika mendefinisikan strategi yang rasional untuk manajemen cairan. Dengan demikian, review artikel ini merangkum pengetahuan tentang fungsi dan disfungsi dinding lapisan pembuluh darah, pada efek dari cairan infus yang berbeda dan pada kesempatan pemantauan hemodinamik untuk memungkinkanya menarik kesimpulan tentang konsep yang benar dalam pemberian cairan perioperatif dan manajemen volume.

Aspek yang mendasariDasar fisiologis: mengapa cairan tinggal dalam pembuluh darah?Dua pertiga dari cairan tubuh manusia berada di intraseluler. Ruang ekstraselular yang tersisa dibagi menjadi plasma darah dan ruang interstitial. Kedua kompartemen tersebut saling berhubungan melintasi lapisan pembuluh darah untuk pertukaran elektrolit dan zat-zat gizi untuk metabolisme sel. Tekanan hidrostatik intravaskular yang positif terus menerus memaksa darah ke ruang interstitial. Dalam kondisi fisiologis, molekul besar, seperti protein dan koloid, tidak dapat melewati sawar pembuluh darah dalam jumlah yang besar, yang merupakan hal yang utama untuk fungsi dari sirkulasi. Jika tidak, tekanan hidrostatik intravaskular akan mengakibatkan hilangnya kendali cairan ke ruang interstitial dan akhirnya akan menyebabkan edema jaringan [1]. Pada tahun 1896, Ernest Starling mengatakan tekanan osmotik interstitial harus berada di bawah tekanan pembuluh darah intraseluler. Konsentrasi gradien melintasi lapisan dinding pembuluh darah menghasilkan aliran yang diarahkan ke pembuluh darah dan membalikkan tekanan hidrostatik mengakibatkan filtrasi menjadi rendah per unit waktu. Menurut prinsip Starling, lapisan sel endotel bertanggung jawab untuk fungsi lapisan pembuluh darah [1]. Dalam percobaan model tikus microvessel, telah ditunjukkan bahwa tekanan osmotik interstitial hampir 70% lebih rendah dari tekanan osmotik intravaskular sehingga tidak menyebabkan edema interstisial, yang tidak jauh berbeda dengan konsep Starling, yang menunjukkan hanya peran kecil untuk konsentrasi protein interstitial [2]. Lapisan membrane endotel glykokalik memainkan peran penting dalam konteks ini. Setiap endotel vaskular yang sehat dilapisi oleh syndecans transmembran dan glypicans terikat membran yang berisi heparan sulfat dan rantai samping kondroitin sulfat, yang bersama-sama merupakan glikokalik endotel [3,4]. Protein terikat plasma, glikosaminoglikan dilarutkan, dan Hyaluronan yang memuat glikokalik ke lapisan permukaan endotel (ESL), yang merupakan subjek dari konstitusi periodik dan degradasi. Dalam kondisi fisiologis, ESL memiliki ketebalan sekitar 1 mm dan mengikat sekitar 800 ml plasma darah, sehingga volume plasma dapat dibagi menjadi sirkulasi dan non sirkulasi [4,5]. Dengan demikian, glikokalik tampaknya bertindak sebagai filter molekuler, mempertahankan protein dan meningkatkan tekanan onkotik dalam lapisan permukaan endotel. Sebuah ruang kecil antara dinding pembuluh anatomi dan ESL selalu terdapat protein bebas [2]. Dengan demikian, cairan akan hilang ketika melewati dinding pembuluh darah yang dibatasi oleh gradien tekanan onkotik dalam ESL [6] Oleh karena itu prinsip klasik Starling 'dimodifikasi dengan "double-barrier-konsep" lapisan sel endotel dan lapisan dinding pembuluh darah [6].

Disfungsi Lapisan Pembuluh darah : Penyebab dan AkibatESL merupakan permukaan yang pertama kali dilewati antara darah dan jaringan dan semua proses serta fungsi terjadi dilapisan pembuluh darah tersebut, seperti peradangan dan sistem koagulasi. Sejumlah penelitian mengidentifikasi berbagai agen dan negara patologis merusak perancah glycocalyx dan ketebalan ESL. Dalam model hati babi, Chappell et al. menunjukkan 30 kali lipat peningkatan penumpahan heparan sulfat setelah reperfusi postischemic [7]. Data ini telah disetujui oleh penyelidikan klinis, yang menunjukkan peningkatan kadar plasma dari syndecan-1 dan heparan sulfat pada pasien dengan iskemia global atau regional yang menjalani operasi besar vaskuler [8]. Selain iskemia cedera / reperfusi, beberapa mediator beredar diketahui memulai degradasi glikokaliks. Tumor necrosis factor (a), sitokin, protease, dan heparanase dari sel mast diaktifkan secara aktor dalam sindrom respon inflamasi sistemik yang mengarah ke pengurangan ketebalan ESL, yang memicu peningkatan adhesi leukosit dan transendotel permeabilitas [7,9 baik dijelaskan, 10]. Menariknya, hypervolemia juga dapat menyebabkan gangguan Glikokaliks dimediasi oleh pembebasan atrial natriuretik peptida [11]. Hypervolemia akibat pemberian cairan yang tidak cukup tinggi karena dapat menyebabkan kerusakan glycocalyx iatrogenik. Seperti ditunjukkan dalam penelitian dasar, konsekuensi dramatis dari glycocalyx dasar, yang kehilangan banyak kemampuannya untuk bertindak sebagai penghalang kedua, sangat peningkatan permeabilitas transendothelial dan pembentukan berikut edema interstitial [7,11]. Relevansi ini data eksperimen yang mengesankan digaris bawahi oleh Nelson et al., Yang menemukan peningkatan kadar plasma dari glikosaminoglikan dan syndecan-1 pada pasien septik, sedangkan tingkat glikosaminoglikan median lebih tinggi pada pasien yang tidak bertahan [12].

Keseimbangan Cairan : Kemana cairan tersebut hilang ?Secara fisiologis produksi urin dan cairan yang tidak dapat diperkirakan yang keluar bisa digantikan dengan absorbsi air bebas yang berasal dari sistem gastrointestinal namun akan memberikan efek yang kurang baik di ruang ekstravaskular, bila keadaan defisiensi cairan tidak ditingkatkan. Secara fisiologis penggantian cairan pada orang yang berpuasa akan terbatas, maka dari itu harus di kompensasi dengan pemberian infus kristaloid. Komposisi dari cairan infus yang digunakan harus disesuaikan dengan kondisi fisiologis untuk menghindari ketidakseimbangan asam basa, yang memerlukan infus kristaloid yang seimbang. Dalam pembedahan, trauma atau syok sepsis yang di sertai dengan kehilangan cairan (perdarahan, kebocoran plasma) akan berdampak buruk terutama pada jaringan intravascular. Akibatnya yang pertama dari kehilangan cairan tersebut adalah kehilangan cairan menurunkan distribusi diintraseluler, interstisial, dan ruang intravaskular yang dimana secara perlahan akan menyebabkan dehidrasi, sedangkan akibat yang kedua dehidrasi dapat menyebabkan hipovolemia akut. Pada saat berpuasa dapat menimbulkan keadaan hipovolemia seperti yang dijelaskan dalam buku teks anestesi [15,16], tidak bisa dijelaskan atau disamakan dengan keadaan diatas karna hal tersebut terjadi secara fisiologis terjadi dan tidak terjadi pada semua pasien [17]. Bahkan pada pasien yang melakukan pembedahan ringan atau pembedahan non invasif dengan keadaan kardiovaskuar yang baik pemberian cairan tidak begitu diindikasikan [17]. Perbedaan muatan cairan atau perbedaan pemberian cairan dapat meningkatkan mediasi pembebasan atrial natriuretic peptide yang menyebabkan degradasi glycocalyx sehingga meningkatkan permeabilitas pembuluh darah, meningkatkan pembentukan edema jaringan hal tersebut merupakan tahap awal dari kebocoran pembuluh darah dan kegagalan organ [11,18]. Kehilangan cairan yang tidak dapat diperkirakan terkadang diberikan secara berlebihan dari yang seharusnya , walaupun saat pembedahan laparotomy hanya kehilangan cairan 1 ml / kg per jam [19]. Secara teori sebenar pemberian cairan yang cukup seharusnya dapat menggantikan cairan yang hilang seperti yang dijelaskan sebelumnya untuk mempertahankan volume darah normal pada pasien sakit kritis. Berdasarkan asumsi bahwa pemberian cairan yang lebih banyak dari seharusnya selama operasi tersebut dapat mencegah hipotensi dan gagal ginjal pasca operasi [20], meskipun tidak adanya gagal ginjal setelah operasi [21]. Selanjutnya, infus kristaloid profilaksis tidak mempengaruhi terjadinya hipotensi yang disebabkan oleh dilatasi pembuluh darah [22]. Walau bagaimanapun menurut pertimbangan fisiologis pasien memerlukan cairan intravena lebih dari yang disarankan. Berdasarkan volume darah, operasi besar menyebabkan defisit cairan 3-6 liter selama operasi dalam [23,24]. Bahkan bertahan hingga 72 jam setelah trauma atau operasi [25]. Hal tersebut terjadi karena adanya fenomena pertukaran cairan ke dalam ruang ketiga. Ruang ketiga ini dapat dibagi menjadi "anatomi" dan "nonanatomi". Pertukaran cairan fisiologi dari intervaskuler menuju ruang interstitial melintasi dinding pembuluh darah mengandung hanya sejumlah kecil protein. Ini tidak menyebabkan edema interstisial selama dibantu oleh sistem limfatik yang baik. Perpindahan cairan ke "anatomi" ruang ketiga didasarkan pada mekanisme ini, tetapi dalam jumlah yang patologis [13,14], yang melampaui batas kapasitas dari sistem limfatik. Ruang ketiga nonanatomic, sebaliknya, diyakini kompartemen terpisah dari ruang interstitial [13,14]. Ketika cairan menuju kompartemen diasumsikan terjebak dan hilang untuk pertukaran ekstraseluler. Hilangnya cairan ke nonanatomic ruang ketiga adalah akumulasi cairan dari jaringan trauma, usus, atau rongga peritoneum [15,16], tetapi meskipun penelitian intensif, ruang seperti tidak pernah diidentifikasi Cairan digeser dari intravaskular ke ruang interstitial. Pergeseran cairan ini dapat diklasifikasikan menjadi dua jenis [13]:Tipe 1, selalu terjadi dan fisiologis, pada saat pertukaran cairan hampir tidak ada protein yang bebaskeluar.Tipe 2, pertukaran cairan patologis disebabkan oleh disfungsi intravaskuler. Berbeda dengan tipe 1, cairan melintasi pembuluh darah bersama protein [13]. Pergeseran ini pada dasarnya memiliki tiga alasan. Pertama, manipulasi pembedahan meningkatkan permeabilitas kapiler sehinggs protein berlebihan [26]. Cairan interstitial meningkat sekitar 10% selama penyambungan pembuluh darah selama operasi [27]. Pemberian kritaloid 5 ml / kg dua kali lipat kemugnkinan dapat menyebabkan edema. Kedua, trauma merusak pembuluh darah mengakibatkan pengeluaran protein secara berlebihan [7-10]. Ketiga, hypervolemia iatrogenik dapat menyebabkan Glikokaliks degradasi dan menyebabkan pergeseran luas cairan dan protein ke jaringan [23,24]. Pergeseran patologis dapat mempengaruhi cairan infus. Berbeda dengan kristaloid, koloid akan tinggal di dalam pembuluh darah, Rehm et al. dijelaskan volume-efek > 90% ketika pemberian tetrastarch diarsorpsikan dengan benar maka kehilangan cairan volume intravaskular dapat diatasi. Diberikan bolus pada pasien normovolemic, dua pertiga dari volume diserap sisanya akan keluar dari pembuluh darah [23,24]. Volume resusitasi dengan koloid jelas membutuhkan titrasi yang baik, sehingga pada saat kehilangan cairan kan menghindari perpindahan protein yang besar ke ruang interstitial [14]. Berdasarkan double barrier concept, hypoproteinemia bahkan mengintensifkan disfungsi menyebabkan disfungsi dari pembuluh darah dan meningkatkan pembentukan edema jaringan. Perioperatif pergeseran cairan tercermin dalam data klinis yang diterbitkan dua dekade lalu. Lowell et al. menunjukkan kenaikan berat badan lebih dari 10% di > 40% dari pasien yang dirawat di unit perawatan intensif setelah operasi besar. Peningkatan berat badan, yang mewakili edema interstitial, berkorelasi kuat dengan kematian [28].

Dehidrasi atau Hipovolemia?Dehidrasi, paling sering memberikan dampak buruk di ekstravaskuler, dan hipovolemia akut adalah merupakan 2 diagnosa yang berbeda serta membutuhkan terapi yang berbeda. Produksi urin dan kehilangan cairan yang tak bisa diperkirakan menyebabkan kehilangan cairan, oleh karena terjadinya redistribusi diantara ruang intravaskuler dan ekstravasluler, dan pada keadaan ini tidak merusak intravaskuler secara langsung. Dengan itu dehidrasi harusnya di terapi dengan mengisi ruang ekstravaskuler dan mengganti cairan yang hilang dengan pemberian kritaloid. Sebaliknya pada keadaan hipovolemia akut akan memberikan dampak yang buruk terhadap intravaskuler. Karena kristaloid bisa secara bebas terdistribusi di intrasitial dan intravaskuler hal tersebut tidak dapat memenuhi volume resusitasi pada akut hipovolemia. Hilangnya cairan dan protein akibat penurunan tekanan onkotik intravaskuler, serta buruknya pemberian cairan koloid intravena yang berlebihan dapat menyebabkan edema interstitial. Dengan itu cairan yang akan bertahan pada vaskuler dan mempertahankan tekanan onkotik adalah kolloids yang dimana diperlukan untuk terapi pada keadaan hilangnya plasma volume.

Cairan intravena: kristaloid dan koloidKristaloidKristaloid bebas mendistribusikan seluruh barrier vaskular. Hanya seperlima dari jumlah intravena infus tetap intravascularly [15,16]. Dicanangkan buku teks, jumlah empat kali lipat dari infus kristaloid diperlukan untuk mencapai efek volume yang sebanding sebagai dicapai dengan pemberian koloid. Padahal ini benar jika penghalang vaskular masih utuh, pada pasien yang menderita rasio kebocoran kapiler dari hanya 1,6: 1 sampai 1: 1 (kristaloid untuk koloid infus) diamati untuk mencapai efek setara [29,30]. Namun demikian, pengobatan koloid menghasilkan peningkatan linear yang lebih besar dalam preload jantung dan output pada pasien hipovolemik septik dan nonseptic dibandingkan dengan pemberian kristaloid [31], dan ekspansi volume berlangsung lebih lama selama perdarahan akut eksperimental [32]. Meskipun saat ini dibahas, mengenai konsep double-penghalang satu bisa berasumsi bahwa koloid mendistribusikan hampir sebebas kristaloid di penghalang vaskular gangguan serius. Namun, resusitasi volume dengan infus kristaloid dikaitkan dengan komplikasi serius, seperti sindrom pernafasan distress, edema serebral, dan sindrom kompartemen abdominal pada pasien dengan trauma besar [33-35] dan mempromosikan pengembangan asidosis hiperkloremik [36]. Bahkan jika ada diskusi yang sedang berlangsung tentang manfaat dan risiko dari larutan kristaloid seimbang, penggunaan yang bermanfaat untuk menghindari gangguan asam-basa [25].koloidSatu-satunya koloid alami yang digunakan dalam hal klinis albumin. Koloid buatan HES (HES) dan gelatin digunakan prevalently di negara-negara Eropa, sedangkan albumin diterapkan kurang umum [37].

AlbuminDalam kondisi fisiologis, albumin adalah molekul terutama bertanggung jawab untuk tekanan osmotik intravaskular dan harus menjadi koloid yang ideal untuk mengembalikan kerugian protein dari pembuluh darah. Namun, sebagai koloid alami, albumin dapat menyebabkan reaksi alergi parah dan komplikasi imunologi. Tanggal mengenai penggunaan albumin untuk mengobati hipovolemia terutama berasal dari pasien sakit kritis. Sebuah Cochrane review 30 acak, percobaan terkontrol, termasuk 1.419 pasien dengan hipovolemia, menunjukkan tidak ada bukti untuk mortalitas membandingkan albumin untuk kristaloid resusitasi volume. Penggunaan albumin mungkin sebaliknya bahkan meningkatkan mortalitas [38]. Baru-baru ini, Studi AMAN, termasuk 6.997 pasien dan membandingkan albumin normal saline resusitasi cairan, ditemukan tidak efek menguntungkan atau mortalitas meningkat pada kelompok albumin. Selain itu, tidak ada perbedaan di hari ventilasi mekanis atau kebutuhan terapi ginjal pengganti yang diamati [39]. Dalam trast con untuk iso albumin onkotik, yang tidak mempengaruhi hasil pasien sakit kritis, pengobatan dengan hyperoncotic albumin peningkatan mortalitas [40]. Oleh karena itu, pemberian albumin isooncotic dapat dibenarkan dalam kasus-kasus tertentu, tetapi tidak sebagai strategi rutin untuk volume resusitasi.

GelatinGelatin adalah polipeptida polydisperse dari terdegradasi sapi kolagen. Berat molekul rata-rata dari solusi gelatin adalah 30.000 sampai 35.000 Da dan volume- mereka memperluas kekuasaan sebanding. Beberapa studi telah meneliti keamanan farmakologi dari gelatin. Singkatnya, semua persiapan dikatakan aman dalam hal koagulasi dan integritas organ [15,16] kecuali fungsi ginjal. Mahmood et al. menunjukkan tingkat yang lebih tinggi dari serum urea dan kreatinin sebagai kerusakan tubular lebih jelas pada pasien yang diobati dengan larutan gelatin 4% dibandingkan dengan HES (HES) solusi saat menjalani operasi aneurisma aorta [41]. Oleh karena itu, penggunaan gelatin terbatas pada pasien ginjal-gangguan.

Hidroksietil patiHidroksietil pati, polimer buatan, berasal dari amilopektin, yang merupakan rantai bercabang molekul glukosa yang diperoleh dari jagung lilin atau kentang. Konservasi dari degradasi dan kelarutan air yang dicapai oleh hydroxymethylation unit glukosa solusi HES tersedia dalam beberapa persiapan dan bervariasi dalam konsentrasi, berat molekul, substitusi molar, C2 rasio / C2, pelarut, dan profil farmakologis. Meskipun molekul HES kecil ( 200 kD menyebabkan pengurangan von Willebrand factor dan faktor VIII, menyebabkan adhesi platelet menurun. Persiapan berat molekul rendah, seperti HES 130 / 0,4, hanya memiliki efek minimal terhadap koagulasi. HES dalam larutan seimbang meningkatkan ekspresi platelet diaktifkan GP IIb / IIIa, menunjukkan hemostasis ditingkatkan [43,44]. Berfokus pada fungsi ginjal, tingkat 80% dari "osmotik lesi nephrosislike" dan gangguan fungsi ginjal dilaporkan pada penerima transplantasi ginjal setelah pemberian HES 200 / 0.62 untuk mati otak donor organ [45,46]. Pada pasien septik, penggunaan 10% HES 200 / 0,5 berkorelasi dengan insiden yang lebih tinggi dari gagal ginjal dibandingkan dengan kristaloid [47]. Diakui, HES diberikan tanpa memperhatikan kriteria eksklusi dan keterbatasan dosis dalam penelitian ini. The pathomechanism kemungkinan gangguan ginjal oleh koloid adalah induksi hiperviskositas urin dengan menanamkan agen hyperoncotic pada pasien dehidrasi. Filtrasi glomerulus molekul hyperoncotic menyebabkan urin hyperviscous dan hasil dalam stasis dari aliran tubular [48]. Peningkatan tekanan onkotik plasma, terlepas dari asal-usul, diketahui menyebabkan gagal ginjal akut sejak lebih dari 20 tahun [49]. Berdasarkan patogenesis ini, semua koloid hyperoncotic dapat menyebabkan kerusakan ginjal, sedangkan solusi pati tetra isooncotic, seperti 6% HES 130 / 0,4, tampaknya tidak merusak fungsi ginjal [41,46]. Setelah administrasi tingkat aplikasi yang sangat tinggi (sampai 66 liter dalam 21 hari) pada pasien dengan cedera kepala berat, ada penurunan fungsi ginjal yang diamati [50]. Berbeda dengan hasil penelitian VISEP [47], studi SOAP, yang mencakup lebih dari 3.000 pasien septik sakit kritis diobati dengan pentastarch dan tetrastarch solusi, juga menunjukkan risiko tidak lebih tinggi untuk gagal ginjal [51]. Hidroksietil pati diberikan dalam jumlah yang jauh lebih rendah (13 vs 70 ml / kg) dan untuk jangka waktu yang lebih pendek dalam studi SOAP. Ada bukti bahwa HES juga memodulasi peradangan. Koloid sintetik menghambat adhesi neutrofil pada endotel dan neutrofil infiltrasi paru [52,53].Selanjutnya, HES dilemahkan respon inflamasi pada tikus septik serta pada tikus volume yang diresusitasi dengan HES 130 / 0,4 pada syok hemoragik berat dengan mengurangi tumor necrosis factor-alpha, interleukin, dan stres oksidatif [53,54]. Meskipun aspek menguntungkan dari penggantian volume dengan apa yang disebut "modern" solusi tetrastarch isooncotic, khususnya dalam mencapai stabilitas hemodinamik dini dipahami [31,32], data difokuskan, didukung memadai, calon uji klinis membuktikan mereka hasil-relevansi diperlukan.

Tujuan dan strategi untuk penggantian volumeKarena tujuan utama dari sistem kardiovaskular adalah menyediakan jumlah oksigen yang cukup ke tubuh dan kebutuhan metabolik untuk mempertahankan perfusi jaringan yang memadai untuk memastikan oksigenasi jaringan. Hipovolemia, serta hypervolemia, dapat mengurangi oksigenasi perfusi jaringan dan dapat mengakibatkan kegagalan organ [55-59]. Bahkan oksigen tambahan tidak dapat meningkatkan oksigenasi di jaringan hipoperfusi [60]. Karena hipovolemia merupakan penyebab tersering untuk ketidakstabilan hemodinamik pada pasien sakit kritis, mengamankan volume intravaskular yang memadai adalah landasan manajemen hemodinamik. Tapi bagaimana kita bisa menilai volume intravaskular "memadai"? Pada keadaan yang sehat hubungan antara variabel hemodinamik sudah cukup komplek, bahkan lebih kompleks dalam penyakit dan interpretasi mereka memerlukan pemahaman yang kuat tentang cardio mekanisme regulasi vaskular.Pada pasien hemodinamik tidak stabil, pada dasarnya empat pertanyaan fungsional perlu dijawab. Karena tujuan utama resusitasi adalah untuk mengamankan oksigenasi jaringan, pertanyaan pertama sudah yang paling menentukan, tetapi juga yang paling sulit satu: Apakah oksigenasi jaringan yang memadai? Karena perwakilan oksigenasi jaringan tidak dapat diukur secara langsung, terutama tiga variabel yang digunakan sebagai pengganti: saturasi oksigen vena campuran; oksigenasi vena sentral; dan laktat serum. Gunakan, interpretasi, dan signifikansi parameter ini mengenai penilaian oksigenasi jaringan dibahas di tempat lain. Singkatnya, tidak satupun dari mereka mampu mendeteksi jaringan kekuranga oksigen secara pasti, karena setiap orang dipengaruhi oleh berbagai morbiditas dan interaksi obat [61-64]. Pertanyaan kedua adalah: Bagaimana cardiac output (CO), sebagai determinate utama pengiriman gen oxy, diperbaiki? Atau, lebih baik mewakili hal-hal klinis: Apakah volume pasien responsif? Pertanyaan ketiga menganggap ada vasomotor: Apakah meningkat, menurun, atau normal pada pasien hipotensi? Keempat, kerja jantung: Apakah jantung bisa mempertahankan CO memadai ketika tekanan arteri dipulihkan tanpa kegagalan [65]?Biasanya dokter menjawab pertanyaan ini dengan mengukur tekanan brata-rata arteri (MAP), tekanan vena sentral (CVP), dan dengan mengamati diuresis [66]. Semua parameter ini mudah untuk mengukur, tapi sebenarnya tidak memungkinkan untuk menilai ketidakstabilan hemodinamik cukup atau untuk membedakan penyebabnya memadai. Jika penyakit menyebabkan penurunan CO, reaksi fisiologis tubuh, dimediasi oleh baroreseptor, adalah untuk mengembalikan penurunan tekanan arteri untuk menjaga tekanan perfusi serebral [67]. Hal ini sering disertai dengan takikardia, disebabkan oleh modulasi nada simpatik. Oleh karena itu, hipotensi mencerminkan kegagalan mekanisme kompensasi ini, sedangkan normotensi tidak secara otomatis menjamin stabilitas hemodinamik [68]. Selain itu, takikardia dan hipotensi dapat absen selama syok hipovolemik sampai intra penyusutan volume vaskular mencapai 20% atau lebih [69,70]. CVP menunjukkan korelasi volume darah [71], tidak memadai untuk mendeteksi hipovolemia andal, dan terutama tidak bisa merasakan utang output dan jaringan oksigen jantung menurun dalam keadaan awal. Selanjutnya, perubahan CVP setelah pemberian volume yang tidak memungkinkan kesimpulan perubahan stroke volume (SV) atau cardiac output (CO) [72]. Mengukur CVP karena itu tidak memadai untuk menilai hemodinamik pasien dan untuk mengelola resusitasi volume. Karena CO adalah determinate utama dimana oksigen terse- but tion ke jaringan bervariasi untuk menyesuaikan kebutuhan metabolik, efektivitas terapi resusitasi dapat dievaluasi terbaik dengan pemantauan terus menerus dari cardiac output. Beberapa metode yang berbeda, mulai dari teknik pengenceran indikator klasik kurang pendekatan invasif, seperti analisis kontur pulsa arteri dan teknik Doppler, secara klinis tersedia. Sebuah penjelasan rinci dan diskusi keuntungan masing-masing dan kerugian adalah di luar lingkup artikel ini dan dapat ditemukan dalam tinjauan baru-baru ini [73,74]. Teknik pemantauan meja Sui untuk mendefinisikan strategi pengobatan dapat menilai cardiac output serta preload jantung dan, pertama-tama, untuk memprediksi respon volume pasien, yang sebagian besar berlaku untuk parameter volumetrik dan fungsional memanfaatkan interaksi jantung-paru di bawah mekanik ventilasi [75-78]. Di masa lalu, berbagai penelitian yang diterbitkan yang disukai konsep individu strategi manajemen volume perioperatif. Kebanyakan dari mereka berasal dari perawatan perioperatif dan difokuskan terutama pada pengobatan di ruang operasi. Tentu saja, strategi tersebut berdampak perawatan ICU pasca operasi juga. "Membatasi" strategi dibandingkan dengan "permisif" atau "liberal" yang. Namun, yang diterima secara umum definisi dari "membatasi" atau "liberal" strategi cairan tidak ada, membuat mereka hampir tak tertandingi studi. Penyidik biasanya berlabel rejimen cairan standar mereka tradisional "standar" kelompok dan membandingkannya dengan membatasi Model pemberian cairan mereka sendiri. "Liberal" di salah satu studi sudah "ketat" di sidang lain dan pemberian cairan diikuti skema kaku atau tujuan yang berbeda. Selain itu, titik akhir dari studi yang diberikan bervariasi dari muntah pasca operasi, nyeri, atau oksigenasi jaringan ke usus waktu pemulihan, yang de facto aturan keluar perbandingan [79-82]. Salah satu studi yang paling dikutip dalam hal ini adalah karya Brandstrup et al., Yang menunjukkan bahwa pembatasan cairan perioperatif (2740 vs 5388 ml) mengurangi kejadian kebocoran anastomosis, edema paru, pneumonia, dan infeksi luka di 141 pasien yang menjalani bedah kolorektal besar tanpa meningkatkan tingkat kegagalan ginjal. Menariknya, melihat lebih dekat pada protokol infus mengungkapkan perbandingan antara kristaloid dibandingkan pemberian cairan koloid. Kelompok membatasi diterima terutama koloid, sedangkan kelompok liberal diperlakukan secara eksklusif dengan kristaloid [79]. Semua dari mereka studi memiliki kesamaan yang ada gol hemodinamik yang ditetapkan, yang berbeda dengan "tujuan-diarahkan terapi (GDT) pendekatan" yang dikenal paling menonjol dari penelitian oleh Rivers et al., Di mana penulis menggunakan vena sentral tekanan, tekanan arteri rata-rata, laktat serum, dan saturasi oksigen vena campuran sebagai tujuan untuk mengoptimalkan pengobatan dini pada pasien septik [83]. Peri lanjut dan studi pasca operasi pada pasien bedah menggarisbawahi pentingnya tujuan hemodinamik "fungsional" untuk meningkatkan hasil pasien. Dalam meta-analisis membungkus empat calon percobaan acak, cardiac output dipandu cairan manajemen berkurang tinggal di rumah sakit dan berkurang tingkat komplikasi [84]. Selain itu, interleukin-6 respon dilemahkan dalam studi bedah kolorektal menggunakan tujuan-diarahkan manajemen cairan Doppler-dioptimalkan [85]. Gpfert et al. melaporkan mengurangi waktu ventilasi mekanik dan unit perawatan intensif tinggal pada pasien bedah jantung menggunakan indeks volume akhir diastolik global dan curah jantung untuk mengelola administrasi Volume [86]. Indeks air paru ekstravaskuler mungkin menjadi alat yang berguna untuk GDT, juga, dan subyek diskusi saat [87]. Selanjutnya, terapi cairan diarahkan pada tujuan mengurangi peradangan, morbiditas, dan mortalitas tidak hanya di sepsis berat dan syok septik, tetapi juga pada pasien yang menjalani operasi besar [88-90].

KesimpulanTemuan konsolidasi mengenai lapisan permukaan endotel menyebabkan pemahaman baru dari penghalang vaskular. Prinsip jalak 'itu disesuaikan dengan "konsep double-penghalang" dan mekanisme ESL perubahan pada pasien sakit kritis tampaknya memainkan peran utama dalam pembentukan edema jaringan. Karena glycocalyx penurunan mengarah ke permeabilitas kapiler meningkat, kehilangan cairan ke ruang interstitial, umumnya dianggap sebagai kerugian terhadap "ruang ketiga," adalah salah satu konsekuensi utama dari degradasi ESL. Dies murid tentang cairan dan terapi volume yang membuktikan efek buruk dari pembentukan edema jaringan pada fungsi organ dan kematian. Oleh karena itu, pengetahuan tentang konsekuensi dari menanamkan berbagai jenis kristaloid dan koloid selama negara fisiologis dan patologis diperlukan. Selanjutnya, cairan dan administrasi Volume dua terapi yang berbeda untuk dua diagnosis yang berbeda. Dehidrasi disebabkan oleh hilangnya urine, puasa pra operasi, dan keringat insensible membutuhkan pemberian cairan terutama didasarkan pada infus kristaloid. Defisit intravaskular volume, yaitu, hipovolemia akut, sehingga curah jantung menurun membutuhkan penggantian volume, di mana administrasi koloid muncul berarti, meskipun data klinis saat ini tidak akhirnya konsisten. Jumlah yang tepat volume diberikan harus dititrasi "tujuan diarahkan" menggunakan strategi berdasarkan parameter makro-hemodinamik aliran dan volume.

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