Sodium citrate is a soluble white powder. It has many uses. Sodium citrate as a anticoagulant which is as an anticoagulant in the collection and processing of animal blood. TriSodium citrate anticoagulant treated blood may be used for production of the soil amendment. Sodium citrate addition to blood prevents it from clotting.
TriSodium citrate anticoagulant reactions or toxicity may occur with the infusion of blood products to patients and return of blood containing citrate anticoagulant to donors. The recipient of the blood containing citrate should be monitored for the signs and symptoms of citrate toxicity. The signs and symptoms of citrate toxicity begin with paresthesia, a “tingling” sensation around the mouth or in the extremities, followed by severe reactions that are characterized by hypotension and possible cardiac arrhythmia. Citrate toxicity may occur more frequently in patients who are hypothermic, have impaired liver or renal function, or have low calcium levels because of an underlying disease.
Background: Sodium citrate anticoagulant has been used as an anticoagulant to stabilize blood and blood products for over 100 years.
Methods: Blood was anticoagulated in three ways: by collection into citrate, CTI and citrate with CTI. Plasma was prepared using each anticoagulation regimen. Functional analyses included calibrated automated thrombography, thromboelastography, plasma clotting, the synthetic coagulation proteome and platelet aggregation this is a Benefits and harms of trisodium citrate.
TriSodium citrate anticoagulant can be associated with disturbance of acid-base balance (usually metabolic alkalosis, but also metabolic acidosis), disturbance of blood calcium concentration (usually hypocalcemia but also hypercalcemia) and disturbance of blood sodium concentration (hypernatremia). These disturbances can arise for a number of reasons but accumulation of citrate in the peripheral circulation is central in most instances. There are three main reasons why citrate may accumulate.
Firstly, the patient may be unable to metabolize (remove) citrate as efficiently as normal; citrate metabolism is diminished in those with advanced liver disease, e.g. cirrhosis, liver failure; and those with any condition associated with poor tissue perfusion (shock).
Secondly, as dialysis progresses, membrane patency may be reduced and consequently less citrate-calcium complex is cleared from blood to the filtrate.
Finally, operational errors can lead to accidental overinfusion of tri-sodium citrate. Since citrate is the anticoagulant used to preserve blood for transfusion, multiple transfusions during continuous RRT can contribute significantly to citrate accumulation.
Irrespective of the cause, accumulation of citrate in the peripheral circulation results in citrate chelation of circulating ionized calcium, with consequent reduced plasma ionized calcium concentration (ionized hypocalcemia). If sufficiently severe (ionized calcium < 0.8 mmol/L), this can have symptomatic effect; indeed, it may actually be life-threatening, because severe ionized hypocalcemia can cause cardiac arrhythmia and, ultimately, cardiac arrest.
Hypo- and hypercalcemia can also occur independently of any effect of citrate if postfilter calcium infusion rate is not well matched to the calcium loss during blood flow through the filter. In this instance there is no effect on calcium ratio; both total and ionized calcium are reduced (or increased) to the same degree.
If tri-sodium citrate is accumulating in a patient who has the capacity to metabolize it, then metabolic alkalosis can ensue. This is because bicarbonate is generated during citrate metabolism; for every mole of tri-sodium citrate metabolized, 3 moles of bicarbonate are generated. The excessive bicarbonate load that causes blood pH to rise merely reflects increased citrate metabolism. Of all metabolic disturbances associated with tri-sodium citrate anticoagulation, metabolic alkalosis is probably the most common, occurring in 50 % of patients in one study.
Failure to metabolize citrate with resulting accumulation of citric acid is the cause of metabolic acidosis that can occur in patients receiving citrate anticoagulation and is therefore usually confined to those with advanced liver disease and/or inadequate tissue perfusion. Pre-existing lactic acidosis in these patients is a likely contributory factor to development of metabolic acidosis.
In practice, the use of hyponatremic dialysis/replacement fluids usually compensates for addition of tri-sodium citrate. An alternative strategy is to use lower strength (2 %) tri-sodium citrate.
Sodium citrate is a white fabric that has many uses. Adding sodium citrate to the blood prevents it from clotting. It has been used for several years as an anticoagulant to stabilize the blood and in blood products. Anticoagulant sodium citrate can impair blood calcium concentration and blood sodium concentration.