For ectopic adrenocorticotropic hormone (ACTH) syndrome (EAS), when surgery is not feasible, or in cases of severe biochemical disturbances, immunosuppression or mental instability, medical therapy with agents such as etomidate is indicated. We present our experience in using etomidate for a 41-year old female with EAS secondary to a malignant mediastinal paraganglioma. We were able to demonstrate that etomidate can be used effectively to control severe hypercortisolism in a lower dose than previously described.
The brain is considered the most eloquent organ in the human body as its activities impacts on all other systems. Though protected physically (in a bony covering), physiologically through the blood-CSF barrier (from invading organisms and toxins) and hemodynamically through the phenomenon of cerebral autoregulation; the brain is open to insults of various kinds which can critically damage this structure. Intracellular Ca++ accumulation, excessive activation of excitatory amino acid receptors, lipid peroxidation and free radical releaserelated damage are but a few of the pathological processes that occur at the neuronal level leading to damage. The mechanism by which the brain can be provided protection when it is in a compromised state or likely to be compromised is known as cerebral protection. There are various modalities of pharmacologic (use of barbiturates, etomidate, isoflurane, steroids, Ca++, corticosteroids etc) and non-pharmacologic therapies (hypothermia, hyperventilation, induced hypotension, electrophysiologic monitoring, endovascular management etc) available for cerebral protection which finds place in the armamentarium of clinicians managing the critically injured brain. Our knowledge of the functioning of the brain at the molecular level and the various biochemico-pathological processes that are set into motion during critical states continues to evolve. This review article attempts to explain present understanding of the biochemical and pathological processes involved in neuronal damage while also looking at current available therapies (pharmacologic & nonpharmacologic) being utilized in different clinical settings.
An ideal anaesthetic for electroconvulsive therapy (ECT) should have rapid onset and offset with no effect on seizure duration, and provide cardiovascular stability during the procedure. Propofol is commonly used, even though it has been shown to shorten seizure duration which might affect the efficacy of ECT Etomidate has been advocated as an alternative. This prospective, randomised, single-blind, crossover study was conducted to compare the effects of etomidate (Etomidate-Lipuro, B. Braun Ltd, Melsungen, Germany) and propofol (Diprivan, AstraZeneca, UK) on seizure duration as well as haemodynamic parameters in patients undergoing ECT Twenty patients aged between 18 and 70 years were recruited. Group I received etomidate 0.3 mg/kg for the first course of ECT (Group IA) and propofol 1.5 mg/kg for the second ECT (Group IB), while Group II received propofol for the first ECT (Group IIA) and etomidate for the second ECT (Group IIB). There was a washout period of two to three days in between procedures. Parameters recorded included motor seizure duration, electroencephalogram seizure duration, blood pressure and heart rate. Analysis demonstrated neither period effect nor treatment period interaction. Etomidate was associated with a significantly longer motor and electroencephalogram seizure duration compared with propofol (P < 0.01). Neither drug demonstrated consistent effects in suppressing the rise in heart rate or blood pressure during ECT Myoclonus and pain on injection were the most common adverse effects in etomidate group and propofol group respectively. Etomidate is a useful anaesthetic agent for ECT and should be considered in patients with inadequate seizure duration with propofol.