Endocrinopathy of the Critically Ill

During critical illness, marked neuroendocrine alterations develop in response to the severe stress. This neuroendocrine response to critical illness is biphasic. The acute phase is characterized by hypercortisolism, hypersecretion of growth hormone uncoupled from insulin-like growth factor-I, and suppression of thyroid and gonadal axes. These changes favor endogenous substrate release, while postponing costly anabolism, and are generally considered adaptive. The chronic phase is characterized by overall diminished hypothalamic output, leading to ineffective stimulation of the pituitary gland and an ongoing state of pronounced hypercatabolism. It is presumed that the neuroendocrine disturbances of prolonged critical illness, or their non-recovery, could contribute to the development of the post-intensive care syndrome. Strategies attempting to counteract these changes have mostly failed, but combined administration of hypothalamic releasing factors has shown to reactivate the neuroendocrine axes. Whether this intervention is able to improve short-term recovery, as well as long-term rehabilitation, needs thorough investigation in appropriately designed, adequately powered randomized controlled clinical trials.