Nursing Interventions for Sepsis: Fluid Management

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Introduction

In clients with septic shock, fluid resuscitation is a critical intervention that restores tissue perfusion. However, there is a great deal of variation in the type of fluid, rate of administration, and the total volume of fluid administered that goes into fluid resuscitation protocol in managing a client with sepsis.

IV fluids should be prescribed like any other drug we give our clients. Each client should undergo a critical evaluation related to the indication and contraindication for different fluid types (14).

Circulatory insufficiency and shock result from inadequate perfusion relative to the tissue demands (7). Early fluid resuscitation is essential in determining the outcome of clients with circulatory insufficiency and shock.

What can cause circulatory insufficiency?

• Pump failure
• Insufficient vascular tone (the vasodilation we see in sepsis)
• Hypovolemia (7)

Clients with distributive shock (the primary shock seen in sepsis) may experience circulatory insufficiency due to the profound vasodilatation associated with the inflammatory reaction to an infection (7).

How Sepsis Affects the Different Organ Systems

Cardiovascular & Neurological

Cerebral blood flow (CBF) is maintained when MAP is between 60 to 150 mmHg. A decrease in CBF is associated with MAP below 60 and is consistently seen in septic shock. This often manifests as a change in level of consciousness or altered mental status, such as delirium (13). The decrease in blood flow can also lead to long-term cognitive decline due to brain ischemia associated with MAP below 70 mmHg (13).

Gastrointestinal & Renal

Increased peripheral vascular resistance in progressive septic shock occurs when the body shunts blood away from non-vital tissues (including the gastrointestinal and genitourinary tract) to vital tissues like the brain and heart (9). Complications can include mesenteric ischemia (or tissue death of the GI tract) and acute/chronic renal injury, as both body systems need optimal blood perfusion to function correctly (9). Maintaining MAP between 60 and 70 mmHg in septic shock may improve blood flow to the superior mesenteric artery, protecting GI function (22).

Overall Metabolism

Secondary to developing tissue hypoxia and as a result of anaerobic metabolism in the absence of adequate tissue oxygenation, clients may create a high lactic acid level as a response to the progressive tissue hypoxia. Serum lactate of 4 or greater is associated with increased severity of illness and poorer outcomes even if hypotension is absent (5).

With this knowledge, providers should be prepared to resuscitate clients who are hypotensive or have a lactate ≥4 mmol/L to expand their circulating blood volume and restore tissue perfusion pressure (5).

The Great Debate: Crystalloid vs. Colloid

Crystalloids

• Low-cost salt solutions are known to be the go-to, easy-to-grab, and often first-choice fluids (4).
• Isotonic crystalloids are the most commonly administered IV fluid internationally.
• Crystalloid solutions were first prepared in response to the cholera pandemic in 1832.
• Only 20-30% of administered crystalloid fluid will stay in the intravascular space. (18).

Examples: Sodium chloride (Normal saline), Lactated Ringers, or Plasmalyte

Colloids

They are suspensions of molecules in a carrier fluid with high enough molecular weight to prevent crossing healthy capillary membranes; thus, a more significant percentage of the administered fluid will remain intravascular (18).

Colloids are more expensive fluids, either artificial (starches, dextrans, or gelatins) or naturally occurring (16, 17).

Examples: Albumin or fresh frozen plasma.

The physiologic rationale behind favoring colloids over crystalloids is that colloids may expand intravascular volume more effectively by remaining in the intravascular space and maintaining colloid oncotic pressure (18).

Choice of Crystalloid Fluid for Resuscitation: Is Normal Saline Really “Normal”?

The use of saline versus a balanced crystalloid solution has been a topic of ongoing debate. Due to the high mortality rate, the burden to society, and increasing awareness surrounding sepsis, extensive research has been performed to identify the optimal fluid treatment protocols. Ultimately, provider preference, hospital protocol, and regional availability dictate much of the choice due to a lack of evidence-based guidelines on specific fluid decisions.

Normal Saline vs. Lactated Ringers

The Saline Against Lactated Ringers or Plasma-Lyte in the Emergency Department (SALT-ED) study is a pragmatic, cluster, multiple-crossover trial at a single center evaluating the clinical outcomes of clients treated with 0.9% NS versus balanced crystalloids in the setting of resuscitation in the emergency department (20). The study found that saline increased the risk of death or renal failure when compared to LR/Plasmalyte (20). The subgroup of clients with renal injury at the time of admission was more susceptible to adverse kidney events from saline administration (adverse kidney events included the inability to recover 50% of baseline estimated glomerular filtration rate up to 90 days after discharge) (20). This trial confirmed that saline increases the risk of renal failure compared to balanced solutions.

These results were then duplicated at Vanderbilt and included critically ill clients. The SMART trial, a pragmatic, cluster-randomized, multiple–crossover trial, was conducted in five intensive care units at an academic center and included 15,802 adult clients (18). Clients were randomized to receive either 0.9% NS or LR/Plasmalyte. Among the 7,942 clients in the balance crystalloid group, 1,139 (14.3%) had an adverse kidney event, compared to 1,211 of the 7,860 (15.4%) clients in the NS group (p = 0.04) (18). In-hospital mortality at 30 days was higher in the NS group compared to the balanced crystalloid group (11.1% vs 10.3%, respectively, p = 0.06) (18). The mortality difference in the two groups suggests that NS may not only be causing renal failure but may also be causing harm to clients via additional mechanisms, including increased inflammation (3).

Normal saline as a resuscitation fluid should not be administered in high amounts as it carries the risk of inducing hyperchloremia, acidosis, and subsequent acidosis (3). Some clients are already highly acidotic, and giving them fluid that will exacerbate their academia is poor practice. The truth is that “normal” saline is not physiologically normal. It is a hypertonic, acidotic fluid that can cause more harm than good, especially in clients who need large-volume resuscitation. The development of electrolyte disturbances secondary to fluid administration also depends on the electrolyte status of the client before resuscitation is initiated.

This is not to say that saline is bad and should never be used but to point out that just because “it’s what we’ve always used,” “it’s easy to grab,” or “the client is hyperkalemic!” are not justifiable reasons to use high volumes of NS in the resuscitation of your clients.

How Much Fluid Do Clients with Sepsis Need?

The concept of prompt IV fluid administration was first accepted after the 2001 study of early goal-directed therapy (EGDT). The results of this landmark study propelled early and protocolized fluid management to the forefront of sepsis management. Because of this study and future studies that replicated the results, the Surviving Sepsis Campaign (SSC) began promoting EGDT fluid resuscitation as a cornerstone of sepsis and septic shock management (18).

EGDT Study Protocol

In the study, clients either received standard therapy, which involved arterial and central venous catheterization and a protocol targeting a CVP 8-12 mmHg, mean arterial pressure (MAP) at least 65 mmHg, and urine output of at least 0.5 ml/kg/hr, or the EDGT group (18). The EDGT group included the components above but also included a catheter to measure central venous oxygen saturation (SvO2), six hours of treatment in the emergency department before admission, and administration of 500 mL of crystalloid fluid every 30 minutes to achieve CVP goals, vasopressors, and vasodilators to maintain MAP goals, and blood transfusions or dobutamine to achieve ScvO2 ≥ 70% (18). Overall, in-hospital mortality was 16% less with EDGT compared to standard therapy (46.5% vs 30.5%; p= 0.009) (18).

The SSC 1-hour bundle recommends the initial administration of 30 mL/kg of crystalloid fluid for hypotension or lactate ≥ 4 mmol/L as a fluid challenge with a target CVP goal ≥ 8 mmHg, ScvO2 of ≥ 70%, and normalization of lactate (3, 7, 19).

*** In the initial phases of sepsis/septic shock, a client may need repeat fluid challenges. This bolus dose is meant to rapidly expand the client’s blood volume, allowing providers to assess the client’s response to fluid resuscitation.

A key concept for dosing fluid therapy in the critically ill population is to actively address ongoing losses (drains, stomas, fistulas, hyperthermia, open wounds, or various causes of polyuria) paired with the frequent reassessment of the need for further hemodynamic support (14). While fluid administration is a critical aspect of resuscitation, excessive fluid accumulation has been associated with worse clinical outcomes- particularly the development of acute kidney injury (AKI), pulmonary edema, pleural effusions, and in some cases, an increase in ventilator days (14).

The idea of interrelated phases of fluid management, coined “ebb and flow,” differentiated according to the client’s clinical status and evolving goals for fluid need, is highly individualized but essential in managing the client with sepsis. This helps to avoid adverse events related to poor fluid management (14).

Phases of Fluid Resuscitation

Initial Phase

In the initial phase of fluid resuscitation, the objective is restoring adequate circulating blood volume, organ perfusion, and tissue oxygenation. Fluid accumulation and a positive fluid balance are expected here (14).

Second Phase

In the second phase, the goal is to maintain intravascular volume homeostasis (14), prevent excessive fluid accumulation, and avoid unnecessary fluid loading. The client should show evidence of adequate tissue perfusion by the second phase.

Third Phase

In the third and final stage, the objective centers around fluid removal and the concept of “de-resuscitation” as dictated by the state of physiologic stabilization, organ injury recovery, and convalescence (14). During this phase, unnecessary fluid accumulation may add to secondary organ injury and adverse events.

Macrocirculation End Points of Sepsis Resuscitation 

As mentioned previously, resuscitation goals for the client with sepsis are to return the client to a physiologic state that promotes adequate organ perfusion and matches metabolic supply and demand. 

Ideally, resuscitation endpoints should assess the adequacy of tissue oxygen delivery (DO2) and oxygen consumption (VO2) and be quantifiable and reproducible. Since there fails to be a single resuscitation endpoint despite years of research, providers must be able to rely on multiple endpoints to determine the client’s overall response to therapy (6). The SSC focuses its resuscitation guidelines on the original EGDT protocol with an emphasis on macro and microcirculatory endpoints (6): 

Phases of Fluid Resuscitation 

Initial Phase 

In the initial phase of fluid resuscitation, the objective is the restoration of effective circulating blood volume, organ perfusion, and tissue oxygenation. Fluid accumulation and a positive fluid balance are to be expected here (10).  

Second Phase 

In the second phase, the goal is a maintenance of intravascular volume homeostasis (10). The goal is to prevent excessive fluid accumulation and to avoid unnecessary fluid loading. By the second phase, the patient should show evidence of adequate tissue perfusion. 

Third Phase 

In the third and final stage, the objective centers around fluid removal and the concept of “de-resuscitation” as dictated by the state of physiologic stabilization, organ injury recovery, and convalescence (10). During this phase, unnecessary fluid accumulation may add to secondary organ injury and adverse events. 

Below is a photo depicting the potential consequences of fluid overload on end-organ function as adapted by Malbrain et al (1).

It is important to be aware of theses potential consequences when using fluid resuscitation as on of your nursing interventions for sepsis. Fluid resuscitation needs to be done properly to ensure the safety of the patient.

Macrocirculation End Points of Sepsis Resuscitation 

As mentioned previously, resuscitation goals for the septic patient are to return the patient to a physiologic state that promotes adequate organ perfusion and matching metabolic supply and demand. 

Ideally, resuscitation end points should assess the adequacy of tissue oxygen delivery (DO2), oxygen consumption (VO2), and should be quantifiable and reproducible. Since there fails to be a single resuscitation endpoint despite years of research, providers must be able to rely on multiple endpoints to determine the patient’s overall response to therapy (11). The SSC focuses their resuscitation guidelines on the original EGDT protocol with an emphasis on macro and microcirculatory endpoints (11): 

Central Venous Pressure

A previously well-established starting point in determining a client’s need and subsequent responsiveness to fluids is to utilize a static measurement, such as the central venous pressure (CVP) or pulmonary artery occlusion pressure (PAOP) (6). As most providers know, using the CVP as an initial resuscitation target and estimating preload adequacy is fundamentally flawed. Factors such as total blood volume, cardiac output/venous return, pulmonary hypertension, cardiac tamponade, arrhythmias, and human error involving leveling of the transducer can potentially impact the central venous pressure (6). The correct interpretation of a CVP value is as follows: a low CVP value of ≤6 almost always indicates hypovolemia. However, a high value does not exclude hypovolemia or guarantee hypervolemia.

Lactate

Moving from a “macro” point of view to a “micro” point of view, providers use several clinical and laboratory values to assess the microcirculation. Most commonly, lactate, central venous oxygenation, and capillary refill time.

Lactic acid (or lactate level) is one of the most widely accepted biomarkers used to diagnose sepsis-related organ dysfunction. The working theory behind increased lactate in septic shock is that as global tissue hypoxia occurs, oxygenation fails to meet tissue oxygen demand, increasing anaerobic metabolism…and lactic acid levels (5). Just like when you show up for that 1st day of spring 5K after spending the last 4 months on your couch watching documentary reruns… need… more… oxygen!!!

Unfortunately, this basic explanation fails to consider other contributors to elevated lactate. Although it continues to be widely accepted and used as a marker of microperfusion, providers should be aware that there are still limitations.

Elevated lactate can be attributed to 4 broad categories:

• Decreased tissue oxygen delivery – you could see elevated lactate in individuals who have had a tonic-clonic seizure, severe asthma attack, severe anemia, carbon monoxide poisoning, or chose to do one of those Spartan Races in July. (5, 11, 21)
• Underlying disease – you could have increased lactate in clients who have fulminant liver failure, lymphoma/leukemia, small cell lung cancer, pheochromocytoma, or thiamine deficiency (sepsis would also fall under this category) (6).
• Drugs & toxins – Drugs and toxins that can often be responsible for increased lactate include Biguanides, Linezolid, Cyanide poisoning, NRTIs, and beta-two agonists (6).
• Inborn errors of metabolism—The rarer inborn metabolism errors are those in clients who have enzyme deficiencies such as pyruvate dehydrogenase, pyruvate carboxylase, Fructose-1-6-diphosphatase, and phosphoenolpyruvate carboxykinase (6).

SvO2/ScvO2

Moving past lactate measurement to more technical measurements of tissue oxygenation, both mixed venous oxygen saturation (SvO2) and ScvO2 have been considered important targets because they can be used to estimate a global balance of cellular oxygen demand vs. delivery (1, 6).

A ScvO2 <70% indicates inadequate oxygen delivery to tissues, increased oxygen extraction, or a combination of the two. It is important to note that a true ScvO2 must be obtained via a central venous catheter with the tip appropriately placed at the junction of the superior vena cava and the right atrium (1, 6).

Assuming it is measured at the correct location, a ScvO2 of 70%-89% suggests a well-balanced VO2/DO2. A ScvO2 ≥90% suggests poor oxygenation utilization at the cellular level, tissue dysoxia, or microcellular shunting (6). Currently, the routine uses of SvO2 and ScvO2 are not supported in the literature, but the role may become more apparent as sepsis end-goal resuscitation research continues to increase in prevalence.

Capillary Refill Time 

While technology and invasive tests offer pertinent information, these interventions should be performed with frequent clinical examinations to assess the response. 

Capillary refill time is an essential skill that new literature is examining as a valuable tool for assessing regional and global tissue perfusion during septic shock resuscitation. 

Capillary refill time is needed for the client’s fingertip to regain color after applying direct pressure to cause blanching. In a healthy adult client, the refill time should be <3.5 seconds (6, 8).  

Table 1. Capillary Refill Measurements Based on Age Group (8) 

It is important to note that skin temperature, room temperature, age, and use of vasoactive medications can impact capillary refill time and should be considered. Assuming the client’s extremities are normothermic, a refill time of >5 seconds suggests the presence of abnormal microcirculatory flow (6). 

Serial assessment with normalization within 6 hours is associated with successful resuscitation compared to traditional resuscitation targets. 

Estimating Fluid Responsiveness with SVV and Bedside Echocardiography

Dynamic indices such as stroke volume variation (SVV), pulse pressure variation, and inferior vena cava variability have all been found to have better predictive value, sensitivity, and specificity than static indices (6). In clients who are spontaneously breathing or have arrhythmias, direct measurement tests such as the expiratory occlusion test and passive leg raise may be preferred (6).

SVV of >12 has an 88% sensitivity and 89% specificity for predicting fluid responsiveness in a client without cardiac arrhythmias and requiring mechanical ventilation. SVV is measured via an intra-arterial line (12).

Sepsis-induced cardiac dysfunction is well described and often presents as a reduction in left ventricular stroke volume and impaired myocardial performance. Noninvasive ways to measure cardiac output and cardiac indexes, including devices or basic bedside echocardiography, have become more common. The use of invasive pulmonary artery catheters is associated with more risk than client benefit, and their use has significantly decreased. The information from bedside echocardiography includes a rough estimate of cardiac output, LV and RV function, chamber fluid status, IVC size and variability, and global cardiac function. This information can be invaluable when utilized in real-time, especially to measure the responsiveness of treatments.

Fluid Challenge Without the Fluid

What could be better than determining a fluid bolus’s effect without infusing any fluid? Though these techniques are imperfect, they can provide insight into a client’s “fluid responsiveness.”

Passive Leg Raise

The passive leg raise test is another noninvasive means to assess fluid need by mimicking a fluid bolus. It involves moving a client from the semi-recumbent position to where the legs are lifted at 45 degrees, and the trunk remains horizontal (15). This induces a transfer of around 300 mL of venous blood from the inferior limbs and the splanchnic compartment to the central circulation, increasing cardiac preload (12, 15). The threshold to define fluid responsiveness with a passive leg raise test is a 10% increase in stroke volume or cardiac output (14). If the blood pressure rises within 60 seconds after passive leg raises, the client will likely respond positively to fluid resuscitation (12). This noninvasive technique is not recommended in clients with increased intrabdominal pressure (i.e., from ascites) (12).

End-Expiration Occlusion Test

The end-expiration occlusion test is another fluid-responsive test, specifically for the subset of clients who require mechanical ventilation. The test consists of stopping mechanical ventilation at end-expiration for 15 seconds and measuring the changes in cardiac output. By pausing mechanical ventilation, the cyclic impediment of venous return that occurs at each ventilator-triggered breath is stopped, increasing cardiac output. An increase in cardiac output above the threshold of 5% indicates fluid responsiveness.

Putting it Together – Performing Nursing Interventions in Sepsis.

The best approach is to use multiple techniques to measure the efficacy of fluid resuscitation. Relying on any single parameter is not ideal practice and may lead to under or over-resuscitation. The best way to use this data is to perform interventions that increase perfusion (usually a fluid bolus in sepsis) and re-measure the endpoint. A trend toward better perfusion (lower lactic acid level, faster capillary refill, etc.) indicates a positive response. A negative response can be either: 1.) inadequate volume of fluid resuscitation OR 2.) a client that is no longer fluid responsive. It can be challenging to discern the difference, but the passive leg raise or occlusion test may be helpful here. There is no fixed rule, but it is generally thought to be better to over-resuscitate than under-resuscitate.

By systematically using this approach, the aim is to properly resuscitate the client while avoiding the pitfalls of both over and under-resuscitation. Endpoints should be measured after each intervention.

For example, if you measure a lactic acid level of 8 and note delayed capillary refill on the exam, you may determine that fluids will augment cardiac output and increase tissue perfusion. Thus, you choose to administer 1L bolus. Once the bolus is complete, you should recheck the lactic acid level and do a capillary refill. It may not normalize, but there should be an improvement.

Sepsis Bundle

While fluid management is critical for restoring hemodynamic stability in clients with suspected sepsis, all sepsis-related assessments and interventions play an intricate role. The one-hour sepsis bundle is a set of formal, evidence-based clinical questions and interventions that guide clinicians in managing sepsis. The bundle starts with identifying symptoms and ends with maintaining hemodynamic stability (2, 7, 19). Follow these steps if sepsis is suspected.

• Are there signs of systemic inflammatory response syndrome (SIRS)? Does the client meet at least two of the following criteria?
  • Temperature > than 38˚C or < than 36˚C
  • Heart rate > 90
  • Respiratory rate > 20 or PaCO2 < 32 mmHg
  • WBC > 12,000 or <4,000 or immature WBCs (bands) > 10%
• Is infection suspected in a client who is immunocompromised?
• If yes to the above questions, perform a rapid clinical assessment to identify the source of infection.
• Assess the client’s hemodynamic status, draw labs, and collect urine (lactate level, blood cultures x2, blood counts, metabolic panel, and urinalysis with culture)
• After blood cultures are drawn, antibiotics are immediately administered.
• Are there signs of hypoperfusion? Are any of the following present?
  • SBP <90
  • SBP 40 mmHg below baseline
  • MAP < 65
  • Lactate level 4 or higher
• If yes, administer a lactated ringer bolus. If no, recheck the lactate level in 3 hours if the initial lactate level was more significant than two but less than 4.
• Perform a physical assessment to check for fluid responsiveness and hemodynamic stability.
• Repeat lactate level.
• Is the client hemodynamically stable now? If yes, continue to monitor. If no, start vasopressors:
  • First choice: norepinephrine (starting dose)
  • Second choice: vasopressin (starting dose)
  • Third choice: epinephrine
• If the IV fluids are responsive, give additional fluids.

Following this bundle is a quick and efficient way of identifying sepsis and ensuring the client receives prompt treatment while remaining hemodynamically stable.

Case Study

A 62-year-old client comes to the ED with lethargy and suspected sepsis. The client has a history of hypertension and depression and no known drug allergies. The client’s baseline blood pressure is 140s/80s. Current vital signs are: blood pressure 94/60, heart rate 121, temperature 38.4˚C, respiratory rate 28, oxygen saturation 87% on room air. The provider performs a rapid clinical assessment and orders to start a peripheral IV, 2 liters oxygen therapy, complete blood count, metabolic panel, lactate level, urinalysis, and urine culture. Based on the provider’s assessment, no source of infection can be identified yet.

Did the provider miss something in their orders?

Yes! You should clarify if the provider meant to order blood cultures x2.

In what order would you fulfill the orders?

First and foremost, administer the oxygen! Your client’s respiratory status is compromised. Second, a blood sample must be obtained for the complete blood count, metabolic panel, lactate level, and blood cultures. It’s essential to draw the blood cultures right away to avoid delaying antimicrobial administration. Next, start an IV. Lastly, try to collect a urine sample if your client is able.

What is the purpose of administering IV fluids to this client?

Your client’s SBP is more than 40 mmHg below the baseline. Their baseline SBP is in the 140s, and current SBP is in the 90s. That’s a difference of about 50 mmHg. This indicates hypoperfusion. The client is at risk for septic shock and needs fluid resuscitation to reach hemodynamic stability.

Lab results are in! WBCs are 23,000, lactate level 3, creatinine 2.4. The urinalysis is negative, and both the blood and urine cultures are pending. You received an order for a 1-liter normal saline IV fluid bolus and meropenem IV.

Do you need to question any of the provider’s orders now?

Yes! You should question the IV fluid bolus order. Lactated ringers are recommended over normal saline.

Now that lab results are in, how many SIRS criteria does the client meet?

The client meets all four SIRS criteria. Their temperature is > 38˚C, heart rate is> 90, respiratory rate is> 20, and WBC is> 12,000.

Is there anything you need to do right now before administering the antibiotic?

No! Blood cultures have already been drawn so that antibiotics may be given now.

What should be done to maintain the client’s creatinine level?

The IV fluids should help revive your client’s kidneys and correct the creatinine level. They have no history of kidney disease, so they are likely to have acute renal failure (or acute kidney injury) related to the infection.

You administer the lactated ringers IV bolus and meropenem IV. You receive a new order to start lactated ringers IV maintenance fluids. You perform a clinical assessment. The client is still somewhat lethargic but is more responsive. Their vital signs have responded positively to all interventions. Vitals are now: blood pressure 110/74, heart rate 93, temperature 37.8˚C, respirations 22, oxygen saturation 98% on 2 liters of oxygen. You monitor the client over the next 3 hours.

Is it time to repeat a specific lab?

Yes! A lactate level should be repeated now or after 3 hours if the initial level was between 2 and 4. Your client’s lactate level was 3.

Lactate levels are in! Your client’s new level is 1.7. Vital signs remain stable.

Should you begin vasopressors now?

No! Vasopressors are only indicated if your client is still not hemodynamically stable after all interventions have been implemented. Your role now is to continue monitoring your client simply.

Let’s say your client was not responding well to fluid resuscitation. What else can you do to redistribute fluid within the body?

In a situation like this, your client might benefit from passive leg raises to help redistribute fluid from the lower limbs to vital organs like the brain and heart. This mimics the increase in cardiac preload that would occur with an IV fluid infusion.

Congratulations! You successfully managed a client with suspected sepsis! You questioned orders appropriately. You completed all interventions promptly and in the appropriate order. Because of your actions, the client is stable, and the infection is improving. You must wait for blood culture results to ensure your client is on the most appropriate antibiotic. In cases where the source of infection is not identifiable, the provider may order additional cultures (i.e., sputum, stool, etc.) if not already ordered initially.

Conclusion

In summary, fluid resuscitation in sepsis is a controversial topic. Nurses should utilize a variety of endpoints to measure fluid and perfusion status. New evidence suggests that LR may have a physiologic benefit over NS, and albumin may have a role in the resuscitation of clients with sepsis. Fluids are vital for restoring the client to hemodynamic stability, preventing the progression of sepsis to septic shock and death. Critical thinking, assessment skills, and excellent interdisciplinary communication are vital when caring for critically ill clients such as these.

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