title: Postoperative sellar hematoma after pituitary surgery: clinical and biochemical characteristics.
abstract: BACKGROUND
  Postoperative sellar hematoma can develop following surgery for pituitary tumors and other sellar masses such a Rathke's cleft cyst (RCC) due to continued blood oozing. Though often mild sellar hematoma can create mass effects that might impair pituitary function.
  
  
  OBJECTIVE
  This study summarizes the clinical and biochemical characteristics of sellar hematoma and explores the potential mechanisms for the associated hypopituitarism.
  
  
  METHODS
  Sellar hematoma was suspected clinically (worsening headaches, visual impairment, and mental status alterations) and confirmed radiographically in 23 patients (18/279 with macroadenomas and in 5/92 with RCC). Postoperatively, patients were monitored without glucocorticoid therapy and all had appropriately normal HPA function before sellar hematoma diagnosis.
  
  
  RESULTS
  The demographics of patients who had sellar hematoma were similar to those who did not. Biochemical changes at diagnosis included decreased plasma ACTH and its dependent steroids (cortisol, DHEA, and DHEA-S), concomitant mild hyperprolactinemia, and mild hyponatremia (P < 0.005 for all parameters). Treatment with glucocorticoids resulted in rapid clinical improvement in most patients. Glucocorticoid therapy was discontinued within 2 weeks and re-testing thereafter showed normal HPA function in 16/23. None of the patients without sellar hematoma had worsening in pituitary function, visual, or neurological symptoms.
  
  
  CONCLUSIONS
  When large, sellar hematoma can lead to mass effect that causes headaches, visual symptoms, and acute and often reversible hypopituitarism manifesting initially as impaired HPA function. Rapid resolution is observed in most patients with glucocorticoid administration The rapid onset and reversibility of hypopituitarism associated with mild hyperprolactinemia suggest that compression of pituitary stalk/ portal vessels is likely the dominant mechanism of pituitary dysfunction in this setting.
authors: Division of Clinical and Molecular EndocrinologyCase Medical Center and Case Western Reserve University, Cleveland, OH, USA.
authors: Nadine
authors: N
authors: El-Asmar
authors: Division of Clinical and Molecular EndocrinologyCase Medical Center and Case Western Reserve University, Cleveland, OH, USA.
authors: Katia
authors: K
authors: El-Sibai
authors: Division of Clinical and Molecular EndocrinologyCase Medical Center and Case Western Reserve University, Cleveland, OH, USA.
authors: Ribal
authors: R
authors: Al-Aridi
authors: The Department of Neurological SurgeryCase Medical Center and Case Western Reserve University, Cleveland, OH, USA.
authors: Warren R
authors: WR
authors: Selman
authors: Division of Clinical and Molecular EndocrinologyCase Medical Center and Case Western Reserve University, Cleveland, OH, USA baha.arafah@case.edu.
authors: Baha M
authors: BM
authors: Arafah
mesh_terms: D000236:Adenoma / Q000601:surgery; D000368:Aged; D003397:Craniopharyngioma / Q000601:surgery; D005260:Female; D005938:Glucocorticoids / Q000627:therapeutic use; D006406:Hematoma / Q000097:blood / Q000188:drug therapy / Q000209:etiology*; D006801:Humans; D007018:Hypopituitarism / Q000097:blood / Q000188:drug therapy / Q000209:etiology*; D019635:Neurosurgical Procedures / Q000009:adverse effects; D010911:Pituitary Neoplasms / Q000601:surgery*; D011183:Postoperative Complications / Q000097:blood / Q000188:drug therapy / Q000209:etiology; D012658:Sella Turcica / Q000473:pathology; D016896:Treatment Outcome
chemical_list: D005938:Glucocorticoids