Additional organs that may be affected include the kidneys and retinas of the eyes. Causes
The first episode of autonomic dysreflexia may occur weeks to years after spinal cord injury takes place, but most people at risk (80%) develop their first episode within the first year after injury. Early AD tends to be associated with less severe increases in blood pressure.One common causative factor may be an undetected urinary tract infection. The difficulty in assessing this may be complicated with the usage of indwelling or suprapubic catheters. Other causes include medication side effects and various disease processes. The use of stimulants such as cocaine and amphetamines which can result in urinary retention, and the use of CNS depressants and other psychoactive drugs can also lead to urinary retention and constipation thus leading to autonomic dysreflexia when in use over an extended period of time. Pain
Current scientific literature suggests that noxious (painful) stimuli are the primary initiators of AD. (Note: Not all noxious stimuli will cause AD. Some otherwise severe noxious stimuli in unaffected people, e.g. broken bones, may not result in AD, and may in fact even go unnoticed.) However, different studies have found that activation of pain receptors in muscle and skin below the lesion in spinal cord injured individuals did not trigger AD. These studies suggests that not all noxious stimuli are reliable triggers of AD, and because non-noxious stimuli can also trigger AD, attribution of an episode of AD to noxious stimuli may cause clinicians to overlook underlying non-noxious triggers.
Since more sodium is reabsorbed than potassium secreted, it also makes the lumen more electrically negative, causing chloride to follow sodium. Water then follows sodium and chloride by osmosis. In Conn syndrome, these actions cause increased extracellular sodium and fluid volume and reduced extracellular potassium. Aldosterone also acts on intercalated cells to stimulate an apical proton ATPase, causing proton secretion that acidifies urine and alkalizes extracellular fluid.In summary, hyperaldosteronism causes hypernatremia, hypokalemia, and metabolic alkalosis.Finer notes on aldosterone include the fact that it stimulates sodium-potassium ATPase in muscle cells, increasing intracellular potassium and also increases sodium reabsorption all along the intestine and nephron, possibly due to widespread stimulation of sodium-potassium ATPase. Finally, epithelial cells of sweat gland ducts and distal colon surface respond exactly the same as the principal cells of the nephron. These responses are important in climate adaptation and as a cause of constipation with elevated aldosterone. The sodium retention leads to plasma volume expansion and elevated blood pressure. The increased blood pressure will lead to increased glomerular filtration rate and cause a decrease in renin released from the granular cells of the juxtaglomerular apparatus in the kidney decreasing sodium reabsorption and returning sodium renal excretion to near normal levels allowing sodium to escape the effect of mineralocorticoids (also known as Aldosterone escape mechanism in primary hyperaldosteronism also contributed to by increased ANP level).