on 30-May-2021 (Sun)

. Zulässigkeit der Klage • Einfache Streitgenossenschaft auf Beklagtenseite (§§ 59, 60 ZPO). • Die Beklagte zu 2) ist als juristische Person gem. § 1 I 1 AktG parteifähig und durch Ihren Vorstand ordnungsgemäß vertreten. • Die örtliche Zuständigkeit bzgl. des Beklagten zu 1) folgt aus § 12, 13 ZPO, dem Gerichtsstand des Wohnortes. • Die örtliche Zuständigkeit bzgl. der Beklagten zu 2) folgt aus § 20 StVG. • Die sachliche Zuständigkeit des Amtsgerichts folgt aus §§ 23 Nr.1 GVG, weil der Streitwert 5.000.- € nicht übersteigt. Der Streitwert der Widerklage bleibt dabei als der niedrigere der beiden Streitwerte nach § 5 ZPO unberücksichtigt, weil bei dem Zuständigkeitsstreitwert - anders als gem. § 45 I 1 GKG bei der Ermittlung des Gebührenstreitwerts - die beiden Einzelstreitwerte nicht addiert werden. Der höhere der beiden Einzelstreitwerte bestimmt die sachliche Zuständigkeit.

er Kläger kann mangels erfolgter Reparatur nur „fiktiv“ auf [...] abrechnen und den Wiederbeschaffungsaufwand, d.h. Schadensersatz i.H.d. [...] abzüglich des Restwertes des Unfall-Kfz verlangen. Beim Wiederbeschaffungswert ist hier vom Netto-Betrag auszugehen, da noch nicht feststeht, ob der Kläger bei einer etwaigen späteren Ersatzbeschaffung überhaupt Mehrwertsteuer zahlen muss (§ 249 II 2 BGB)

zulässig und insbesondere gem. § 338 ZPO statthaft

Volume depletion results from loss of sodium and water from the following anatomic sites:

● Gastrointestinal losses, including vomiting, diarrhea, bleeding, and external drainage

● Renal losses, including the effects of diuretics, osmotic diuresis, salt-wasting nephropathies, and hypoaldosteronism

● Skin losses, including sweat, burns, and other dermatological conditions

● Third-space sequestration, including intestinal obstruction, crush injury, fracture, and acute pancreatitis

Gastrointestinal losses — Each day, approximately 3 to 6 liters of fluid are secreted by the stomach, pancreas, gallbladder, and intestines into the lumen of the gastrointestinal tract. Almost all of the secreted fluid is reabsorbed, so that only 100 to 200 mL are lost in the stool.

Renal losses — Under normal conditions, renal sodium and water excretion are adjusted to match intake. In a normal adult, approximately 130 to 180 liters is filtered across the glomerular capillaries each day. More than 98 to 99 percent of the filtrate is then reabsorbed by the tubules, resulting in a urine output averaging 1 to 2 L/day. Thus, a small (1 to 2 percent) reduction in tubular reabsorption can lead to a 2- to 4-liter increase in sodium and water excretion, which, if not replaced, can result in severe volume depletion.

Diuretic therapy and osmotic diuresis caused by glucosuria are the most common causes of excessive renal salt and water loss. Variable degrees of sodium wasting are also present in many different kidney diseases. As an example, most patients with chronic kidney disease and a glomerular filtration rate (GFR) of less than 25 mL/min are unable to maximally conserve sodium if acutely placed on a low-sodium diet. These patients may have an obligatory sodium loss of 10 to 40 mEq/day, in contrast to normal subjects who can lower sodium excretion to less than 5 mEq/day [1,2].

Skin losses — Although sweat production is low in the basal state, it can exceed 1 to 2 L/h in a subject exercising in a hot, dry climate [3].

Sequestration into a third-space — Volume depletion can be produced by the loss of interstitial and intravascular fluid into a third-space that is not in equilibrium with the extracellular fluid. As an example, a patient with a fractured hip may lose 1500 to 2000 mL of blood into the tissues adjacent to the fracture. Although this fluid will be resorbed back into the extracellular fluid over a period of days to weeks, the acute reduction in blood volume, if not replaced, can lead to severe volume depletion.

Symptoms — Three sets of symptoms may occur in hypovolemic patients:

● Those due to volume depletion

● Those related to the cause of fluid loss

● Those due to the electrolyte and acid-base disorders that can accompany volume depletion

Symptoms induced by hypovolemia are primarily related to decreased tissue perfusion. The earliest complaints include lassitude, easy fatigability, thirst, muscle cramps, and postural dizziness. More severe fluid loss can lead to abdominal pain, chest pain, or lethargy and confusion due to ischemia of the mesenteric, coronary, or cerebral vascular beds, respectively. These symptoms are usually reversible, although tissue necrosis may develop if the low-flow state is allowed to persist.

Patients may also report decreased urine volume or frequency. Low urine volume (oliguria) is common in hypovolemic patients due to the combination of sodium and water avidity. If, however, concentrating ability is impaired, or if there is increased urea excretion due to catabolism, oliguria may not be present.

Symptomatic hypovolemia most often occurs in patients with isosmotic sodium and water depletion in whom most of the fluid deficit comes from the extracellular fluid. This contrasts with pure water loss due to insensible losses or diabetes insipidus, in which the elevation in the plasma osmolality (and sodium concentration) causes water to move down an osmotic gradient from the cells into the extracellular fluid. The net result of pure water loss is that approximately two-thirds of the water lost comes from the intracellular fluid, a condition which is called "dehydration" rather than "hypovolemia." Patients with pure water losses exhibit the symptoms of hypernatremia (produced by the water deficit) before those of marked extracellular fluid depletion.

● Muscle weakness due to hypokalemia or hyperkalemia (see "Approach to the patient with muscle weakness")

● Polyuria and polydipsia due to severe hypokalemia (see "Clinical manifestations and treatment of hypokalemia in adults", section on 'Renal abnormalities')

● Tachypnea due to acidosis (see "Approach to the adult with metabolic acidosis")

● Neuromuscular irritability and confusion due to metabolic alkalosis (see "Clinical manifestations and evaluation of metabolic alkalosis")

● Lethargy, confusion, seizures, and coma due to hyponatremia or hypernatremia (see "Manifestations of hyponatremia and hypernatremia in adults")

An additional symptom that occurs only in primary adrenal insufficiency is extreme salt craving. Patients with this disease frequently give a history of heavily salting all foods (including those not usually salted) and even of eating salt that they have sprinkled on their hands. The mechanism responsible for this appropriate increase in salt intake is not known.

If the skin on the thigh, calf, or forearm is pinched in normal subjects, it will immediately return to its normally flat state when the pinch is released. This elastic property, called turgor, is partially dependent upon the interstitial volume of the skin and subcutaneous tissue. Interstitial fluid loss leads to diminished skin turgor, and the skin flattens more slowly after the pinch is released. In younger patients, the presence of decreased skin turgor is a reliable indicator of volume depletion.

By comparison, elasticity diminishes with age, so that reduced skin turgor does not necessarily reflect hypovolemia in older patients (more than 55 to 60 years old). In these patients, skin elasticity is usually best preserved on the inner aspect of the thighs and the skin overlying the sternum. Decreased turgor at these sites is suggestive of volume depletion. (See below.)

The skin is also usually dry in hypovolemic patients, and a dry axilla is particularly suggestive of the diagnosis [4]. The tongue and oral mucosa may also be dry since salivary secretions are commonly decreased in this setting.

Examination of the skin may be helpful in the diagnosis of primary adrenal insufficiency. The impaired release of cortisol leads to hypersecretion of ACTH, which can result in increased pigmentation of the skin, especially in the palmar creases and buccal mucosa.

Although reduced skin turgor is an important clinical finding, normal turgor does not exclude the presence of hypovolemia. This is particularly true with mild volume deficits, in young patients whose skin is very elastic, and in obese patients, since fat deposits under the skin prevent the changes in subcutaneous turgor from being appreciated.

Postural hypotension leading to dizziness may be the patient's major complaint and is strongly suggestive of hypovolemia in the absence of an autonomic neuropathy or the use of sympatholytic drugs for hypertension.

An important change that can occur with marked fluid loss is that the secondary neurohumoral vasoconstriction leads to decreased intensity of both the Korotkoff sounds (when the blood pressure is being measured with a sphygmomanometer) and the radial pulse [5,6]. As a result, a very low blood pressure suggested by auscultation or palpation may actually be associated with a near-normal pressure when measured directly by an intraarterial catheter.

Jugular venous pressure — The reduction in the vascular volume observed with hypovolemia occurs primarily in the venous circulation (which normally contains 70 percent of the blood volume), thereby leading to a decrease in venous pressure. In most patients, the venous pressure can be estimated with sufficient accuracy by physical examination. The height of the jugular venous pulse above the right atrium (5 cm above the sternal angle of Louis) approximates the atrial pressure. However, characterization of the venous pressure as either low (less than or equal to 5 cm H₂0) or high (greater than or equal to10 cm H₂0) is probably as precise an estimate as can be achieved.

However, an elevation in the BUN can also be produced by an increase in the rate of urea production or tubular reabsorption. As a result, the serum creatinine concentration is a more reliable estimate of the GFR since it is produced at a relatively constant rate by skeletal muscle and is not reabsorbed by the renal tubules. (See "Assessment of kidney function".)

In normal subjects and those with uncomplicated kidney disease, the BUN/serum creatinine ratio is approximately 10:1. However, this value may be substantially elevated in hypovolemic states because of the associated increase in urea reabsorption [8]. In general, approximately 40 to 50 percent of filtered urea is reabsorbed, much of this occurring in the proximal tubule, where it is passively linked to the reabsorption of sodium and water. Thus, the increase in proximal sodium reabsorption in volume depletion produces a parallel increase in urea reabsorption. The net effect is a fall in urea excretion and elevations in the BUN and the BUN/serum creatinine ratio, frequently to greater than 20:1. This selective rise in the BUN is called prerenal azotemia. The serum creatinine concentration will increase in this setting only if the degree of hypovolemia is severe enough to lower the GFR. (See "Etiology and diagnosis of prerenal disease and acute tubular necrosis in acute kidney injury in adults".)

Although an elevated BUN/serum creatinine may indicate hypovolemia, it is subject to misinterpretation for two major reasons: 1) the BUN is affected by the rate of urea production; a high ratio may be due solely to increased urea production (as with steroid therapy) rather than hypovolemia, whereas a normal ratio may occur in patients with hypovolemia if urea production is reduced (eg, due to decreased protein intake); 2) the serum creatinine is affected by muscle mass as well as GFR; a high ratio may be due to a low muscle mass (which lowers the serum creatinine concentration), increasing the BUN/serum creatinine ratio in the absence of hypovolemia.

A special case is the increased BUN/serum creatinine ratio in patients with upper gastrointestinal bleeding. In such patients, the ratio increases markedly for two reasons: the extracellular fluid volume is decreased due to the blood loss, which increases proximal tubule urea reabsorption; and the rate of urea production is increased due to the catabolism and absorption of blood proteins from the gastrointestinal tract.

Metabolic alkalosis and acidosis — The effect of fluid loss on acid-base balance also is variable. Although many patients maintain a normal extracellular pH, either metabolic alkalosis or metabolic acidosis can occur. Patients with vomiting or nasogastric suction or those given diuretics tend to develop metabolic alkalosis because of hydrogen ion loss and volume contraction. On the other hand, bicarbonate loss (due to diarrhea or intestinal fistulas) can lead to metabolic acidosis. In addition, lactic acidosis can occur in shock and ketoacidosis in uncontrolled diabetes mellitus.

Hematocrit and serum albumin concentration — Since red blood cells and albumin are essentially limited to the vascular space, a reduction in the plasma volume due to volume depletion tends to elevate both the hematocrit (ie, relative polycythemia) and serum albumin concentration. However, these changes are frequently absent because of underlying hypoalbuminemia and/or anemia, due, for example, to bleeding.

Manifestations of shock — The symptoms and physical findings that have been described apply to patients with mild to moderate volume depletion who are still able to maintain an adequate level of tissue perfusion. However, as the degree of hypovolemia becomes more severe, due, for example, to the loss of 30 percent of the blood volume from a ruptured aortic aneurysm, there is a marked reduction in tissue perfusion, resulting in a clinical syndrome referred to as hypovolemic shock [5,9]. This syndrome is associated with a marked increase in sympathetic activity and is characterized by tachycardia, cold, clammy extremities, cyanosis, a low urine output (usually less than 15 mL/h), and agitation and confusion due to reduced cerebral blood flow.

Manifestations in older adults — Unlike in younger individuals, excessive fluid loss in older individuals often presents with nonspecific signs and symptoms. The most specific for hypovolemia is acute weight loss; however, obtaining an accurate weight over time may be difficult in older adults. Weight loss is particularly important to identify because older adults, compared with the young, have a greater proportion of fat (relative to lean) muscle mass. Since there is less water in fat than in muscle, older individuals have a lower total body water (relative to weight) and therefore, for a given degree of fluid loss, will have a greater reduction in extracellular fluid volume.

In almost all cases, hypovolemia is a clinical diagnosis based upon the characteristic manifestations mentioned above and confirmed by a low urine sodium concentration.

An additional problem is the frequent inability to detect relative hypovolemia in patients with underlying edematous disorders or kidney failure. Although clinical and/or laboratory abnormalities may suggest relative volume depletion in some cases, others may require empiric fluid replacement therapy and/or intravascular monitoring to reverse the consequences of hypovolemia.

Urine sodium concentration — A low urine sodium concentration (or low urine chloride concentration in patients who have metabolic alkalosis) is strongly suggestive of reduced tissue perfusion, and it is usually present in hypovolemic patients unless there is a salt-wasting state (eg, diuretics, underlying kidney disease), selective renal ischemia (eg, acute glomerulonephritis or bilateral renal artery stenosis), or a very low-sodium diet.

However, the presence of a low urine sodium does not necessarily mean that the patient has true volume depletion, since edematous patients with heart failure, cirrhosis with ascites, and the nephrotic syndrome also avidly conserve sodium. These disorders are characterized by reduced effective arterial blood volume due to a primary reduction in cardiac output (heart failure), to splanchnic vasodilatation and sequestration of fluid in the peritoneal cavity and arterial shunts (cirrhosis), and to a low plasma oncotic pressure (in some patients with severe or acute nephrotic syndrome).

With the exception of those disorders in which sodium reabsorption is impaired, the urine sodium concentration in hypovolemic states should be less than 20 mEq/L and may be as low as 1 mEq/L.

There are two additional exceptions in which the urine sodium concentration may be higher than 20 mEq/L despite the presence of hypovolemia:

● When there is also a high rate of water reabsorption; in this setting, the rate of sodium excretion and urine volume are low, but the urine sodium concentration is higher than expected due to concentration of the urine.

● When sodium is excreted with another anion [10]. This most often occurs in metabolic alkalosis due to vomiting or nasogastric suction. In such disorders, the metabolic alkalosis is associated with a high filtered bicarbonate load. The stimuli that increase renal sodium and bicarbonate reabsorption (volume depletion and hypokalemia) may sometimes be inadequate to remove all of the filtered sodium and bicarbonate from the urine. Under these conditions, urinary bicarbonate excretion occurs (with sodium as the accompanying cation). This occurs early in the disorder and also intermittently during established alkalosis, usually when transient further increases in serum bicarbonate occur (disequilibration phases of metabolic alkalosis). In such settings, the urine chloride concentration remains low (ie, below 20 mEq/L) and is a better index of extracellular fluid volume.

Other laboratory tests can provide evidence for the presence of hypovolemia or reduced effective arterial blood volume, but are less specific than a low urine sodium or chloride concentration. These include the fractional excretion of sodium, the urine osmolality and specific gravity, and the urinalysis.

The FENa is most useful in the differential diagnosis of oliguric acute kidney injury with a reduced glomerular filtration rate (GFR). In this setting, the FENa is usually under 1 percent in hypovolemic patients and above 1 percent when the oliguria is due to acute tubule necrosis [11,12]. By comparison, this measurement is more difficult to evaluate in patients with a normal GFR since the filtered sodium load is so high in this setting that a different value (FENa <0.1 to 0.2 percent) must be used to diagnose volume depletion.

Urine osmolality — In hypovolemic states, the urine is relatively concentrated with an osmolality often exceeding 450 mosmol/kg [11-13]. This response may not be seen, however, if concentrating ability is impaired by kidney disease, an osmotic diuresis, the administration of diuretics, or central or nephrogenic diabetes insipidus. As an example, both severe volume depletion (which impairs urea accumulation in the renal medulla) [14] and hypokalemia (which induces antidiuretic hormone [ADH] resistance) can limit the increase in the urine osmolality in some patients. Thus, a high urine osmolality is consistent with hypovolemia, but a relatively isosmotic value does not exclude the disorder [13].

Urinary concentration can also be assessed by measuring the specific gravity. The results are less reliable than the urine osmolality because specific gravity is determined by the mass rather than number of solute particles in the urine. A value above 1.015 is suggestive, but not diagnostic, of a concentrated urine, as is usually seen with hypovolemia. The urine specific gravity is misleadingly high with proteinuria or after administration of radiocontrast agents.

Central venous pressure — It is the left ventricular end-diastolic pressures (LVEDP), and not the right atrial pressure, that is the important determinant of left ventricular output which, together with vascular resistance, determines tissue perfusion. Although an estimate of central venous pressure can help determine a patient's volume status, the central venous pressure does not adequately predict whether or not an intravenous fluid challenge will increase stroke volume and cardiac index [15].

There are two major clinical settings in which the central venous or right atrial pressure provides an unreliable estimate of the LVEDP:

● In patients with pure left-sided heart failure, the wedge pressure is increased, but the central venous pressure may remain unchanged if right ventricular function is normal. In this setting, treating a low central venous pressure with volume expanders can precipitate pulmonary edema.

● The central venous pressure tends to exceed the LVEDP in patients with pure right-sided heart failure (as with cor pulmonale or following an acute right-sided myocardial infarction). These patients may have high central venous pressures even in the presence of volume depletion; as a result, the central venous pressure cannot be used as a guide to therapy.

Bedside ultrasound — Bedside ultrasound examination of the respiratory variation of the inferior vena cava diameter has been used to augment physical examination. However, this tool has not been shown to reliably predict fluid responsiveness [16].

However, persistently edematous patients with congestive heart failure who are aggressively treated with diuretics may develop a fall in cardiac output due to relative volume depletion, and the decrease in tissue perfusion will result in a rise in the BUN. It can be difficult to distinguish clinically between progression of intrinsic heart disease and relative hypovolemia. Such patients may require a cautious therapeutic trial of saline infusion or placement of a pulmonary artery catheter for optimal fluid management.

Cirrhosis — As in congestive heart failure, the low urine sodium concentration found in cirrhotic patients with ascites and, in many cases, peripheral edema should not be confused with true volume depletion. The progressive vasodilation seen in cirrhosis leads to the activation of endogenous vasoconstrictors, sodium and water retention, and increasing renal vasoconstriction, thereby leading to a very low urine sodium concentration, hyponatremia, decreased tissue perfusion, and occasionally the hepatorenal syndrome.

The hepatorenal syndrome is a prerenal disease, as the kidneys are normal histologically and have been used successfully for kidney transplantation. However, decreased renal perfusion in this setting can also be induced by concurrent volume losses, including gastrointestinal losses, bleeding, or overly aggressive diuretic therapy. As a result, diagnosis of the hepatorenal syndrome requires the lack of improvement in kidney function following discontinuation of potential nephrotoxins and a trial of fluid repletion.

Kidney disease — The laboratory diagnosis of hypovolemia may be difficult to establish in patients with underlying kidney disease. In this setting, the urine sodium concentration may exceed 20 mEq/L, and the urine osmolality may be less than 350 mosmol/kg, since renal insufficiency impairs the ability to maximally conserve sodium and to concentrate the urine [2,13,17].

Despite this difficulty, making the correct diagnosis is important since volume depletion is a reversible cause of worsening kidney function, in contrast to progression of the underlying kidney disease. The history and physical examination may be helpful in some patients, but these findings are not always present. As a result, a cautious trial of fluid repletion may be warranted in the patient whose kidney function has deteriorated without obvious cause.

The diagnosis of intravascular volume depletion in the patient with nephrotic syndrome is particularly difficult. Despite a great deal of study, the relative roles of underfilling due to hypoalbuminemia and overflow due to renal sodium retention remain unclear and probably vary among patients [18,19]. Patients with "underfill" edema are more commonly those with a GFR greater than 75 percent of normal and with either minimal change disease of acute onset or severe hypoalbuminemia (often below 1 g/dL) [20,21]. The ability to distinguish between these two possibilities is extremely important, as diuretic therapy may be useful in those with elevated intravascular volumes but deleterious in patients with underfilling

Older adults — Although associated with nonspecific manifestations among older adults, the findings of hypernatremia and/or weight loss are suggestive for fluid loss. Additional helpful objective clinical signs, although less specific than in younger individuals, include an elevated BUN-to-creatinine ratio and a low urinary sodium concentration.

Water balance — Water losses lead to an increase in serum sodium and osmolality, resulting in stimulation of thirst and increased release of antidiuretic hormone (ADH). In normal individuals, these changes will lead to increased water intake and reduced water excretion, which will restore normal water balance. Thus, patients who are alert, have an intact thirst mechanism, and access to water will not become hypernatremic.

On a normal diet, the minimum water intake is estimated at 500 mL/day (assuming there are no increased losses). This value is based upon the balance of total water intake and production and the minimum rate of urinary loss. Individuals who can concentrate their urine to 1200 mosmol/L who excrete 600 mosmol of solute (sodium and potassium salts and urea) per day will have a minimum urine output of 500 mL (600 mosmol ÷ 1200 mosmol/L).

There are two other sources of water in addition to fluid ingestion: the water content of food (fruits and vegetables are almost 100 percent water by weight) and the water generated by oxidation of carbohydrates. There are also other sources of water loss in addition to the urine output: insensible losses and sweat.

Normal adults are considered to have a minimal obligatory water intake or generation of approximately 1600 mL per day, composed of the following:

● Ingested water – 500 mL

● Water in food – 800 mL

● Water from oxidation – 300 mL

The sources of obligatory water output in normal adults are composed of the following:

● Urine – 500 mL

● Skin – 500 mL

● Respiratory tract – 400 mL

● Stool – 200 mL

However, the water of oxidation and much of the water lost from the lungs during respiration are linked [2]. The metabolic production of CO2 and water occur in a 1:1 proportion during the oxidation of carbohydrates and fatty acids and, if the arterial pCO2 is close to 40 mmHg, these two end-products are eliminated together in alveolar air in a 1:1 proportion. Water and CO2 are eliminated in parallel because the partial pressures of water vapor (47 mmHg) and CO2 (40 mmHg) are virtually equal in alveolar air, and because both CO2 and water are nearly absent in inspired air.

Thus, the water of oxidation and most of the water normally lost from the lungs during respiration can probably be removed from estimates of water balance [2]. In most patients, only the small amount of water evaporation from the upper respiratory tract results in a negative water balance. This does not apply to patients who are hyperventilating (which increases alveolar water losses) or are on a ventilator and inspiring humidified air warmed to body temperature (which decreases alveolar water losses).

Evaporation of water from the skin as sweat (which usually has a sodium concentration of 15 to 30 mEq/L [15 to 30 mmol/L] and is therefore mostly water) is required to dissipate heat. When additional heat loss is needed, there is an increase in evaporative water losses from the skin. On the other hand, these losses diminish during fasting and inactivity.

Water — Hospitalized patients who are afebrile, not eating, and physically inactive require less than one liter of electrolyte (sodium and potassium)-free water as maintenance fluid. Maintenance water requirements can be increased or decreased by a number of factors:

● Increased water intake is required if the patient has fever, sweating, burns, tachypnea, surgical drains, polyuria, or ongoing significant gastrointestinal losses. As an example, water requirements increase by 100 to 150 mL/day for each degree of body temperature elevation over 37ºC.

● Decreased water intake is required in a number of clinical settings, including oliguric renal failure, the use of humidified air, edematous states, and hypothyroidism. In addition, sick patients may be unable to excrete excess water due to the presence of nonosmotic stimuli for the release of antidiuretic hormone (ie, syndrome of inappropriate ADH secretion).

Since the maintenance requirement for electrolyte-free water intake is less than one liter per day, a reasonable approach is to begin with two liters per day of one-half isotonic saline in 5 percent dextrose to which 20 mEq (ie, 20 mmol) of potassium chloride is added per liter. This regimen provides 9 g of sodium chloride (3.4 g of sodium), which is similar to the sodium content of a hospital diet. The presence of dextrose in the solution does not alter its tonicity, and infusion of two liters of the dextrose-containing solution provides 400 kilocalories, enough to suppress catabolism. Patients with gastrointestinal or third-space losses may require a higher rate of saline (or blood) administration to maintain volume balance.

The original solution can be continued unless one of the following occurs:

● If the serum sodium starts to fall, a more concentrated solution should be given (eg, isotonic saline in 5 percent dextrose)

● If the serum sodium starts to rise due, for example, to increased insensible losses from high fever, a more dilute solution should be given (eg, one-quarter isotonic saline in 5 percent dextrose)

● If the serum potassium starts to fall, more potassium should be added and, should it rise above normal, potassium should be eliminated

In patients with normal or near-normal renal function, hyperkalemia is a rare problem.

These parameters should be followed to assess the efficacy of volume replacement. If, for example, the urine sodium concentration remains below 15 mEq/L (15 mmol/L), then the kidney is sensing persistent volume depletion and more fluid should be given. Use of the urine sodium concentration does not apply to edematous patients with heart failure or cirrhosis in whom the urine sodium concentration is a marker of effective circulating volume depletion but not of the need for more fluid or more salt. (See "Pathophysiology and etiology of edema in adults", section on 'Renal sodium retention'.)

Rate of replacement — The rate of correction of volume depletion depends upon its severity. With severe volume depletion or hypovolemic shock, at least 1 to 2 liters of isotonic fluids are generally given as rapidly as possible in an attempt to restore tissue perfusion. Fluid replacement is continued at a rapid rate until the clinical signs of hypovolemia improve (eg, low blood pressure, low urine output, and/or impaired mental status).

In comparison, rapid fluid resuscitation is not necessary in patients with mild to moderate hypovolemia. To avoid worsening of the volume deficit, the rate of fluid administration must be greater than the rate of continued fluid losses, which is equal to the urine output plus estimated insensible losses (usually 30 to 50 mL/hour) plus any other fluid losses (eg, gastrointestinal losses) that may be present. One regimen that we have used to induce positive fluid balance in such patients is the administration of fluid at a rate that is 50 to 100 mL/hour greater than estimated fluid losses.

As examples, hypotonic solutions should be used in hypernatremia, isotonic or hypertonic saline should be used in hyponatremia, and isotonic saline and/or blood should be used in patients with blood loss. Potassium or bicarbonate may need to be added in patients with hypokalemia or metabolic acidosis.

Choosing a replacement fluid in patients with severe volume depletion, including a discussion about the use of crystalloid versus colloid, and the use of balanced crystalloid solutions versus isotonic saline are presented separately. (See "Treatment of severe hypovolemia or hypovolemic shock in adults", section on 'Choice of replacement fluid'.)

Hypernatremia — In infants, water deficits resulting in hypernatremia should generally be corrected slowly since overly rapid correction of chronic hypernatremia can cause cerebral edema, and water deficits usually develop gradually. Because this complication has only been reported in infants, the proper rate of rehydration in adults is uncertain. If, however, it is known that the water deficit developed in less than 48 hours, hypernatremia can and should be corrected rapidly. The preferred rate of correction and the supportive data are reviewed elsewhere. (See "Treatment of hypernatremia in adults", section on 'Choosing a rate of correction'.)

Sodium and/or potassium can be added to the intravenous fluid as necessary to treat concurrent volume depletion and/or hypokalemia (due, for example, to diarrhea). However, the addition of sodium and/or potassium decreases the amount of free water that is being given. If, for example, one-quarter isotonic saline is infused, then only three-quarters of the solution is free water. In this setting, approximately 1333 mL of isotonic saline must be given to provide 1000 mL of free water. If potassium is also added to the intravenous fluid, then even less free water is present and a further adjustment to the rate of infusion must be made. These adjustments are only estimates that are then guided by serial monitoring of the serum sodium.

Hyponatremia — As with hypernatremia, overly rapid correction of hyponatremia is potentially harmful if there has been time for adaptation to the electrolyte disturbance (greater than 48 hours). The administration of isotonic saline in hyponatremic patients will initially tend to raise the serum sodium since it has a higher sodium concentration than the serum.

If the cause of hyponatremia is a hypovolemic stimulus to antidiuretic hormone (ADH) secretion, then once the volume deficit is largely repaired, the stimulus to ADH secretion will be removed. This will result in the excretion of a maximally dilute urine and possible overly rapid correction of the hyponatremia that can lead to severe neurologic dysfunction.

On the other hand, if the cause of hyponatremia is the syndrome of inappropriate ADH secretion (SIADH), the urine will remain concentrated and the sodium contained in the intravenous isotonic fluid will be excreted in the urine at a higher concentration than in the infused intravenous fluid. This "desalination" phenomenon will result in a net gain of electrolyte-free water that may cause the serum sodium to fall during the infusion of isotonic saline. (See "Osmotic demyelination syndrome (ODS) and overly rapid correction of hyponatremia" and "Overview of the treatment of hyponatremia in adults".)

There are also settings in which potassium depletion is present but the serum potassium is normal or even increased. A classic example is diabetic ketoacidosis or nonketotic hyperglycemia in which both hyperosmolality and insulin deficiency promote potassium movement out of the cells, masking the presence of potassium depletion. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis", section on 'Serum potassium'.)

Rarely, the serum potassium may be low in the absence of potassium depletion, as may be seen in patients with thyrotoxic or familial hypokalemic periodic paralysis; potassium replacement in such patients can lead to hyperkalemia [7].

If potassium is added to isotonic saline or one-half isotonic saline, it limits the potential rate of infusion. In most cases, the desired rate of potassium replacement is no greater than 10 mEq per hour; in patients with life-threatening hypokalemia, the rate can be increased to 20 mEq per hour, although electrocardiographic monitoring is required. Thus, if 40 mEq of potassium has been added to a liter of intravenous (IV) solution, the rate of infusion should generally be limited to 250 mL per hour, or 500 mL per hour with electrocardiographic monitoring if the patient has life-threatening hypokalemia.

Addition of bicarbonate — A more complex solution may be required in patients with metabolic acidosis. In this setting, sodium bicarbonate may be added, particularly if the acidemia is severe (arterial pH less than 7.15 to 7.2 or less than 7 in diabetic ketoacidosis) or bicarbonate losses persist (as with severe diarrhea).

Suppose a patient with diarrhea presents with mild hypernatremia, mild hypokalemia, and a serum bicarbonate concentration of 10 mEq/L. An appropriate dilute replacement fluid in this setting might be one-quarter isotonic saline in 5 percent dextrose (containing 38.5 mEq of sodium chloride) to which 20 mEq of potassium chloride and 25 mEq (one-half ampule) of sodium bicarbonate have been added. The total cation concentration is 83.5 mEq/L, roughly equivalent to one-half isotonic saline. It is important to add potassium to the intravenous fluid in hypokalemic patients since both the administration of bicarbonate and increased insulin secretion induced by dextrose will tend to drive potassium into the cells, which will further reduce the serum potassium concentration.

An alternative regimen that can be used in patients with metabolic acidosis without hypokalemia is the addition of three ampules of sodium bicarbonate (each containing 50 mEq of sodium and 50 mL of water) to one liter of 5 percent dextrose in water, which results in a nearly isotonic solution with a sodium concentration of approximately 130 mEq/L. In contrast, addition of the same three ampules of sodium bicarbonate to one-liter of half isotonic saline (containing 77 mEq/L of sodium) results in a hypertonic solution with a sodium concentration of 197 mEq/L, which will tend to raise the serum sodium concentration. Such a solution should not be used unless the patient is hyponatremic (such as in a patient with short bowel syndrome who has mild hyponatremia and metabolic acidosis).

There is little evidence that a dextrose-saline solution has any benefit or harm compared to a saline solution alone for most patients. However, there are some exceptions to this general rule:

● Dextrose-containing solutions should be used in patients with hypoglycemia or alcohol or fasting ketoacidosis and should be given with insulin in patients with hyperkalemia and no hyperglycemia since insulin-mediated entry of potassium into cells will lower the serum potassium concentration. (See "Hypoglycemia in adults with diabetes mellitus", section on 'Reversing hypoglycemia' and "Treatment and prevention of hyperkalemia in adults", section on 'Insulin with glucose' and "Fasting ketosis and alcoholic ketoacidosis".)

● Dextrose-containing solutions should not be used in patients with uncontrolled diabetes mellitus or hypokalemia. With respect to hypokalemia, the administration of dextrose stimulates the release of insulin, which promotes potassium entry into cells with possible worsening of the hypokalemia. (See "Clinical manifestations and treatment of hypokalemia in adults", section on 'Intravenous therapy'.)

In studies of patients without diabetes who are treated with total parenteral nutrition (TPN) or in normal individuals given glucose infusions, hyperglycemia is primarily seen when glucose is given at a rate exceeding 4 to 5 mg/kg per minute, a rate that exceeds the body's ability to metabolize glucose, even with maximum doses of insulin [9-11]. In a patient weighing 70 kg, a glucose dose of 4 to 5 mg/kg per minute translates into an infusion rate greater than 5.6 to 7 mL/min (336 to 420 mL/hour) with 5 percent dextrose solutions and greater than 0.8 to 1 mL/min (48 to 60 mL/hour) with the 25 to 35 percent glucose solutions that may be used in TPN.

The usual safety of lower glucose infusion rates was demonstrated in a report of TPN in hematopoietic stem cell transplant recipients, who are typically highly stressed [12]. The proportion of hyperglycemic days was not increased compared to patients not treated with TPN at an average glucose infusion rate of 2.7 mg/kg per min (range 1.3 to 3.9 mg/kg per min).

Dextrose-induced hyperglycemia — The administration of large volumes of dextrose-containing solutions to critically ill patients can promote the development of hyperglycemia [8-10], which is in part mediated by both administering dextrose at a rate that exceeds the maximum rate of metabolism and by the counterregulatory hormone response (eg, increased epinephrine secretion) and perhaps cytokine responses [8].

● For patients who require maintenance fluid and have normal or near-normal renal function and are otherwise stable, we suggest beginning with two liters per day of one-half isotonic saline in 5 percent dextrose to which 20 mEq (ie, 20 mmol) of potassium chloride is added per liter (Grade 2C). (See 'Electrolytes' above.)

Choosing between 0.9 percent saline and buffered crystalloid — Normal saline (0.9 percent saline) is hyperchloremic relative to plasma, such that large volume resuscitation using 0.9 percent saline may be associated with the development of a hyperchloremic metabolic acidosis (table 1) [14-16].

This has led to suggestions that isotonic fluids with lower chloride concentration be used instead of 0.9 percent saline for large volume resuscitation; such fluids are termed buffered, balanced, or chloride-restrictive crystalloids and include fluids such as Lactated Ringer solution (or Hartmann solution), 0.45 percent saline solution with 75 mmol/L of sodium bicarbonate, or Plasma-Lyte.

The rationale for this recommendation is based upon the lack of an ideal standard crystalloid resuscitation solution, and data from randomized trials that are conflicting but may suggest potential benefit from buffered crystalloids in those in whom large volumes of fluids are administered (eg, >2 L). As an example, patients with hypernatremia from hypovolemia may benefit from fluids with lower concentrations of sodium or free water while those with symptomatic acute hyponatremia may benefit from hypertonic saline. Similarly, in patients with hyperchloremic acidosis, buffered crystalloids may be preferred while 0.9 percent saline may be preferred in those with hypochloremic contraction alkalosis. Potassium-containing solutions such as Lactated Ringer are traditionally avoided in patients with hyperkalemia; however, data in patients undergoing renal transplantation suggest that Lactated Ringer does not significantly increase the potassium level when compared with normal saline [17,18].

A meta-analysis of 21 randomized controlled trials (over 20,000 patients), eight of which were of high methodologic quality, found no convincing evidence of an effect of buffered solutions (balanced crystalloids) on in-hospital mortality or acute kidney injury, when compared with 0.9 percent saline (odds ratio [OR] 0.92, 95% CI 0.84-1.00; OR 0.80, 95% CI 0.40-1.62, respectively) [27]. The certainty of evidence that buffered solutions are no better than 0.9 percent saline in preventing in-hospital mortality was considered high, indicating that further research would detect little or no difference in mortality. The certainty of evidence showing that buffered solutions and 0.9 percent saline are similar in preventing acute kidney injury was considered low, so that further research could change this conclusion.

Normal saline (crystalloid) — For most patients, normal saline (0.9 percent saline) (table 1), which contains 154 mEq/L of sodium chloride, is an effective and inexpensive initial resuscitation fluid for the management of patients with hypovolemia and hypovolemic shock not due to bleeding [7,8,12,13,28,29]. This assessment is based upon several trials and meta-analyses which consistently report that although colloids expand plasma volume more effectively than isotonic crystalloids, clinically meaningful outcomes are similar [7-13,28,29].

● Hyperchloremic acidosis is due to the high concentrations of chloride relative to that in plasma and may be resolved by the administration of buffered crystalloid, provided continued fluid resuscitation is required. Hyperchloremia associated with 0.9 percent saline has also been associated with hyperkalemia due to transcellular shifts of potassium. For example, in patients undergoing renal transplantation, 0.9 percent saline administration has been associated with more cases of hyperkalemic acidosis than Lactated Ringer [17,18].

● Peripheral edema occurs because of the significant extravascular distribution of normal saline when compared with colloids (table 2 and table 3); for this reason, it has been estimated that 1.5 to 3 times as much saline must be given when compared with colloid-containing solutions [8,30-32]. However, this is not necessarily deleterious, since fluid loss also leads to an interstitial fluid deficit that is repaired by saline administration.

Buffered crystalloid — Buffered crystalloids are a reasonable alternative as either the initial resuscitation fluid or as a secondary fluid to be used if large volumes of resuscitation fluids are necessary or if hyperchloremic acidosis is a concern. Several buffered crystalloids are available (table 1). Some of these have a lower sodium concentration than 0.9 percent saline, and were associated with greater hyponatremia than saline in the SMART/SALT-ED trials [24,25]. Although buffered fluids also contain small amounts of potassium, their contribution to extracellular potassium concentration is small unless very large volumes are infused. Buffered crystalloids have nearly the same plasma-expanding properties as isotonic crystalloid solutions (table 2 and table 3).