标题: Treatment of severe hypovolemia or hypovolemic shock in adults [打印本页] 作者: shenxiu2 时间: 2009-12-7 18:00 标题: Treatment of severe hypovolemia or hypovolemic shock in adults 本帖最后由 shenxiu2 于 2009-12-7 19:08 编辑
Treatment of severe hypovolemia or hypovolemic shock in adults
INTRODUCTION — Rapid volume repletion is indicated in patients with severe hypovolemia or hypovolemic shock. Delayed therapy can lead to ischemic injury and possibly to irreversible shock and multiorgan system failure. Three issues generally need to be considered in this setting: the rate of fluid replacement; the type of fluid infused; and the role for buffer therapy in patients with concurrent lactic acidosis . Vasopressors, such as norepinephrine and dopamine, generally should NOT be administered since they do not correct the primary problem and tend to further reduce tissue perfusion .
RATE AND ASSESSMENT OF FLUID REPLETION — It is not possible to precisely predict the total fluid deficit in a given patient with hypovolemic shock, particularly if fluid loss continues due, for example, to bleeding or third space sequestration. In general, at least one to two liters of isotonic saline are given as rapidly as possible in an attempt to restore tissue perfusion.
Early correction of the volume deficit is essential in hypovolemic shock to prevent the decline in tissue perfusion from becoming irreversible. Irreversible shock is associated with loss of vascular tone, a drop in systemic vascular resistance, pooling of blood in the capillaries and tissues, and an impaired response to vasoactive medications.
Fluid repletion should continue at the initial rapid rate as long as the systemic blood pressure remains low. Clinical signs, including blood pressure, urine output, mental status, and peripheral perfusion, are often adequate to guide resuscitation. The development of peripheral edema is often due to acute dilutional hypoalbuminemia and should not be used as a marker for adequate fluid resuscitation or fluid overload.
An arterial line should be placed in all patients who fail to respond promptly to initial fluid resuscitation. In such patients, monitoring of central venous pressure can help direct therapy. There is little added value from measurement of the pulmonary capillary wedge pressure unless the patient has underlying cardiopulmonary disease.
If the patient does not respond promptly and central venous pressure monitoring is not available or cannot be performed, some data suggest that respiratory variation in the arterial pressure tracing can be used to estimate the adequacy of fluid resuscitation . Large respirophasic variations in the arterial systolic pressure and pulse pressure are qualitatively linked to persistent hypovolemia and right ventricular underfilling . These changes are accentuated in patients receiving mechanical ventilation.
However, despite efforts to quantify the respirophasic variations that are likely to predict persistent hypovolemia, there currently are insufficient data to support the use of definitive cutoff values for these parameters . Other potential confounders include variability among patients with respect to respiratory and heart rate, elastic recoil of the aorta, tidal volume, and the compliance of the respiratory system .
DELAYED FLUID RESUSCITATION/CONTROLLED HYPOTENSION — A different therapeutic approach that emphasizes limiting fluid resuscitation and allowing a mild degree of hypotension until hemorrhage can be controlled may be beneficial in patients with hypovolemic shock due to gunshot injuries or stab wounds. This approach is discussed separately.
CHOICE OF REPLACEMENT FLUID — The choice of replacement fluid depends in part upon the type of fluid that has been lost . As an obvious example, blood components are indicated in patients who are bleeding. In general, the hematocrit should not be raised above 35 percent; a further increase is not necessary for oxygen transport and may increase blood viscosity, potentially leading to stasis in the already compromised capillary circulation.
Colloid versus crystalloid — Both isotonic saline solutions and colloid-containing solutions have been used to replace the extracellular fluid deficit. Some physicians have advocated the administration of a colloid-containing solution (such as albumin or hetastarch) because of two possible advantages over fluid repletion with saline: (1) more rapid plasma volume expansion, since the colloid solution remains in the vascular space (in contrast to saline, two-thirds of which enters the interstitium); and (2) a lesser risk of pulmonary edema, since dilutional hypoalbuminemia will not occur
However, randomized controlled trials and systematic meta-analyses have failed to demonstrate either of these theoretical benefits :
A well-executed multicenter trial randomly assigned nearly 7000 hypovolemic medical and surgical ICU patients to fluid resuscitation using either 4 percent albumin or normal saline. All-cause mortality at 28 days (the primary end point of the study), multiorgan failure, the duration of hospitalization, and effect upon systemic pH were similar in both groups .
A meta-analysis of 55 studies, published before the above trial, pooled and analyzed data from nearly 3000 critically ill patients randomly assigned to treatment with albumin or crystalloid . There was no evidence for either improved outcome or increased mortality in patients given albumin. Subset analysis identified no group of patients, including those with trauma, burns, hypoalbuminemia, or ascites, that derived statistically significant benefit or harm from albumin transfusion.
In addition, colloid-containing solutions are not more effective in preserving pulmonary function . This lack of protection is due at least in part to the relatively high permeability of the alveolar capillaries to albumin, leading to a higher interstitial oncotic pressure than in subcutaneous tissue . As hypoalbuminemia occurs, there is a parallel reduction in alveolar interstitial protein concentration since less albumin moves across the capillary wall. The net effect is little or no change in the transcapillary oncotic pressure gradient and therefore little tendency to the development of pulmonary edema . In comparison, acute saline-induced hypoalbuminemia can lead to peripheral edema, which is a cosmetic but not life-threatening problem.
Saline solutions are equally effective in expanding the plasma volume, although 1.5 to 3 times as much saline must be given because of its extravascular distribution . This is not deleterious, however, since fluid loss also leads to an interstitial fluid deficit that is repaired by saline administration.
In summary, saline solutions are generally preferred in patients with severe volume depletion not due to bleeding; they seem to be as safe and as effective as colloid-containing solutions, and are much less expensive .
Blood substitutes — Because animal data suggest the outcome of hemorrhagic shock correlates with tissue hypoxia, acellular, oxygen carrying resuscitation fluids may improve outcome when blood transfusion is not immediately available. This subject is covered separately.
BUFFER THERAPY — Patients with marked hypoperfusion also may develop lactic acidosis, leading to a reduction in extracellular pH below 7.10. Sodium bicarbonate can be added to the replacement fluid in this setting, in an attempt to correct both the acidemia and the volume deficit. However, the efficacy of alkali therapy in lactic acidosis remains controversial. Furthermore, optimal monitoring of acid-base status may require measurement of mixed venous as well as arterial blood gases.
SUMMARY — Severe hypovolemia and particularly hypovolemic shock are life-threatening complications of a range of medical and surgical disorders. The cause is immediately apparent in patients with trauma or a massive gastrointestinal bleed, but is more difficult to identify in patients with pancreatitis or retroperitoneal hemorrhage.
Clinical clues to the presence of severe hypovolemia include tachycardia, hypotension, peripheral vasoconstriction, oliguria, and a narrowed pulse pressure in the absence of jugular venous distention or pulmonary edema.
Once the diagnosis of severe hypovolemia with or without shock is established, treatment is centered on rapid correction of the intravascular fluid deficit via crystalloid infusion; red blood cells should be used if there is ongoing hemorrhage or severe anemia. There are no strong data to support the routine use of colloid-based solutions, including albumin, in the management of severe hypovolemia.
Reversal of the clinical manifestations of severe hypovolemia is often adequate to guide resuscitation. However, in complex cases, invasive monitoring may be required.
The use of delayed fluid resuscitation or controlled hypotension in traumatically injured patients has shown some promise in animal and human studies, but more data are needed before this practice can be unequivocally endorsed. These approaches should be reserved for well-designed trials and should not be undertaken unless emergent surgical intervention is available. The role of bicarbonate therapy in patients with hypovolemia complicated by profound lactic acidosis is uncertain and at present generally limited to patients with severe academia.