Monitoring of the Effect of Synthetic Vasopressin in Vasodilatory Shock Using Esophageal Doppler Probe
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- Category: Vol. 79, June 2011
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Monitoring of the Effect of Synthetic Vasopressin in Vasodilatory Shock Using Esophageal Doppler Probe,FAHEEM RAGAB, NASHWA ABED and MOHAMED IBRAHEM AFIFY
Abstract
Background: Septic shock is a form of vasodilatory shock chractrized by arteiolar vasodilation the objective of treatment is to elevate tissue perfusion and mean arterial pressure to allow adequate organ perfusion, noradeenaline and dopamine was the usual catecholamines used in the treatment of septic shock. Loss of response was the common problem that lead to patient loss after large continous dose of noradrenalien which was termed as catecholamines refractory septic shock. Recently vasopressin and its alnalog namely terlipressin used in the treatment of such catastrophic condition.
Methods and Results: In a prospective controlled study we included 40 patients with catecholamine resistant septic shock i.e. noradrenalien dose exceeded 0.7mg/kg/min divided into two groups 20 patients was treated conventionally ac-cording to survving sepsis compagm 2008 served as control group and the other 20 patients treated conventionally and when noradrenaline dose exceeded 0.7mic/kg/min terlipresin in a dose of 1mg I.V bolus every 12 hours for a study time of 48 hours was started terlipressin therapy was associated with increased MAP from 58±14mmHg at baseline to 73±20 mmHg with p value: 0.008 after 48 hours that allowed signif-icant reduction of noradrenalien dose from 50mic/min on day 0 to <25±8 mic/min after 48 horus terlipressin therapy was associated with elevated systemic vascular resistant from 546±260dyne.sec/cm–5 to 986±390dyne.sec/cm–5 after 48 hour which represent normalized arterilor tone that expected to allow better organ bed perfusion.
There was reduction of both stroke volume and cardiac output 63±16ml/beat to 51ml/beat and 78liter/m to 5.3litre/min, respectively yet this was not associated with abnormal organ perfusion marked by improved urine output from 49ml/hour to 133ml/h and improved global perfusion which was marked by improved base deficint which represent lactic acidosis from 9.3±3mEq/L to 5.7±3mEq/L p value: <0.002.
Terlipressin therapy was not associated with deleterious effect on PO2/FiO2 ratio 208±74 to 211±118 after 48 hours.
Yet there was significant reduction of oxygen delivery Do2 from 848ml/min to 610±47ml/min after 48 hours (p>0.02).
There was no effect on length of ICU stay in both groups which was 16±6 in the terlipressin group and 12±6 days in control group (p<0.06) shorter length of stay in control group may be due to the rapid deterioration of hemodynamics and death without terlipressin support. Which was true as mortality in control group was 70% versus 60% (12/20) in terlipressin group with absolute risk reduction 10% and relative risk reduction 25% regarding organ function terlipressin could improve SOFA score form 11±3.2 to 8±5 with p value: <0.02.
Conclusion: Terlipressin is a rather safe inexpensive easy to administer alternative in the treatment of septic shock-further studies are needed to propose the ideal timing for initiation of its therapy early Vs. late, adjuvant or as an initial treatment.