DOI: 10.1097/CCM.0b013e31823d77e9

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PMID: 22249046

Issn Print: 0090-3493

Publication Date: 2012/02/01


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Why guess when you can see? Heart function and fluid management in dengue shock*

Ian M. Seppelt; Sam R. Orde

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It is increasingly recognized that cardiac dysfunction forms a component of most shock states. In sepsis, this is a complex process that is only imperfectly characterized, but the more it is studied, it appears that there is no such thing as “pure” high cardiac output vasodilated shock and that all septic patients have some degree of myocardial dysfunction (1, 2). Dengue viral infection is one of the most common vector-borne diseases in the world and shock and low cardiac output are commonly seen in severe dengue, but as yet, the exact mechanism is not well understood. Intravascular hypovolemia from increased capillary permeability and plasma leak have been suggested as causes (3) and have led to caution in fluid resuscitation recommendations, but in the generally resource-poor environments where dengue is treated, the management is by necessity empirical.
Fluid resuscitation is one of the most controversial areas in current intensive care practice. We have moved from a comfortable understanding in the 1980s of pulmonary artery occlusion pressures and central venous pressures to the realization that pressure actually has no correlation with volume (or preload) at all (4, 5) and is a poor predictor of fluid responsiveness (6, 7). Although it is well understood that hypovolemia associated with shock leads to poor outcomes and must be treated, in the last decade, there is an increasing awareness that fluid overload is also extremely harmful. In a recent analysis of the Vasopressin in Septic Shock Trial (VASST), Boyd and colleagues (8) demonstrated an increased mortality in those with a positive fluid balance and elevated central venous pressure, and in the associated editorial, Ytrebø (9) pleaded to “Stop filling patients against central venous pressure, please.”
The key question is not volume status per se, but fluid responsiveness, and particularly dynamic fluid responsiveness, but always with the underlying question not “can I give fluid?” but “should I give fluid?” This has been vividly highlighted in sub-Saharan Africa in the Fluid Expansion as Supportive Therapy (FEAST) trial (10) in which, contrary to expectations, fluid boluses significantly increased mortality in critically ill children with impaired perfusion.
The available data on cardiac function in dengue are limited, coming from small observational studies predominantly in the pediatric population. There is evidence of significantly low ejection fraction during the toxic stage of the more severe dengue fever (11, 12). Measurement of ejection fraction is problematic, however, because it remains sensitive to changes in preload and afterload, so for more detailed study, assessment of cardiac function using indices independent of preload is necessary.
In this issue of Critical Care Medicine, Yacoub and colleagues (13) describe comprehensive echocardiographic assessment of intravascular volume and relatively preload-independent of cardiac function parameters (myocardial tissue Doppler imaging) to estimate the effect of different severities of dengue fever on the heart. They studied 79 patients (adult and children) with dengue viral infection of varying severity and performed a comprehensive echocardiographic examination after immediate resuscitation, at 24 hrs, and at hospital discharge. The least severe patients with dengue had transient evidence of systolic and diastolic impairment with possible segmental wall abnormalities of the septum and right ventricular wall. The more severe the dengue infection, the more likely it was these cardiac abnormalities occurred and the more severe they were.
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