Prognostic Assessment of Endocrine Disturbances in Posttraumatic Subarachnoid Hemorrhage

Abstract

Traumatic subarachnoid hemorrhage (SAH) is a condition with high risk for the development of hypopituitarism. Hormonal assessment is not a part of routine assessment after traumatic SAH. This study is a prospective screening study from our center focusing on the prognostic assessment of endocrine disturbances in posttraumatic SAH. A total of 150 consecutive patients with head injuries with SAH were included irrespective of their age and sex. Patients were divided into three groups: with normal hormonal status (group 1), patients with endocrine disturbances with no hormonal replacement (group 2), and patients with endocrine disturbances with replacement therapy (group 3). Hormonal assessment was done within 24 hours of admission and repeated at 7 to 15 days and at 1-month interval. Most commonly affected was pituitary-thyroid axis, and the most common hormone to increase was cortisol. In group 3, a statistically significant improvement was seen in Glasgow outcome score (GOS) as compared with the other two groups at 1 month. A statistically significant positive correlation has been found between thyroxine (T₄) at 30 days and Glasgow coma scale (GCS) at discharge in group 3, a negative correlation has been found between GCS at admission and serum cortisol at days 7 to 15 in group3. A positive correlation has been found between GCS at admission and GOS at 1 month in group 3. The authors have demonstrated evidence of pituitary dysfunction following traumatic brain injury (TBI) with SAH. Patients with traumatic SAH should be screened for hypopituitarism, so that appropriate hormone replacement is given to improve the outcome of these patients.

Keywords

head injury - subarachnoid hemorrhage - endocrine dysfunction - hormone replacement

• References

• 1 Mahapatra AK, Patnaik A. Introduction. In: Mahapatra AK, Kamal R. eds. Textbook of Head Injury. 4th ed.. New Delhi, India: CBS Publishers; 2014: 1
• 2 Cyran E. HypophysenschA~ digung durch schA~ delbasisfraktur. Dtsch Med Wochenschr 1918; 44: 1261
• 3 Kelly DF, Gonzalo IT, Cohan P, Berman N, Swerdloff R, Wang C. Hypopituitarism following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a preliminary report. J Neurosurg 2000; 93 (05) 743-752
• 4 Lieberman SA, Oberoi AL, Gilkison CR, Masel BE, Urban RJ. Prevalence of neuroendocrine dysfunction in patients recovering from traumatic brain injury. J Clin Endocrinol Metab 2001; 86 (06) 2752-2756
• 5 Leal-Cerro A, Flores JM, Rincon M. et al. Prevalence of hypopituitarism and growth hormone deficiency in adults long-term after severe traumatic brain injury. Clin Endocrinol (Oxf) 2005; 62 (05) 525-532
• 6 Aimaretti G, Ambrosio MR, Di Somma C. et al. Traumatic brain injury and subarachnoid hemorrhage are conditions at high risk for hypopituitarism: screening study at 3 months after the brain injury. Clin Endocrinol (Oxf) 2004; 61 (03) 320-326
• 7 Springer J, Chollet A. A traumatic car crash. Lancet 2001; 357 9271 1848
• 8 Schneider HJ, Aimaretti G, Kreitschmann-Andermahr I, Stalla GK, Ghigo E. Hypopituitarism. Lancet 2007; 369 9571 1461-1470
• 9 Bondanelli M, Ambrosio MR, Zatelli MC, De Marinis L, degli UbertiEC. Hypopituitarism after traumatic brain injury. Eur J Endocrinol 2005; 152 (05) 679-691
• 10 Behan LA, Phillips J, Thompson CJ, Agha A. Neuroendocrine disorders after traumatic brain injury. J Neurol Neurosurg Psychiatry 2008; 79 (07) 753-759
• 11 Edwards OM, Clark JD. Post-traumatic hypopituitarism. Six cases and a review of the literature. Medicine (Baltimore) 1986; 65 (05) 281-290
• 12 Niederland T, Makovi H, Gál V, Andréka B, Abrahám CS, Kovács J. Abnormalities of pituitary function after traumatic brain injury in children. J Neurotrauma 2007; 24 (01) 119-127
• 13 Kelestimur F, Tanriverdi F, Atmaca H, Unluhizarci K, Selcuklu A, Casanueva FF. Boxing as a sport activity associated with isolated GH deficiency. J Endocrinol Invest 2004; 27 (11) RC28-RC32
• 14 Yuan XQ, Wade CE. Neuroendocrine abnormalities in patients with traumatic brain injury. Front Neuroendocrinol 1991; 12 (03) 209-230
• 15 Greenwald BD, Burnett DM, Miller MA. Congenital and acquired brain injury. 1. Brain injury: epidemiology and patho-physiology. Arch Phys Med Rehabil 2003; 84 (03) Suppl 1) S3-S7
• 16 Wartofsky L, Burman KD. Alterations in thyroid function in patients with systemic illness: the “euthyroid sick syndrome.”. Endocr Rev 1982; 3 (02) 164-217
• 17 Agha A, Rogers B, Sherlock M. et al. Anterior pituitary dysfunction in survivors of traumatic brain injury. J Clin Endocrinol Metab 2004; 89 (10) 4929-4936
• 18 Feibel J, Kelly M, Lee L, Woolf P. Loss of adrenocortical suppression after acute brain injury: role of increased intracranial pressure and brain stem function. J Clin Endocrinol Metab 1983; 57 (06) 1245-1250
• 19 King LR, McLaurin RL, Lewis HP, Knowles Jr HC. Plasma cortisol levels after head injury. Ann Surg 1970; 172 (06) 975-984
• 20 Benvenga S, Campenní A, Ruggeri RM, Trimarchi F. Clinical review 113: hypopituitarism secondary to head trauma. J Clin Endocrinol Metab 2000; 85 (04) 1353-1361
• 21 Woolf PD. Hormonal responses to trauma. Crit Care Med 1992; 20 (02) 216-226
• 22 Van den Berghe G, de Zegher F, Bouillon R. Clinical review 95: acute and prolonged critical illness as different neuroendocrine paradigms. J Clin Endocrinol Metab 1998; 83 (06) 1827-1834
• 23 Van den Berghe G. Novel insights into the neuroendocrinology of critical illness. Eur J Endocrinol 2000; 143 (01) 1-13
• 24 Aimaretti G, Ambrosio MR, Di Somma C. et al. Residual pituitary function after brain injury-induced hypopituitarism: a prospective 12-month study. J Clin Endocrinol Metab 2005; 90 (11) 6085-6092