How fast does ddavp work

Patients with mild von Willebrand disease so mild that…. Submit a Comment Cancel reply Your email address will not be published. Recent Comments Kristine said Yes! Ambereen Imran said Oh wow! There is so much we seniors can learn from the young Over-correction of hypovolemic hyponatremia is a common example of failure of the Adrogue-Madias formula. The physiology of hypovolemic hyponatremia is shown below.

In response to cerebral hypoperfusion, the brain secretes vasopressin a. Vasopressin has vasopressor effects and also causes retention of free water by the kidneys, both in efforts to support perfusion.

Free water retention causes hyponatremia. If a patient with hypovolemic hyponatremia is volume resuscitated, at a certain point perfusion improves and this shuts off vasopressin figures below.

Without vasopressin, the kidneys rapidly excrete water, causing a dangerously fast normalization of the serum sodium. Although this example focuses on hypovolemic hyponatremia, overcorrection will also occur after treatment of any reversible cause of hyponatremia e. There are two treatments to managing water over-excretion.

This requires careful attention to urine output and serum sodium, with ongoing titration of the D5W. Wrestling with normal kidneys is difficult. Usually at some point something exciting happens in the ICU, attention is diverted, and before you know it the sodium is too high. High rates of D5W may induce hyperglycemia. Others have reported difficulty with this strategy Perianayagam ; Gharaibeh DDAVP stimulates the V2-vasopressin receptors in the kidney, causing renal retention of water figure above.

This eliminates unpredictable excretion of water from the kidneys:. With blockade of renal water excretion, the Adrogue-Madias equation will be more accurate. This allows control of the sodium based on fluid administration:. This will halt intake and output of free water, so the sodium should remain stable.

If the patient is neglected for a few hours, the sodium will probably be fine. The risk of osmotic demyelination syndrome depends on the average change in sodium over time, so if the sodium over-corrects this can still be remedied by decreasing the sodium to its original target. This is obviously not the preferred strategy for managing sodium. However, it is important to recognize that sodium over-correction is not an unfixable problem.

Even if the patient seems OK neurologically, it is probably safest to lower the sodium. By the time symptoms of osmotic demyelination syndrome emerge, the optimal window for intervention has passed. Consider a patient admitted with chronic, asymptomatic hyponatremia due to hypovolemia.

Nothing dramatic must be done initially. Fluid resuscitation may be undertaken with careful monitoring of the serum sodium concentration. At some point, vasopressin levels will fall and the sodium will start really climbing. Once the sodium has increased a fair amount i. The physiology underlying this strategy is supported by an observational study of this approach by Rafat They showed that DDAVP administration decreased the urine output and increased the urine tonicity, causing a halt in the rate of sodium correction over time:.

The weakness of this strategy is that it initially requires constant vigilance to detect overcorrection, with intervention at just the right moment. This is not foolproof. For example, in the Rafat series, about half of patients still over-corrected their sodium. This is performed as follows:. How long does ddavp last. Common Questions and Answers about How long does ddavp last.

I've been taking this medicine for many years only to find out my tests say I don't need it I had small injury to pituitary in brain. Unfortunately I find it almost impossible to wean off because it makes you go to the bathroom ALOT after the medicine ware's off! Confusing and tricky. Read More. I still have diabetes insipidus and almost zero testosterone.

I have to resume work in a week and feel so so tired. How long did it take for your diabetes insipidus to resolve? My endo refuses to prescribed the testosterone as he says that should recover by itself, however I am exhausted all day. I am on ddavp sublingual pill and 10mg of prednisone. Desmopressin has no effect on platelet count or aggregation, but enhances platelet adhesion to the vessel wall. Because these factors increase rapidly and transiently, it is most likely that desmopressin causes them to be released from storage sites.

The vascular endothelium is presumably the main source of vWF. This view is supported by the observation that in rats injections of desmopressin elicit biological responses that are clearly related to the activation of endothelial cells, like surface expression of P selectin and subsequent margination of leukocytes.

In the search of such a second messenger, it was shown that release of vWF from endothelial cells occurred after the addition of desmopressin to monocytes. Desmopressin acts on storage sites via its strong V 2 agonist activity, since patients with nephrogenic diabetes insipidus, who are unresponsive to V 2 agonists, do not have increased factor VIII and vWF levels after treatment with desmopressin. Their location is currently unknown.

A puzzling, unresolved question is how desmopressin is efficacious in bleeding disorders other than hemophilia and vWD, in patients who have normal or even high levels of factor VIII and vWF.

The favorable effects of the compound may be mediated by increased platelet adhesion to the vessel wall, 18 , 19 due not only to the rise of plasma vWF but also to the abluminal secretion of the protein toward the subendothelium 22 ; by heightened coagulability, due to supranormal levels of factor VIII, a rate-accelerating factor in the process of fibrin formation 27 ; and by the fresh appearance in plasma of ultralarge vWF multimers.

For instance, the compound induces the adhesion of erythrocytes to the endothelium 30 and decreases the endothelial production of hydroxyoctadecadienoic acid HODE , a derivative of linoleic acid that powerfully inhibits platelet adhesion to the vessel wall.

In hemophilia and vWD, desmopressin is efficacious because it provides a form of autologous replacement therapy. Table 1 summarizes the routes of administration, the recommended dosages, and the pharmacokinetic properties of desmopressin-induced factor VIII and vWF.

The prototypes of patients who respond to desmopressin and avoid the use of coagulation factor concentrates are those with measurable levels of factor VIII and vWF, ie, patients with mild hemophilia A and type 1 vWD, 1 , whereas patients with unmeasurable levels do not respond at all. Clinical failures of desmopressin can usually be explained by the attainment of factor VIII levels in plasma that are insufficient to control bleeding.

On the other hand, these levels should be sufficient for the patient to have a minor procedure, such as circumcision or dental extractions. Although in type 1 vWD this effect is usually achieved in proportion to the levels of normally functioning vWF attained in plasma, 28 the bleeding times of patients with type 3, characterized by complete deficiency of vWF, and of those with dysfunctional molecules are usually not shortened.

Table 2 summarizes the indications for desmopressin in patients with different types of vWD. Patients treated repeatedly with desmopressin may become less responsive, perhaps because stores are exhausted.

In these situations, which occur relatively seldom in the clinical management of mild hemophilia and type 1 vWD, it may become necessary to use plasma-derived or recombinant factors, or to supplement desmopressin with them.

Subcutaneous and intranasal desmopressin are at least as efficacious as intravenous desmopressin and can be self-administered. Although intravenous desmopressin is recommended before surgery or for treating severe hemorrhages, because very consistent responses are required in these situations, subcutaneous desmopressin can be used at home to prevent or treat minor bleeding episodes and in women with vWD who have excessive bleeding at menstruation.

Despite the fact that neither in vitro nor in vivo studies have clearly proved a direct stimulatory effect of desmopressin on platelets reviewed by Wun et al 38 , the drug shortens or normalizes the bleeding time of some patients with congenital defects of platelet function.

Most patients with storage pool deficiency respond to desmopressin but a few do not, 40 so a test dose is recommended to select responders. Whether the effect on a laboratory test such as the bleeding time corresponds to a hemostatic effect is not well established. On the other hand, the data obtained from a few well-conducted but nonrandomized studies would indicate that desmopressin can be a useful alternative to blood products during or after surgery or delivery, assuring satisfactory hemostasis.

To sum up, desmopressin is efficacious in mild hemophilia and type 1 vWD and usually permits the avoidance of concentrates, with significant reductions in costs. The benefits of desmopressin are not limited to cost savings. The compound may be needed to meet religious requests, such as the avoidance of blood products in Jehovah's Witnesses. More importantly, it is likely to have spared many patients from infection with the human immunodeficiency virus type 1 HIV.

In Italy, where desmopressin was used earlier and more extensively than in other countries, the prevalence of HIV infection in patients with mild hemophilia 2. Hence, they could only be treated with plasma concentrates during the critical years between when desmopressin was first used clinically and the HIV outbreak started and when the outbreak was halted by the development of virus-inactivation methods and their application to plasma concentrates.

Additional evidence of the HIV-sparing effect of desmopressin stems from the comparison of the prevalence of HIV infection in Italian patients with mild hemophilia A to the corresponding patients from other countries where the compound was used later. In the United States, for instance, where in the period mild hemophiliacs were mainly treated with plasma concentrates because desmopressin was not licensed until , anti-HIV prevalence is The hemostatic defect in uremia is characterized by a prolonged bleeding time, a laboratory abnormality that correlates strongly with the hemorrhagic symptoms of these patients, mainly epistaxis and bleeding from the gastrointestinal tract.

Dialysis may improve the bleeding time and the bleeding tendency, but this is not always the case. In the search for pharmacological agents that could improve hemostasis in uremia, intravenous desmopressin was considered, despite the fact that factor VIII and vWF are normal in uremic patients. Currently, most patients with chronic renal insufficiency are regularly treated with erythropoietin. This practice has led to the sustained improvement not only of anemia but also of the hemostatic defect, 44 so that short-acting compounds such as desmopressin and conjugated estrogens are now less frequently needed.

The bleeding time is prolonged in some patients with liver cirrhosis.