It is important for the nurse to be aware of the physiological dynamics of surgical diuresis. After a major surgical procedure that produces high physiologic and psychological stress, increased secretion of antidiuretic hormone causes fluid retention within the vascular space. As stress after surgery decreases, ADH and other hormones, such as glucocorticosteroids, begin to drop to normal values, and the fluid that was held in reserve is excreted. This increase in urine volume a few days after surgery is sometimes referred to as a surgical diuresis. It is important for nurses to consider this type of fluid retention and related increase in urine specific gravity in the immediate post-operative patient to avoid excessive fluid replacement.
The drug's most common side effects are poor or reduced appetite, vomiting, lack of energy, diarrhea, and weakness. Occasionally, more serious side effects, including bloody diarrhea, collapse, severe sodium/potassium imbalance, and destruction of the adrenal gland may occur, and may result in death. In 2014, with input from CVM, the manufacturer updated the information about patient monitoring and side effects on the package insert. Although not proven to be caused by Vetoryl, some additional side effects reported to CVM and now included on the package insert are adrenal insufficiency, shaking, elevated liver enzymes and elevated kidney tests.
Glucocorticosteroids are the most effective anti-inflammatory therapy for asthma but are relatively ineffective in COPD. Glucocorticoids are broad-spectrum anti-inflammatory drugs that suppress inflammation via several molecular mechanisms. Glucocorticoids suppress the multiple inflammatory genes that are activated in asthma by reversing histone acetylation of activated inflammatory genes through binding of ligand-bound glucocorticoid receptors (GR) to coactivator molecules and recruitment of histone deacetylase-2 (HDAC2) to the activated inflammatory gene transcription complex (trans-repression). At higher concentrations of glucocorticoids GR homodimers interact with DNA recognition sites to activate transcription through increased histone acetylation of anti-inflammatory genes and transcription of several genes linked to glucocorticoid side effects (trans-activation). Glucocorticoids also have post-transcriptional effects and decrease stability of some proinflammatory mRNAs. Decreased glucocorticoid responsiveness is found in patients with severe asthma and asthmatics who smoke, as well as in all patients with COPD. Several molecular mechanisms of glucocorticoid resistance have now been identified which involve phosphorylation and other post-translational modifications of GR. HDAC2 is markedly reduced in activity and expression as a result of oxidative/nitrative stress and pi3 kinase-δ inhibition, so that inflammation is resistant to the anti-inflammatory actions of glucocorticoids. Dissociated glucocorticoids and selective GR modulators which show improved trans-repression over trans-activation effects have been developed to reduce side effects, but so far it has been difficult to dissociate anti-inflammatory effects from adverse effects. In patients with glucocorticoid resistance alternative anti-inflammatory treatments are being investigated as well as drugs that may reverse the molecular mechanisms of glucocorticoid resistance.