Does Pituitary Dysfunction Always Occur Following Penetrating Head Trauma?

Abstract

Background: Pituitary dysfunction and panhypopituitarism remain underdiagnosed in penetrating and blunt head trauma and can occur in both acute and chronic settings. Case: A 56 years old male with no significant PMH was admitted with a gunshot wound to the left T9 rib paraspinally with bullet deflection cranially along the left lung, left sternocleidomastoid, and resting anterior to the suprasellar cistern just above the midline of the sphenoid sinus close to the pituitary gland. Moderate volume pneumocephalus, chest hemopneumothorax, and sudden loss of right-sided vision required neurosurgical and pulmonary intervention. Endocrinology was consulted to evaluate pituitary function in the context of the bullet within the cranium. Physical examination showed intact mental status, non-focal exam, right-sided blindness, and foley catheter with normal urine output. Laboratory hormonal assessment for hypothalamic-pituitary axis (HPA) was performed consistent with normal sodium, potassium, FSH of 14.2 mIU/ml (1.0-13.0 mIU/ml), LH of 4.5 mIU/ml (1.0-9.0 mIU/ml), AM cortisol of 13.6 ug/dl (5-25 ug/dl), free cortisol of 2.06, ACTH of 10 pg/ml (10-60 pg/ml), IGF-1 of 80 ng/ml (78-220 ng/ml), TSH 1.93 mIU/L (0.5-5.0 mIU/L), FT4 1.05 ng/dl (0.8-1.8 ng/dl), Prolactin of 14.2 ng/ml (4-23 ng/ml) and HbA1c 5.1%. He reported no symptoms of adrenal insufficiency and remained hemodynamically stable. He was monitored for symptoms of pituitary insufficiency and suppression of the HPA axis along with urine output which remained normal and reassuring for the absence of central DI. The patient will continue outpatient endocrine surveillance. Discussion: The development of hormone deficiencies is directly related to the severity of head trauma. Mild traumatic brain injury (TBI) patients discharged from the ED, without loss of consciousness or post-traumatic amnesia less than 30 minutes do not require endocrine surveillance. Pituitary dysfunction occurs in 20-40% of patients with moderate to severe TBI. Pituitary ischemia leads to pituitary injury, due to changes in cerebral blood flow, cerebral hypoxia, and increased intracranial pressure. Compressive effects on the stalk from increased intracranial pressure is another indirect mechanism for pituitary dysfunction. Hospitalizations longer than 48 hours following TBI, require pituitary screening at 3-6 months. Chronic hypopituitarism develops in 15-20% of patients within 2-3 years with ACTH and GH deficiencies. Other changes in LH, FSH, TSH, and development of central diabetes insipidus can occur. However, despite severe TBI, acute pituitary hormonal involvement may not always occur, as in our patient.