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Ischemic skin lesions and microcirculatory collapse during vasopressin therapy: a possible role of the microcirculation?

Sir, We would like to thank Drs Boerma and colleagues for their interesting case report (1). By presenting orthogonal polarization spectrophotometric pictures, they gave a great insight into the microcirculatory system of a patient with severe cardiovascular failure, who responded to an increase in vascular tone with signs of tissue hypoperfusion. In a retrospective analysis, our working group observed that 30% of severe shock patients treated with a supplementary arginine—vasopressin (AVP) infusion developed signs of skin or tongue ischemia (2), which seemed to be accompanied by disturbances of the microcirculation as presented by Boerma et al. However, in a prospective study comparing combined AVP/norepinephrine infusion with norepinephrine infusion alone in otherwise refractory cardiovascular failure, there was no difference in the incidence of ischemic skin lesions between the study groups (29.2% vs. 25%, P 1⁄4 1) (3). Typically, ischemic skin lesions developed more rapidly during supplementary AVP infusion than during norepinephrine therapy alone. This is most probably attributable to the fact that vascular tone is immediately restored after the initiation of AVP infusion, but only gradually by incremental doses of norepinephrine. These data may indicate that it is not the choice of vasopressor applied, but other factors, that cause a collapse of capillary perfusion and end-organ ischemia in severe cardiovascular failure. In these shock patients, who might particularly benefit from new innovative strategies targeting the microcirculation, the microcirculatory system may be functionally impaired to such a degree that the restoration of vascular tone to achieve an adequate mean arterial blood pressure (MAP) results in major impairments of microvascular flow. In our retrospective study, sepsis [odds ratio (OR), 3.46; 95% confidence interval (CI), 1.004—12.14] and peripheral arterial occlusive disease (OR, 12.02; 95% CI, 1.006—143.74) were independent risk factors for the development of ischemic skin lesions during AVP therapy (2). Although sepsis was proven in the presented patient, it is very likely that this 80-year-old patient suffered at least some degree of arteriosclerosis or peripheral arterial occlusive disease. In the univariate model, high norepinephrine doses (P 1⁄4 0.005) and increased requirements for the transfusion of fresh frozen plasma (P 1⁄4 0.03) and thrombocyte concentrates (P 1⁄4 0.034) were significantly associated with the development of ischemic skin lesions (2). Both variables reflect the severity of multiple organ dysfunction, and were observed in the presented patient. In addition, Boerma et al. did not present data on the volume status and cardiac output of their patient. It is conceivable that hypovolemia and low cardiac output were still present despite aggressive fluid resuscitation and infusion of dopamine. Strong and uncontrollable terlipressininduced vasoconstriction, combined with reduced systemic blood flow, may also have contributed to a decrease in peripheral tissue perfusion. However, if adequate cardiac output is maintained by both volume and inotropic therapy, the cardiac index is not associated with the occurrence of ischemic skin lesions during AVP therapy (P 1⁄4 0.367) (2). In conclusion, it may be speculated whether microcirculatory collapse would have developed in the presented patient if: (i) AVP had been initiated at an earlier stage of the disease; (ii) norepinephrine had been increased to doses attaining similar MAP as terlipressin; and (iii) the volume status and cardiac output had been accurately monitored.