Shock: Fluid therapy remains a basic tenet for successful resuscitation

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Oct 01, 2005

Q. Please review shock fluid therapy for small animals.

A. Dr. Deborah Silverstein at the 2005 American College of Veterinary Internal Medicine Forum in Baltimore gave a lecture on shock fluid therapy. Some relevant points in this lecture are provided below.

Shock fluid therapy remains a basic tenet of therapy for the resuscitation of animals with non-cardiogenic shock. Volume replacement for the treatment of non-cardiogenic shock helps to restore tissue perfusion, attenuate the cytokine response, and reverse cellular swelling and injury that commonly occurs. The perfect fluid does not exist, but science has progressed in helping clinicians to better understand the use and abuse of fluid therapy for the treatment of shock. By reviewing the past, present and future of shock fluid therapy, the veterinarian might better understand the art of fluid resuscitation.

The past

During and after World War I, shock was thought to be secondary to an excessive neurogenic discharge, thus the word "shock". It was considered an over-response to the popular concept of "fight or flight". In 1960, Fogelman and Wilson found that dogs subjected to two hours of hemorrhagic hypotension followed by resuscitation with reinfusion of shed blood had 80 percent mortality. If these dogs were also given lactated Ringer's solution during resuscitation, mortality decreased to only 40 percent. Thus, the beginning of resuscitative fluid therapy commenced. Initially, blood-volume replacers not only included isotonic crystalloids but also exotic substances such as gum acacia, bovine and human plasma, plasma fractions and albumin.

The main therapeutic strategies include the arrest of bleeding and replacement of circulating blood volume. During most of the second half of the 20th century, aggressive fluid administration was recommended. The last decade re-examined this practice, and the adverse consequences of overaggressive fluid resuscitation have been recognized.

"Supranormal" endpoints of resuscitation will not increase survival and may actually do the opposite. Overzealous fluid administration to the bleeding patient may exacerbate bleeding tendencies and lead to clot disruption from increased blood flow, decreased viscosity and increased perfusion pressure. The goal is to restore effective circulating blood volume while minimizing the risk of further bleeding.

In addition, vigorous fluid resuscitation may potentiate the cellular injury caused by hemorrhagic shock and may predispose patients to interstitial edema throughout the body.

Normotensive versus hypotensive resuscitation

Hypotensive resuscitation has been advocated in order to prevent the resuscitation injury mentioned above. This technique calls for fluid administration to a goal mean arterial pressure of 60 mm Hg or systolic pressure of 90 mm Hg, the minimum pressure necessary to maintain vital organ perfusion.

It would appear that bolus administration of large quantities of crystalloids (the only fluid that is dosed using a full-blood volume) might increase blood pressure excessively and cause bleeding problems. One more recently proposed strategy for hypotensive resuscitation uses the presence or absence of a palpable peripheral pulse as a guide for fluid therapy. The British and American armed forces currently recommend that fluids be administered to maintain the presence of a radial pulse in soldiers with ongoing hemorrhage. It is important to keep in mind that the long-term effects of permissive hypotension are still unknown.

Early versus delayed resuscitation for hemorrhagic shock

The potential risks of early intravenous fluid therapy before surgical control of bleeding continue to be investigated. In an attempt to avoid the disruption of an early clot at the site of vascular injury, delayed resuscitation has been studied.

Although there is evidence to support both early and delayed resuscitation techniques, early resuscitation does appear to cause marked hepatic stability, an increase in urine output, decreased IL-6 levels and a lower mortality rate than delayed resuscitation strategies. However, the volume of fluid delivered is obviously very important. Not only are larger volumes of crystalloids more likely to dislodge early clots, but overzealous fluid administration may also lead to an increased inflammatory cytokine response and mortality.

A study performed by Siegel et al examined 40 dogs that were bled to a mean oxygen debt of 104 mL/kg and partial resuscitation strategies were investigated.

Animals that survived the shock were given 0 percent, 8.4 percent, 15 percent, 30 percent or 120 percent of the shed volume (as 5 percent albumin), held for two hours, and then administered the remaining portion of resuscitation fluid.