SAT-100 - A Diagnostic Trap: Delayed Recognition of Post-Traumatic Panhypopituitarism

Acquired hypopituitarism (HP) is a recognized complication of traumatic brain injury (TBI), affecting approximately 20–40% of patients with moderate to severe head injury. [1] Pituitary dysfunction may emerge in both acute and chronic phases, with deficiencies developing up to five years of post-injury, often leading to delayed diagnosis and ongoing morbidity.[2] We report a case of a patient with prior TBI in whom incomplete hypopituitarism screening and inadequate follow up resulted in delayed diagnosis and intervention of hypogonadism leading to severe osteoporosis.


A 55-year-old male was initially admitted to the intensive care unit following a motor vehicle accident complicated by complete lack of arousal. MRI revealed subdural hematoma, and a vertebral artery contusion.

Laboratory results showed morning ACTH level of 4.7 pg/mL ( 7.2-63.3 pg/ml) and a serum cortisol level of 1.1 µg/dL (10-20 mg/dl); TSH level < 0.01 µIU/mL (n. 0.8-1.8 ng/dl) and a free thyroxine level (FT4) of 0.2 ng/dL (n. 0.8-1.8 ng/dl), were consistent with central adrenal insufficiency and central hypothyroidism. Hydrocortisone (HC) 20 mg oral (po) and levothyroxine (LT4) 175 µg po daily were initiated.

Patient presents in clinic for the evaluation of chronic fatigue and poor libido ten years after the vehicle accident, when he was on prednisone 7.5 mg daily, and LT4 150 µg po daily. Pituitary hormone workup showed morning cortisol 1.1mcg/dL with ACTH < 5 pg/ml (after holing on prednisone for 24hrs); LH < 0.2 IU/L (n. 1.8 to 8.6 IU/L), FSH < 0.7 IU/L (n. 1.42 to 15.4 IU/L), total testosterone < 1ng/dL (n. 250 to 1100 ng/dL); prolactin < 0.1 ng/mL (n. < 20 ng/mL); IGF-1 level was 24 ng/mL (50-317 ng/dL); TSH < 0.01 with FT4 1.1 ng/dL (0.8-1.8 ng/dL), suggestive of panhypopituitarism. He denies polyuria and polydipsia; serum sodium is normal. Testosterone cypionate injections 100 mg weekly was initiated.

The patient also underwent dual-energy X-ray absorptiometry, which revealed severe osteoporosis of the anteroposterior lumbar spine (BMD 0.794 g/cm2, T-score −3.7). Patient was started on a Bisphosphonate infusion with Vitamin D supplement.

Clinicians should maintain a high index of suspicion for evolving pituitary dysfunction after TBI and ensure periodic reassessment of all pituitary axes. This monitoring should be performed not only by endocrinologists but also by primary care providers and could be integrated into the long-term follow-up of patients with severe TBI. Early recognition and appropriate hormone replacement therapy may prevent irreversible complications and improve long-term quality of life.

Incomplete screening for pituitary hormone deficiency and lack of long-term follow-up for the patients with moderate to severe TBI led to delayed recognition and treatment of post-traumatic panhypopituitarism, including central hypogonadism resulting in severe osteoporosis.

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