Resuscitation of hypovolemic shock


Alfred Blalock demonstrated that injury precipitates local and regional fluid loss, the effects of which can be ameliorated by vigorous restoration of intravascular volume. This concept is foundational to understanding the pathophysiology of shock and provides the rationale underlying intravenous (IV) therapy for hemorrhage and hypovolemia.

Severe hypovolemia consists of loss of intravascular or total body fluid volume necessary to cause insufficient tissue perfusion at the local and cellular level. If not rapidly corrected, hypovolemic shock leads to refractory end-organ damage, multisystem organ failure, and death. Broadly, hypovolemic shock can be divided into two etiologies with concomitant differences in treatment ( Fig. 141.1 ). Nonhemorrhagic hypovolemic shock consists of body fluid loss and is treated primarily with fluid replacement to restore intravascular volume. Hemorrhagic shock results from blood loss and is treated with hemorrhage control, replacement of whole blood or its components, and avoidance or correction of coagulopathy.

Fig. 141.1
Etiology and Treatment of Hypovolemic Shock.

Nonhemorrhagic hypovolemic shock

Management of nonhemorrhagic hypovolemic shock centers around rapid replacement of intravascular volume and subsequent restoration of tissue perfusion. Additional priorities include management of concomitant electrolyte and acid/base abnormalities and diagnosis and treatment of the etiology of the patient’s underlying fluid loss.

Fluid resuscitation principles

For the majority of patients with hypovolemia, resuscitation should consist of rapid bolus infusion of isotonic crystalloid solution with ongoing monitoring of physiologic and laboratory data to evaluate response and dictate termination of therapy. Potential resuscitation products to treat hypovolemia include crystalloid solutions (0.9% normal saline and buffered solutions), colloid solutions (albumin, dextran, hyperoncotic starch) and blood products (fresh frozen plasma [FFP], packed red blood cells [PRBCs], platelets). Multiple large, randomized control trials (SAFE, CRISTAL ) and subsequent meta-analyses comparing outcomes with crystalloid versus colloid solutions have demonstrated no significant advantage to colloid resuscitation in terms of 28-day mortality. Data on secondary outcomes, including renal replacement and intensive care unit (ICU) and hospital length of stay have been mixed, but no clear benefit to colloid resuscitation has been demonstrated. Notably, in subgroup analysis of the SAFE trial, resuscitation with albumin was associated with higher mortality among patients with head injuries. Because of a lack of demonstrable benefit and higher cost of colloid, crystalloid resuscitation should be used as the first-line resuscitation fluid for severe hypovolemia in critically ill patients. Despite a paucity of data favoring colloid use, albumin may be an appropriate resuscitation adjunct in cases of refractory hypovolemia thought to be secondary to low oncotic pressure. Other colloid solutions, including hyperoncotic starch, have been associated in large, randomized trials with increased risk of renal failure and death and should not be used to treat hypovolemia. ,

There is ongoing debate regarding the most appropriate crystalloid product for resuscitation for hypovolemia. Normal saline contains high levels of sodium and chloride compared with plasma (154 mEq/L each of Na and Cl), raising concerns that particularly large volume resuscitations of 0.9% normal saline may precipitate hyperchloremic metabolic acidosis. Buffered isotonic solutions, including PlasmaLyte-A and lactated Ringer’s, have been suggested as potential first-line alternatives in resuscitation. The 2018 Balanced Crystalloids versus Saline in Critically Ill Adults (SMART) trial randomized over 15,000 critically ill patients to either 0.9% normal saline or buffered crystalloids. The authors reported a lower composite rate of 30- day all-cause mortality, new need for renal replacement therapy, or renal dysfunction among patients resuscitated with buffered solutions compared with 0.9% normal saline (odds ratio [OR] 0.91, P = .04). However, a 2019 Cochrane database meta-analysis of 21 randomized controlled trials and 20,000 patients failed to find an advantage of buffered solutions over 0.9% normal saline with regard to hospital mortality or renal failure. Overall, data suggest that infusion of buffered isotonic crystalloids is likely a reasonable first-line approach for resuscitation of hypovolemic shock among critically ill patients, although specific fluid choice should continue to be tailored to each patient’s specific metabolic and physiologic parameters.

Electrolyte and acid/base disturbances

Nonhemorrhagic hypovolemic shock often occurs concomitantly with or results in metabolic disturbances, including critical excesses or deficiencies of electrolytes such as sodium, potassium, magnesium, chloride, bicarbonate, and disordered acid/base balance. Although the detailed discussion of the management of electrolyte abnormalities is addressed elsewhere in this text, it is important to rapidly identify and correct these disturbances to restore physiologic homeostasis to the patient in hypovolemic shock.

Etiologies of nonhemorrhagic hypovolemic shock

Although the cornerstone of managing nonhemorrhagic hypovolemic shock is rapid fluid replacement, identification and treatment of the underlying cause of fluid loss is necessary to avoid further hypovolemia and tailor resuscitation strategy. Etiologies of hypovolemic shock include inadequate fluid intake (often in hospitalized, elderly, debilitated, or restrained patients) or losses of fluid from the skin or soft tissue (exertional and insensible losses during strenuous activity, burns and desquamating conditions, open wound and abdomens), the gastrointestinal tract (vomiting, diarrhea, nasoenteric tube, biliary drain, or ostomy losses), third-spacing conditions (sepsis, small bowel obstruction, cirrhosis, heart failure, pancreatitis), and renal conditions in which resorption of electrolytes or water is impaired (diabetes insipidus, cerebral salt wasting, diuretic overuse). Clinical work-up, laboratory, and imaging studies should focus on diagnosis of these conditions.

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