Hypopituitarism following traumatic brain injury:† Is there a role for routine screening?
Chia J, Brockett K, Raj S, Clark J, Field B, Zachariah S.
Abstract: A 51 year old male presented in April 2014 to a district general hospital with a painful, swollen left leg. Three weeks previously he had slipped from his wheelchair onto both knees. Plain radiography disclosed a comminuted fracture of the left distal femur and generalised osteopenia. In 1995 the patient had sustained a severe head injury during a cycling accident, resulting in left hemiplegia.
During the current admission, initial blood tests demonstrated a normochromic, normocytic anaemia (Hb 73 g/L, MCV 91 fL) but serum electrolytes were normal (Na+ 141 mmol/L, K+ 4.4 mmol/L, urea 5.5 mmol/L, creatinine 76 umol/L). The patient underwent manipulation under anaesthesia and initially recovered well. A fortnight later he deteriorated over the space of three days, gradually becoming drowsy. Blood tests revealed serum Na+ 112 mmol/L. Intravenous fluid resuscitation was started and an endocrine opinion was requested. Characteristic signs and symptoms of chronic untreated panhypopituitarism were apparent. Further investigations revealed 9 a.m. cortisol 82 nmol/L, prolactin 271 mu/L, free T4 8.2 pmol/L, TSH 3.6 mIU/L, testosterone <0.1 nmol/L, FSH 0.3 iu/L, LH <0.1 iu/L and IGF-1 4.2 nmol/L (age-adjusted reference range 9 to 40). Hydrocortisone treatment was commenced, followed by levothyroxine. The patient made a swift recovery and his electrolytes normalised. Magnetic resonance imaging was not tolerated but a CT scan showed an atrophic pituitary gland. Since discharge from hospital the patient reports symptomatic improvement; testosterone replacement has been started and assessment of growth hormone secretion is planned. There is no suggestion of diabetes insipidus.
Anterior pituitary hormone deficiency after traumatic brain injury is an increasingly well-recognised phenomenon. Possible mechanisms1 include haemorrhage, necrosis or fibrosis affecting the hypothalamus and pituitary. The reported prevalence varies widely, owing to case identification bias and the multiplicity of dynamic tests and assays used for diagnosis. However, deficiencies are more common after blast-related traumatic brain injury than after blunt trauma.2 With relevance to ongoing debate on the cost-effectiveness of screening for hypopituitarism after traumatic brain injury, it is interesting that the consequences of our patientís condition did not become apparent until nineteen years after the original injury. It is also striking that metabolic decompensation, resulting primarily from cortisol deficiency, was delayed for five weeks after the femoral fracture.†
References: (1) Wilkinson CW et al.† High prevalence of chronic pituitary and target-organ hormone abnormalities after blast-related mild traumatic brain injury.† Front Neurol. 2012; 3. doi: 10.3389/fneur.2012.00011.† (2) Baxter D et al. Pituitary dysfunction after blast traumatic brain injury: The UK BIOSAP study. Ann Neurol. 2013; 74(4): 527-36.