Chapter outlines
| History |
| Clinical Examination |
| Monitoring of Fluid Balance |
| Hemodynamic Monitoring |
| Laboratory Investigations |
| Serum lactate |
Both inadequate or excessive fluid replacement is detrimental [1, 2], and optimum fluid replacement is beneficial and, at times, lifesaving. So, meticulous evaluation and, on its basis, planning of proper administration of intravenous (IV) fluid is critical.
The accurate assessment of body fluid volume status requires proper history, clinical examination, hemodynamic monitoring, and laboratory investigations (Table 15.1). There is no single parameter that alone can precisely assess the hydration status [3]. Therefore, after initial resuscitation, frequent reassessment and monitoring are mandatory for the appropriate subsequent fluid administration.
| Table 15.1 Assessment of volume status |
- History
- Clinical examination and monitoring
- Hemodynamic monitoring
- Laboratory investigations
|
HISTORY
Detailed history provides valuable information about body fluid volume status and associated illnesses. Important history to be elicited are:
Fluid intake (volume and type of oral, nasogastric, or intravenous fluids).
Abnormal loss of fluid (diarrhea, vomiting, drains, high fever, and insensible losses).
Urine volume.
Symptoms of hypovolemia (increased thirst, oliguria, fatigue, weakness, or dizziness on standing).
Symptoms of hypervolemia (swelling, weight gain, shortness of breath with aggravation on exertion or lying down flat).
Coexisting illness and comorbidities (diabetes, hypertension, ischemic heart diseases, congestive heart failure, kidney failure, cirrhosis of the liver, hypoproteinemia, and malnutrition).
Medication (antihypertensive, diuretics, laxatives).
CLINICAL EXAMINATION
It is essential to assess the volume status of the patient by proper physical examination. Based on the clinical examination, the predictability of the severity of volume depletion is poor. However, in critical patients with severe volume depletion and shock, prompt clinical assessment and proper medical history are sufficient to initiate the right treatment [4]. It is essential to know the features of hypovolemia and hypervolemia to determine the volume status.
Signs of hypovolemia: Signs of volume depletion on clinical evaluation do not always correlate with the severity of hypovolemia. However, the features, based on the degree of extracellular fluid (ECF) volume depletion, are summarized below.
Mild volume depletion (<5% reduction of ECF)
- Diminished skin turgor
- Concentrated urine
- Loss of weight
Moderate volume depletion (5 to 10% reduction of ECF), as above plus
- Oliguria (<400 ml/day)
- Orthostatic tachycardia and hypotension (fall of ≥20 mm Hg systolic blood pressure or 10 mm Hg diastolic blood pressure)
Severe volume depletion (>10% reduction of ECF), as above plus
- Hypotension
- Low pulse volume, tachycardia, tachypnea
- Cold extremities, dry tongue, sunken eyeballs
- Prolonged capillary refill time (>2 seconds), and reduced skin turgor (doughy feel)
- Abnormal mental status and confusion
Difference between dehydration and hypovolemia: Terms dehydration and hypovolemia are often confusing and used interchangeably. But dehydration and hypovolemia are fundamentally different clinical disorders with different pathogenesis, clinical presentations, biochemical features, and management [5, 6]. The term dehydration refers to pure water loss producing hypertonicity and intracellular volume contraction. While hypovolemia refers to a combined loss of salt and water, causing extracellular fluid volume deficit and contraction of the blood volume. Characteristic features of dehydration are normal blood pressure, no orthostatic hypotension, and hypernatremia. Hypovolemia is characterized by orthostatic hypotension, tachycardia, decreased skin turgor, and normal or low serum sodium.
Signs of hypervolemia: Common signs of volume overload on clinical evaluation are:
- Peripheral edema, sacral edema in bedridden, and recent weight gain.
- Distended jugular vein.
- The third spacing of intravascular fluid causing ascites and pleural fluid.
- Tachycardia, tachypnea, and orthopnea.
- On auscultation, basal crepitation in the chest and third heart sounds.
MONITORING OF FLUID BALANCE
Important steps to monitor fluid balance are:
- Intake and output chart: Maintain a proper chart of fluid administered (enterally or parenterally) and fluid losses (urine output, abnormal losses such as diarrhea, vomiting, or losses from gastrointestinal drainage tubes, and insensible losses) to assess the fluid balance.
- Urine flow rate: Maintaining hourly urine output is a standard practice in all hemodynamically unstable patients. Urine output reflects tissue perfusion and is an important indicator of hydration (in the absence of glycosuria, osmotic diuresis, or diuretic therapy). Fluid therapy aims to achieve a urine output of approximately 0.5 mL/kg/h or more.
- Daily weight: The day-to-day weight chart is an accurate indicator for detecting the changes in the patient’s volume status. Weight gain suggests fluid excess, while weight loss suggests fluid deficit. The inability to obtain weight is a limitation in sick patients.
HEMODYNAMIC MONITORING
Hemodynamic monitoring is a cornerstone in the management of hemodynamically unstable patients. The goal of hemodynamic monitoring is to ensure optimal tissue perfusion and to optimize the oxygenation of the tissues. Less than 50% of hemodynamically unstable critical patients are ‘fluid responders,’ and in the rest 50% of patients, fluid administration may be harmful [7, 8], and therefore proper evaluation before administration of fluid is advisable.
Various hemodynamic monitoring techniques and parameters ranging from simple bedside examination to advanced complex methods are available (Table 15.2).
| Table 15.2 Techniques and parameters used for hemodynamic monitoring |
| A. Basic and non-invasive hemodynamic monitoring techniques
Non-invasive blood pressure measurement, pulse oximetry, continuous electrocardiography, ultra-sonogram, echocardiography, and X-ray chest
|
| B. Static hemodynamic monitoring techniques
Inferior vena cava assessment, central venous pressure monitoring, arterial cannulation, and pulmonary artery catheter monitoring
|
| C. Dynamic hemodynamic monitoring
1. Provocative techniques to detect fluid responsiveness
The fluid challenge, passive leg raising, and end-expiratory occlusion test
2. Dynamic parameters to predict fluid responsiveness
Pulse pressure variation, stroke volume variation, cardiac output, and plethysmographic variability index
3. Methods and monitors used for the assessment
a. Noninvasive cardiac output monitoring
Transthoracic echocardiography, bioimpedance or bioreactance, radial applanation tonometry, volume clamp method, ultrasound cardiac output monitoring (USCOM), and plethysmographic variability index
b. Minimally invasive cardiac output monitoring
Transesophageal echocardiography, transpulmonary thermodilution, lithium dilution, arterial pulse contour analysis, and partial CO2 rebreathing
c. Invasive cardiac output monitoring
Pulmonary thermodilution (Intermittent bolus or continuous)
|
The selection of modality varies depending on the severity of the underlying disease, resources and local expertise available at each institution, predictability of the modality, and cost-effectiveness.
There is no single hemodynamic technique or parameter which is enough to provide sufficient information in all patients [9]. Less invasive systems are safer and therefore preferred for the initial evaluation. But invasive methods provide more predictable information and therefore are preferred in critical, unstable patients or patients with shock who do not respond to initial therapy.
Non-critical patients who are hemodynamically stable require non-invasive monitoring techniques such as continuous ECG monitoring, frequent non-invasive blood pressure measurement, and peripheral pulse oximetry to assess their oxygen saturation.
The limitations of this primary monitoring modalities is a less precise or inaccurate data, but it avoids risks of harmful invasive approaches.
On the other hand, hemodynamically unstable critical patients need more precise or highly accurate data, so they require advanced hemodynamic monitoring approaches such as arterial pulse contour analysis, transesophageal echocardiography, and transpulmonary thermodilution for continuous hemodynamic monitoring [3, 10].
Noninvasive echocardiography and ultrasonogram are currently rapidly growing and preferred modalities for the initial hemodynamic assessment of shock and perioperative evaluation instead of more invasive technologies.
Dynamic parameters such as pulse pressure variation (PPV), stroke volume variation (SVV), and cardiac output (CO) are shown to be more accurate for the assessment of the volume status. Therefore, they are preferred in predicting fluid responsiveness over static invasive measures (e.g., central venous pressure and pulmonary artery catheters) [3].
However, monitoring these dynamic parameters is not routinely recommended for patients in shock who are responding well to initial treatment. Complex, high-risk patients who do not respond to initial fluid administration need measurements of dynamic parameters to evaluate the response to fluids or inotropes [3].
LABORATORY INVESTIGATIONS
Various laboratory investigations performed considering the clinical context for the monitoring of fluid therapy are:
- Routine investigations: CBC, BUN/creatinine, transaminases, and serum electrolytes.
- Additional investigations: Serum lactate level, arterial blood gas (ABG) analysis, cardiac biomarkers, coagulation profile, and urinary electrolytes.
Serum lactate
Serum lactate estimation is the most useful and valuable laboratory parameter for monitoring critically ill patients, and the high lactate level is strongly associated with the severity of sepsis [11, 12].
Elevated lactate is multifactorial: Increased serum lactate level reflects tissue hypoxia is a misconception [13]. Increased serum lactate level is a non-specific finding which can occur due to multiple causes such as impaired tissue oxygenation, stimulation of beta-2 adrenergic receptors due to increased aerobic glycolysis, medications (adrenaline, beta-2 agonists), liver failure, thiamine deficiency, or other causes [14]. So always interpret the value of serum lactate carefully in the clinical context.
Clinical application of lactate measurement
- A tool to diagnose severe sepsis or septic shock: The measurement of lactate is useful to establish the diagnosis of severe sepsis [15] and is included in the definition of recent major sepsis guidelines such as National Quality Forum Sepsis Update [16], and third international consensus definitions for sepsis and septic shock [17, 18].
- Prognostic marker on admission: Increased lactate level in the prehospital measurement or the emergency department is associated with increased mortality even in patients with initial normal vital signs [18–22]. So early elevated lactate is useful to detect occult shock, uncover subtle organ hypoperfusion, and help to detect patients who are at higher risk for deterioration and require aggressive management.
- As a component of resuscitative algorithms: Serum lactate is included as a component of resuscitative algorithms in different guidelines (e.g., Surviving Sepsis Campaign Bundle and Surviving Sepsis Campaign International Guidelines) [23, 24].
- Lactate monitoring for a shock: In addition to clinical assessment, trends in the blood lactate levels are useful to guide resuscitation [25]. Serial serum lactate measurements during resuscitation predict mortality among septic shock patients [26, 27]. So, serum lactate level is generally remeasured every 6 hours until it becomes normal [27, 28]. Lactate-guided therapy significantly reduces hospital mortality [29–31] and has a greater mortality benefit than even early goal-directed therapy [32].
- Lactate normalization predicts a favorable prognosis: Normalization of lactate within 6 hours of initial resuscitation is the strong predictor of survival [33–36]. In a recent study, even delayed normalization of lactate (i.e., within 24 hours), independently predicts decreased mortality [37].
- Lactate clearance as a prognostic marker: Early lactate clearance reduces in-hospital mortality and strongly predicts the survivor [33, 38–41]. On the contrary, persistent hyperlactatemia increases morbidity and mortality and is a strong adverse prognostic factor [38, 42, 43].
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