A Thesis submitted to The University of Arizona College of Medicine - Phoenix in partial fulfillment of the requirements for the Degree of Doctor of Medicine.Introduction: Traumatic brain injury (TBI) in children can result in cognitive, emotional and somatic neurological impairments. In adults, post-traumatic hypopituitarism can extend or exacerbate these impairments, likely due to mechanical damage to the pituitary and hypothalamus. The pituitary in the pediatric brain likely suffers similar mechanical damage, inducing endocrinopathies as in adults, but injury-induced endocrinopathies are infrequently reported in children. Unrecognized hypopituitarism may lead to elevated risks of metabolic syndrome, diabetes, delayed or absent puberty, short stature, and other endocrinopathies. However, screening for endocrine deficiencies in susceptible patients and initiating appropriate hormone replacement therapy may prevent these sequelae and improve the prospects for recovery.
Results: We determined that TBI victims were 3.18-times higher risk of developing a central
endocrinopathy compared with the general population (CI=0.264), pediatric AHCCCS patients
with a central endocrinopathy had a 3.2-fold higher odds of a history with TBI than those without a central endocrinopathy (CI=0.266), of the central endocrinopathy in TBI victims is attributable to the TBI, and the number of patients who need to be exposed to a TBI for 1 patient to develop an endocrinopathy was 154.2 (CI=7.11). We also determined that more males than females presented with central endocrinopathies after TBI compared with the general population of TBI victims.This item is part of the College of Medicine - Phoenix Scholarly Projects 2018 collection. For more information, contact the Phoenix Biomedical Campus Library at [email protected]
