Why is triple whammy bad?
Triple Whammy – ‘three simultaneous deleterious blows with compounded effect’. The combination of medicines above can result in significant harm. Used individually or combined, these three types of medicines are involved in more than half of all reported iatrogenic acute renal failure cases.
What is the triple whammy and what combination of drugs combine to cause this adverse outcome?
Recent articles have coined the term ‘triple whammy’ for the adverse effect of combinations of angiotensin converting enzyme inhibitors (ACEI)/angiotensin receptor antagonists (ARA), diuretics and nonsteroidal anti-inflammatory drugs (NSAIDs), particularly in the elderly [1, 2].
Why do you stop ACE inhibitors in Aki?
Clinicians managing patients with AKI therefore frequently stop drugs that lower blood pressure (particularly ACEI and ARBs, which selectively reduce glomerular pressure) and diuretics. ACEIs, ARBs and potassium-sparing diuretics may also be stopped because of hyperkalaemia.
Are ACE and ARBs nephrotoxic?
This triple therapy can increase the risk of acute renal failure. This triple therapy can increase the risk of acute renal failure.
Is aspirin an NSAID?
Aspirin is an NSAID, too. It increases the risk of bleeding, but when used appropriately, it has a net benefit for heart health for those at high risk of future heart problems because it prevents the clotting that leads to heart attacks and strokes.
What does triple whammy cause?
The mechanism of the triple whammy NSAIDs are associated with an increased risk of AKI, due to blockade of the COX-2 enzyme preventing prostacyclin synthesis, which causes afferent arteriolar vasoconstriction.
Why does Acei cause Aki?
ACE-I in the setting of hypovolemia can cause acute kidney injury due to inadequate renal perfusion. The RAAS is activated when decreased blood flow is detected in the kidneys, which can happen in normal states such as dehydration but can also happen in pathological states such as heart or liver failure.
Do you hold furosemide in AKI?
The clearance of furosemide is delayed in patients with AKI; however, torsemide and bumetanide are metabolized in the liver and their half-lives are not prolonged in AKI.
At what creatinine level should ACE inhibitors be stopped?
The authors recommend that ACE inhibitor therapy should not be discontinued unless serum creatinine level rise above 30% over baseline during the first 2 months after initiation of therapy or hyperkalemia (serum potassium level >or=5.6 mmol/L) develops.
Do ARBs increase creatinine?
Many such patients experience a transient rise in serum creatinine levels after treatment with an ACEI or angiotensin receptor blocker (ARB) is started or after blood pressure is adequately reduced. A rise in the serum creatinine level consequently leads to physician reticence to stay the course with a given therapy.
What is the meaning of the triple whammy?
The term “triple whammy” refers to the concurrent use of an angiotensin converting enzyme (ACE) inhibitor or an angiotensin-II receptor blocker (ARB), with a diuretic and a non-steroidal anti-inflammatory drug (NSAID), including cyclo-oxygenase-2 (COX-2) inhibitors.
What happens if you take a triple whammy medicine?
Triple Whammy – ‘three simultaneous deleterious blows with compounded effect’.1 The combination of medicines above can result in significant harm. Used individually or combined, these three types of medicines are involved in more than half of all reported iatrogenic acute renal failure cases.2 AVOID THIS COMBINATION OF MEDICINES IF POSSIBLE
What are the risk factors for triple whammy Aki?
Risk factors for triple whammy-induced AKI are similar to other forms of kidney injury and include:3–5. Any stage of chronic kidney disease (CKD) Older age, e.g. over 75 years. Volume depletion, e.g. due to vomiting, diarrhoea, sepsis or low fluid intake. Māori, Pacific or Indo-Asian ethnicity. Diabetes. Heart failure.