An Elderly Man Presents with Septic Shock and Oliguria. Best Way to Maintain Renal Perfusion Is
RNSH 2003 Renal
Question 4
An elderly man presents with septic shock and oliguria. Best way to maintain renal perfusion is:
(a)renal dose dopamine
(b)adrenaline infusion
(c)intermittent frusemide
(d)continuous frusemide infusion
Ultimately need to increase blood pressure and volume to improve renal perfusion. First line therapy would be adequate fluid resuscitation.
Frusemide is a loop diuretic which inhibits the Na-K-Cl co transporter in the loop of Henle.
In general, agents that augment peripheral vascular resistance, such as dopamine, norepinephrine, epinephrine, or phenylephrine, are required for initial stabilization [9]. However, large trials comparing outcomes with different vasopressors have not been performed, and therefore there is no definitive evidence of the superiority of one vasopressor over another
Dopamine
Dopamine is synthesized within the kidney in the proximal tubule from circulating L-dopa, via the enzyme L-amino acid decarboxylase [1-3].
RENAL ACTIONS – Circulating and locally formed dopamine can affect both sodium excretion and renal hemodynamics via activation of the DA1 and DA2 receptors [1].
Natriuresis – Dopamine is a natriuretic hormone, increasing sodium excretion by diminishing reabsorption, primarily in the proximal tubule [1,2,4,5]. This effect of dopamine appears to involve both of the steps involved in transtubular sodium transport:
- decreases the activity of the Na-H exchanger in the luminal membrane
- inhibits the Na-K-ATPase pump in the basolateral membrane, and thus inhibits Na reabsorption
In addition to these proximal effects, dopamine can also reduce sodium reabsorption in the collecting tubules.
Vasodilation – When infused in low doses (0.5 to 3 µg/kg per minute), dopamine dilates the interlobular arteries and both the afferent (preglomerular) and efferent (postglomerular) arterioles [4,9]. The net effect is a relatively large increase in renal blood flow with a lesser or no elevation in glomerular filtration rate (GFR) [5]; the relative lack of increase in GFR is due to the efferent dilatation which minimizes the rise in intraglomerular pressure. At higher concentrations (above 5 µg/kg per minute), however, dopamine induces renal vasoconstriction, a response that is mediated by activation of the alpha-adrenergic receptors.
CLINICAL UTILITY – These findings have led to the frequent use of low-dose, "renal-dose" dopamine (0.5 to 3 µg/kg per minute) both to increase the urine output and to preserve renal function in oliguric patients at risk for postischemic ATN. Although dopamine can raise the urine output and increase renal blood flow, there is at present little evidence for a renal protective effect. When renal ischemia is induced in experimental animals, for example, dopamine alone does not appear to be more effective than saline infusion.
There are few studies that have evaluated the effect of dopamine in humans at risk for or with early or established ATN:
• One controlled trial performed in patients after elective major abdominal vascular surgery compared the effects of fluid repletion with saline alone to saline plus low-dose dopamine. No difference in renal function was noted between the two groups. However, acute renal failure was an infrequent occurrence in these well hydrated patients; as a result, improvement with dopamine would have been difficult to demonstrate.
• In the NORASEPT II study of nearly 400 patients with oliguria and shock due to sepsis, 174 patients nonrandomly received low-dose dopamine (44 percent), high-dose dopamine (32 percent), or no dopamine (24 percent) [16]. The incidence of acute renal failure and the requirement for dialysis was similar among the three patient groups.
In summary, there is at present no clear experimental or clinical support for a renal protective effect of dopamine. Furthermore, there are potential risks associated with even low-dose regimens. These include tachycardia, cardiac arrhythmia, myocardial ischemia, and possibly intestinal ischemia (due to precapillary vasoconstriction), which might promote bacterial translocation from the intestinal lumen into the systemic circulation. Thus, we cannot recommend the use of dopamine to protect patients considered to be at risk for ATN or in those with early and/or established ATN.
Norepinephrine/Epinephrine
MECHANISM OF ACTION – Stimulates beta1-adrenergic receptors and alpha-adrenergic receptors causing increased contractility and heart rate as well as vasoconstriction, thereby increasing systemic blood pressure and coronary blood flow; clinically alpha effects (vasoconstriction) are greater than beta effects (inotropic and chronotropic effects)