Special Feature -- End Points in Shock Resuscitation: Current Concepts
January 1, 2001 8 minutes read
Special Feature
End Points in Shock Resuscitation: Current Concepts
By Karen Johnson, PhD, RN, CCRN
The issue of end points in resuscitation in the critically injured patient is one of the greatest sources of confusion and controversies in trauma care.1 What constitutes adequate resuscitation? What clinical parameters can be used to determine adequacy of shock resuscitation? The initial step in managing shock in the injured patient is to recognize its presence. According to Advanced Trauma Life Support, the diagnosis is based on clinical appreciation of the presence of inadequate organ perfusion and tissue oxygenation.2 This provides us with a good working definition because it contains the end points of resuscitation: correction of inadequate organ perfusion and tissue oxygenation. What are the clinical manifestations of inadequate perfusion and impaired oxygenation?
Traditional End Points of Resuscitation: Global Oxygenation Variables
Traditional clinical signs of inadequate perfusion and impaired oxygenation include hypotension, tachycardia, decreased mentation, and urine output. However, these signs can be misleading in trauma patients. They are sensitive but nonspecific indicators of physiologic abnormalities. "Normal" blood pressure is individualized. A blood pressure of 80/40 mm Hg may be normal for one patient, yet extremely hypotensive for another. Tachycardia can occur in response to shock, but may also be present in patients with anxiety, pain, fever, or substance abuse/withdrawal. Mentation is difficult to assess in trauma patients due to head injury and the presence of alcohol or other drugs. Clinicians often use urine output as a marker of adequate fluid resuscitation. However, adequate urine output in the face of hypoperfusion can occur during the initial neuroendocrine response to trauma as hyperglycemia results in osmotic diuresis. Similarly, massive amounts of diuresis may occur in head injured patients with diabetes insipidus.
A shock state may persist despite normalization of blood pressure, heart rate, and urine output. Scalea and colleagues reported that in 30 trauma patients, 24 (80%) had normal blood pressure, heart rate, and urine output despite the presence of elevated lactated levels and decreased mixed venous oxygen saturation.3 Abou-Khalil and colleagues evaluated 39 penetrating trauma patients who were younger than 40 years old.4 They reported that despite normal heart rate, blood pressure, and urine output, only 15% had achieved an optimal state one-hour postoperatively. They concluded that traditional end points of resuscitation underestimate the degree of shock, particularly in young trauma patients who have compliant capacitance vessels and arterioles that maximally vasoconstrict. These studies demonstrate that trauma patients can remain in a state of inadequate tissue perfusion and oxygenation if resuscitation measures cease after traditional end points (blood pressure, heart rate, and urine output) have been normalized.
Lactate Levels
Inadequate tissue perfusion results in anaerobic metabolism, the byproduct of which is lactate. Therefore, monitoring serum lactate levels has been proposed as a clinical marker of inadequate perfusion. Abramson and colleagues prospectively studied lactate clearance and survival following injury in 76 critically ill trauma patients.5 They reported 100% survival in 27 patients whose lactate level normalized (< 2 mMol/L) in 24 hours. If lactate levels cleared to normal between 24 and 48 hours, the survival rate was 75%. They concluded that time needed to normalize serum lactate levels may be an important prognostic factor for survival.
Abou-Khalil and colleagues prospectively studied 39 patients who had required operative intervention for penetrating trauma.4 They found that at one hour and 24 hours post-operatively, survivors had significantly lower serum lactate concentrations than nonsurvivors. Manikis and colleagues investigated the correlation between blood lactate, morality, and organ failure in 129 critically ill trauma patients (100 survivors, 29 nonsurvivors).6 Nonsurvivors and patients who developed organ failure had higher initial lactate levels and higher overall lactate levels. The duration of hyperlactatemia averaged 2.2 days in patients with organ failure and one day in patients who did not develop organ failure.
These studies suggest the magnitude and duration of lactic acidosis may be predictors of mortality and morbidity following trauma. However, there are multiple factors that can contribute to elevated lactate levels. Serum lactate levels are an aggregate of lactate production and lactate metabolism. As underperfused tissue beds are reperfused, accumulated lactate may be washed out into the circulation, thus spuriously increasing serum lactate levels.7 Cancer can cause elevated lactate levels because tumors have a high rate of anaerobic glycolysis. The larger the tumor burden, the greater that lactate production. Patients with Type II diabetes mellitus have a defect in pyruvate oxidation that can lead to mild hyperlactatemia. Acute ETOH intoxication can contribute to elevated lactate levels because oxidation of ethanol in liver produces acetaldehyde and acetate which fosters the conversion of pyruvate to lactate.
In summary, lactate is a byproduct of anaerobic metabolism that may reflect inadequate oxygen delivery at the cellular level. Blood lactate levels may be used to assess adequacy of perfusion and prognosis in the critically ill trauma patient. If lactate is progressively clearing, shock may be in the process of reversing. If lactate fails to clear, then it is reasonable to look for a missed cause of shock.5 To address the problem of interpretation of a single lactate level, using serial measurements as an indicator of improving or worsening organ perfusion and oxygen delivery has been advocated.1
Base Deficit
Base deficit is defined as the amount of base (mMol) required to titrate 1 liter of whole arterial blood to a pH of 7.40 with the sample fully saturated with oxygen at 37°C and PCO2 of 40 mm Hg. It is calculated from an arterial blood gas and, thus, is widely available and readily obtained. Normal base deficit is +3 mMol to -3 mMol. It is used as an approximation of global tissue acidosis.
Rutherford and colleagues conducted a retrospective chart review of 3791 patients to determine the association of base deficit with mortality.8 Data suggested that a base deficit of -15 mMol/L within 24 hours post-injury in a patient younger than 55 years of age (no head injury) was a significant marker of mortality. A base deficit of -8 mMol/L within 24 hours post-injury in a patient older than 55 years old (no head injury), or a young patient with a head injury, was a significant marker of mortality. They concluded that base deficit is an expedient and sensitive measure of both the degree and duration of inadequate perfusion.
The advantage of base deficit is that it is readily obtained by arterial blood gas analysis and is more rapidly estimated in the laboratory than serum lactate levels.7 However, limitations of base deficit do exist and should be considered in their interpretation. Administration of sodium bicarbonate may alter the base deficit irrespective of the tissue oxygen debt. A normal base deficit can exist with hyperlactatemia when the lactate load has not overwhelmed the body’s buffer system or when a preinjury base excess exists, such as in patients with emphysema who are chronic CO2 retainers.1
Although a prospective study showing an improvement in base deficit during volume resuscitation improves survival has yet to be performed, many trauma centers support the use of a normal base deficit—an appropriate end point of trauma resuscitation.8
Regional Markers: Gastric Tonometry
Global markers of tissue perfusion, such as lactate and base deficit, reflect the sum perfusion of all tissue beds in the body. However, blood flow is not uniformly distributed to all tissue beds and regions during shock when blood flow to the gut is redistributed to the systemic circulation to increase perfusion to vital organs. Therefore, monitoring gut mucosa may provide information about systemic oxygenation.
Gut perfusion can be estimated by gastrointestinal tonometry. The gastric tonometer is a conventional nasogastric tube that has a silicone balloon at its tip that is filled with normal saline. The tonometer is inserted into the stomach like a standard nasogastric tube. The balloon lies in close proximity to the gastric mucosa. The balloon which is permeable to CO2, allows CO2 to diffuse freely from the gastric mucosa into the saline filled balloon. After an equilibration period, the CO2 of the saline balloon should equal that of the gastric mucosa. A sample of saline is withdrawn from the balloon, followed immediately by an arterial blood sample. The two samples are analyzed by a blood gas analyzer. The pCO2 of the saline sample and the HCO3 form the arterial blood gas sample and are used in the Henderson-Hasselbalch equation to determine intramucosal pHi.
There are several studies using gastric pHi in the evaluation and management of the resuscitation of trauma patients. Roumen and colleagues prospectively evaluated 15 multiple trauma patients.10 Eight of the 15 patients had a low pHi once or more within the first 48 hours of admission. Two of these patients subsequently died and three developed organ failure. Patients whose pHi remained normal were discharged without complications. Chang and colleagues prospectively studied 20 multiple trauma patients and compared global oxygen transport parameters, lactate, base deficit, and pHi over the first 24 hours of admission.11 Patients with low pHi on admission who did not normalize within 24 hours had a higher mortality (50% vs 0%, P = 0.03) and a higher incidence of organ dysfunction (2.6 organs/patient vs 0.62 organs/patient, P = 0.02) than those patients whose pHi corrected to normal within 24 hours. Chang and Meredith prospectively studied 20 critically ill trauma patients and compared global oxygen transport parameters, lactate, base deficit, and pHi.12 They found that patients with a persistently low pHi had a higher mortality and higher incidence of organ dysfunction than patients whose pHi normalized within 24 hours post-admission.
The limitations of gastric tonometry have been extensively reviewed by Russell.13 Calculation of pHi is based on the assumption that HCO3 of the gastric mucosal tissue is in equilibrium with the systemic arterial HCO3. This assumption may not always be correct. When gastric mucosal blood flow decreases in shock, local gastric tissue HCO3 may be significantly lower than the systemic arterial HCO3. Therefore, use of systemic HCO3 to calculate pHi may overestimate gastric pHi. Calculation of pHi is also based on the assumption that systemic arterial pCO2 is normal and, thus, does not need to be considered to interpret abnormal gastric pCO2i. While this may be true in healthy volunteers, critically ill patients frequently have abnormal systemic arterial PCO2 and acute changes in systemic PCO2 can change gastric PCO2 directly.
Although gastric tonometry may not be ready for routine clinical practice,13 as its technology becomes more accurate, timely, and user friendly, pHi may become an established end point of resuscitation in trauma.7
Conclusions: Guidelines for Resuscitation
The optimal resuscitation end point in trauma remains elusive and is a major focus of research in trauma care.7 There is not a definitive answer as to what constitutes adequate resuscitation. Several clinical parameters appear to be useful in determining end points of resuscitation. Elevated serum lactate concentrations, elevated base deficit, and low gastric pHi appear to be clinical manifestations of inadequate tissue perfusion and impaired oxygenation. Resuscitation end points used in combination appear to be superior to those used alone. 7,9 Current data support the use of base deficit, lactate, and gastric pHi as appropriate end points for the resuscitation of trauma patients and the goal should be to correct at least one, if not all three parameters (lactate, base deficit, pHi), to normal within 24 hours after injury.9
References
1. Cornwell EE, et al. Surg Clin North Am 1996;76:959-969.
2. American College of Surgeons. Advanced Trauma Life Support. 6th ed. Chicago, Ill: American College of Surgeons; 1997.
3. Scalea T, et al. Crit Care Med 1994;22:1610-1615.
4. Abou-Khalil B, et al. Crit Care Med 1994;22:633-639.
5. Abramson D, et al. J Trauma 1993;35:584-589.
6. Manikis P, et al. Am J Emerg Med 1995;13:619-622.
7. Mikhail J. AACN Clinical Issues 1999;10(1):10-21.
8. Rutherford EJ, et al. J Trauma 1992;33:417-423.
9. Porter JM, Ivatury RR. J Trauma 1998;44:908-914.
10. Roumen RMH, et al. J Trauma 1994;36:313-316.
11. Chang MC, et al. J Trauma 1994;37:488-492.
12. Chang MC, Meredeth W. J Trauma 1997;42:577-582.
13. Russell JA. Intensive Care Med 1997;23:3-6.
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