Trauma Unmasking Pituitary Apoplexy: Coexisting Epidural Hematoma and Sellar Mass - A Case Report with Selected Cases from the Literature

Abstract

Background

Pituitary incidentalomas are sellar lesions identified on imaging performed for unrelated reasons. Lesions measuring 1 cm or larger are classified as macroincidentalomas. Pituitary apoplexy is an acute clinical syndrome caused by hemorrhage or infarction within the pituitary gland and may present with headache, ophthalmoplegia, altered consciousness, visual dysfunction, and hypopituitarism.

Case Presentation

A 36-year-old man presented with decreased consciousness after a motor vehicle crash. Noncontrast CT revealed a right parietal epidural hematoma with approximately 5 mm of midline shift and an incidental sellar mass. Emergency craniotomy and hematoma evacuation were performed, after which his Glasgow Coma Scale score improved to 15. Family members reported that left eyelid ptosis had begun 10 days before the crash. Subsequent MRI demonstrated a large heterogeneous sellar-suprasellar mass with T1-hyperintense components compatible with pituitary apoplexy. Endocrine evaluation showed central hypothyroidism, reduced gonadotropins, low prolactin, normal morning cortisol, and low-normal ACTH. Following endocrinology consultation, perioperative hydrocortisone was administered and later tapered. Endoscopic transsphenoidal resection revealed chronic motor oil-like blood and fragmented dark clot within the tumor. Histopathology confirmed a gonadotroph pituitary neuroendocrine tumor with a Ki-67 labeling index below 1%. The left ptosis resolved completely by the 3-month follow-up.

Conclusion

Life-threatening traumatic lesions may coexist with sellar emergencies and obscure their neurological and endocrine manifestations. In this case, pre-injury left ptosis suggested that the sellar process preceded the crash, whereas the role of trauma as a precipitating or aggravating factor could not be established. After stabilization of the traumatic lesion, targeted sellar imaging and early endocrine involvement should be considered when cranial nerve findings or endocrine abnormalities remain unexplained.

Background

Pituitary incidentalomas are increasingly identified because CT and MRI are frequently performed for head trauma, headache, and other unrelated indications.^1,2 Incidental pituitary lesions are reported in approximately 10% of MRI examinations in the general population.³ Although most lesions identified in radiologic and autopsy series are microadenomas, clinically detected incidental lesions may include macroadenomas.⁴ Demographic patterns vary among cohorts, although men are often diagnosed with larger adenomas.^5,6

Natural-history studies indicate that many clinically nonfunctioning pituitary incidentalomas remain stable, although enlargement and apoplexy can occur.⁷ Pituitary apoplexy may present with acute headache, visual impairment, cranial nerve palsies, altered consciousness, and acute hypopituitarism.^8,9 In contrast, non-apoplectic macroadenomas may cause gradual hypopituitarism and optic chiasm compression.^10,11

We report a patient with a traumatic epidural hematoma requiring emergency evacuation and a coexisting sellar-suprasellar mass with clinical, MRI, and intraoperative findings consistent with pituitary apoplexy. The coexistence of these lesions complicated attribution of the left ptosis and right mydriasis and required prioritization of the immediately life-threatening epidural hematoma before definitive sellar management. Selected comparable cases from the literature are summarized to place this management sequence in context.

Case Presentation

A 36-year-old man presented to the emergency department with decreased consciousness after a motor vehicle crash. On admission, his Glasgow Coma Scale score was E3V2M6. The right upper and lower limbs moved spontaneously. The left upper limb was paralyzed, and the left lower limb was plegic to the extent that could be assessed. Deep tendon reflexes were symmetric and normal (+2). There were no clinical signs of cerebrospinal fluid rhinorrhea or otorrhea.

Pupillary examination revealed a reactive, mid-sized left pupil and a fixed, dilated right pupil. A complete cranial nerve examination was not possible because of limited cooperation. Family members reported a 10-day history of left eyelid ptosis before the crash, which had not been evaluated. Plantar responses were downgoing bilaterally. Initial laboratory testing showed no immediately life-threatening abnormality. Noncontrast CT demonstrated a right parietal epidural hematoma with a maximum thickness of 3 cm and approximately 5 mm of midline shift, requiring urgent evacuation. The same CT showed an incidental sellar mass enlarging the sella and measuring approximately 4.0×2.0 x 2.5 cm.

The patient underwent emergency right parietal craniotomy and epidural hematoma evacuation. Postoperatively, he stabilized and improved to a Glasgow Coma Scale score of 15. Endocrinology was consulted after epidural hematoma evacuation. MRI then showed a large sellar-suprasellar mass consistent with a pituitary macroadenoma, with suprasellar extension compressing the optic chiasm and parasellar extension corresponding to Knosp grade IIIa. Heterogeneous internal signal and T1-hyperintense components suggested intratumoral hemorrhage compatible with pituitary apoplexy (Figure 1).^8,12

Figure 1.

(A) Axial noncontrast CT at the skull base shows an iso- to mildly hyperdense sellar lesion with sellar enlargement (arrow). (B) Axial T2-weighted MRI shows a heterogeneous sellar mass with suprasellar extension (arrow). (C) Coronal gadolinium-enhanced T1-weighted MRI shows heterogeneous enhancement and signal within the expansile sellar lesion (arrow). (D) Sagittal T2-weighted MRI shows a sellar-suprasellar mass with heterogeneous signal compatible with apoplexy (arrow).

Serial endocrine measurements during admission showed low TSH with low total T4 and low/low-normal total T3, supporting central hypothyroidism. LH and FSH were reduced, consistent with gonadotropin deficiency; testosterone was not available, so hypogonadotropic hypogonadism could not be confirmed biochemically. Prolactin was low. Morning cortisol remained within the laboratory reference interval (9.5–12.5 µg/dL), whereas ACTH ranged from borderline low to within range (7.1–8.0 pg/mL). Basal GH and IGF-1 were within their respective reference intervals. Serum sodium ranged from 138 to 154 mEq/L, and urine specific gravity ranged from 1.004 to 1.030 during admission. Paired serum and urine osmolality measurements were not available; therefore, the available data were insufficient to determine whether transient diabetes insipidus occurred. Given the acute clinical setting and concern for pituitary apoplexy, hydrocortisone 100 mg every 8 hours was initiated before transsphenoidal surgery after endocrinology consultation, continued during the immediate postoperative period, and subsequently tapered under endocrinology supervision. The serial hormonal results are summarized in Table 1.

Table 1.

Serial Hormonal Profile During Admission

Hormone	Result During Admission	Reference Range
Cortisol (8 AM)	9.5–12.5 µg/dL	4.82–19.54 µg/dL
ACTH (8 AM)	7.1–8.0 pg/mL	7.2–46 pg/mL
GH (basal)	0.2–0.6 ng/mL	<3.0 ng/mL
IGF-1	70.5–211 ng/mL	69–227 ng/mL
TSH	0.05–0.47 µIU/mL	0.35–4.94 µIU/mL
Total T4	3.6–5.4 µg/dL	4.87–11.72 µg/dL
Total T3	0.4–0.6 ng/mL	0.35–1.93 ng/mL
LH	0.1–0.6 mIU/mL	0.57–12.07 mIU/mL
FSH	0.2–2.6 mIU/mL	Adult male: 0.95–11.95 mIU/mL
Prolactin	1.0–2.1 ng/mL	3.46–19.4 ng/mL

Endoscopic endonasal transsphenoidal resection was performed following partial middle turbinectomy/ethmoidectomy and wide sphenoidotomy. On opening the sellar dura, chronic motor oil-like blood and fragmented dark clot, consistent with chronic and subacute hemorrhage, were clearly identified within the tumor. Gross-total tumor removal, including the capsule, was achieved. An intraoperative cerebrospinal fluid leak was repaired with a multilayer underlay fat graft and an overlay vascularized nasoseptal flap reinforced with hemostatic agents. The patient remained intubated and hemodynamically stable and was transferred to the intensive care unit.

Histopathology

Histopathological examination of the resected sellar mass demonstrated a pituitary neuroendocrine tumor composed of uniform cells arranged in micropapillary structures, with round-to-oval nuclei, finely granular chromatin, and moderate eosinophilic cytoplasm. No mitotic activity was identified. Immunohistochemical findings were consistent with a gonadotroph pituitary neuroendocrine tumor (pituitary adenoma), and the Ki-67 (MIB-1) labeling index was below 1%, indicating low proliferative activity. The pathology report did not describe hemorrhage, necrosis, or hemosiderin deposition in the submitted sections.

Postoperative Recovery

Postoperative MRI demonstrated complete tumor removal and decompression of the optic apparatus (Figure 2). The left-sided ptosis persisted after epidural hematoma evacuation and transsphenoidal resection and then resolved completely by the 3-month follow-up (Figure 3). The clinical sequence is summarized in Table 2.

Figure 2.

(A) Postoperative sagittal T2-weighted MRI shows postoperative changes in the sellar region and reduction of the suprasellar component (arrow). (B) Postoperative coronal gadolinium-enhanced T1-weighted MRI shows decompression of the optic apparatus (arrows).

Figure 3.

Clinical photographs showing (A) complete left ptosis before recovery and (B) complete resolution at the 3-month follow-up. The original photographs were obtained as selfies and are horizontally mirrored; therefore, the patient’s affected left eye appears on the right side of the displayed images.

Table 2.

Clinical Timeline

Time Point	Neurological/Ocular Findings	Investigation or Intervention
10 days before the crash	Left eyelid ptosis began; no right ptosis was reported.	No prior evaluation or imaging was available.
Emergency admission after motor vehicle crash	Decreased consciousness (GCS E3V2M6); reactive mid-sized left pupil; fixed, dilated right pupil; family confirmed pre-existing left ptosis.	CT showed a right parietal epidural hematoma with approximately 5 mm midline shift and an incidental sellar mass.
Emergency operation	Neurological status improved after surgery.	Right parietal craniotomy and epidural hematoma evacuation.
Early postoperative assessment	GCS improved to 15; left ptosis persisted; no right ptosis was present.	Endocrinology consultation; serial pituitary testing; hydrocortisone 100 mg every 8 hours was started before sellar surgery.
Sellar MRI	Persistent left ptosis.	MRI showed a large heterogeneous sellar-suprasellar mass with T1-hyperintense components.
Transsphenoidal surgery	No new right-sided ptosis.	Endoscopic endonasal resection; chronic motor oil-like blood and fragmented dark clot were observed; intraoperative CSF leak was repaired.
Histopathology	Not applicable.	Gonadotroph pituitary neuroendocrine tumor; Ki-67 below 1%. The pathology report did not describe hemorrhage, necrosis, or hemosiderin in the submitted sections.
Three-month follow-up	Left ptosis resolved completely.	Clinical follow-up photograph.

Discussion

This case illustrates a time-critical management problem in which a surgical epidural hematoma coexisted with pituitary apoplexy. Epidural hematoma can cause rapid neurological deterioration and herniation and therefore requires immediate evacuation.¹³ Pituitary apoplexy can likewise cause altered consciousness, cranial nerve palsies, visual dysfunction, and acute endocrine impairment; early endocrine assessment and empirical corticosteroid coverage may be lifesaving.^9,12,14 In this patient, epidural hematoma evacuation was prioritized, followed by endocrinology consultation, stress-dose hydrocortisone, sellar MRI, and transsphenoidal decompression. The educational value of the case lies not in either diagnosis alone, but in their uncommon coexistence, competing treatment priorities, discordant ocular findings, and direct operative evidence of hemorrhage despite nonconfirmatory histological sampling.

Selected previously reported cases are summarized in Table 3 to provide clinical context. These reports are heterogeneous single-case observations with variable timing of presentation, endocrine assessment, imaging, operative sequencing, and follow-up. They therefore cannot establish a causal relationship between trauma and apoplexy or define a uniform management algorithm; their value is illustrative and supports individualized treatment according to the immediately life-threatening lesion, neuro-ophthalmological deficits, and endocrine status.

Table 3.

Selected Published Reports Relevant to Trauma-Associated Pituitary Apoplexy and Incidental Sellar Lesions

Case	Age/Sex	Presentation/Symptoms	Imaging Findings	Hormonal Findings	Associated Pathology	Management	Outcome
Dev, 200715	40/M	Sudden severe headache, vomiting, acute visual loss	CT/MRI: sellar–suprasellar hemorrhagic mass + basifrontal ICH	Panhypopituitarism	Road traffic accident → apoplexy in occult NFPA + basifrontal ICH	Endonasal TSS; tumor + basifrontal hematoma evacuated	Vision improved, residual hemianopia; hormone replacement continued
Ishigaki, 201716	66/M	Delayed isolated left CN III palsy (diplopia, ptosis) 4 days post-fall	CT/MRI: hemorrhage with left cavernous sinus compression; sphenoid thickening	Normal hormonal profile	Minor head trauma → apoplexy in incidental NFPA	Endonasal TSS on day 6	CN III palsy resolved by day 14; no DI or hypopituitarism
Noriega-Jalil, 201817	46/M	Severe TBI (GCS 8), hypotension; multiple CN deficits; left ptosis/mydriasis	MRI: hemorrhagic macroadenoma 21×42×52 mm with cavernous sinus invasion	Hypocortisolism + central hypothyroidism + hypogonadotropic hypogonadism; prolactin 6213 ng/mL	Post-traumatic apoplexy in macroprolactinoma	Conservative: stabilization + hydrocortisone, levothyroxine, cabergoline	Tumor shrank; prolactin normalized; persistent hypopituitarism on replacement; residual low left visual acuity
Morinaga, 201918	42/M	Post-trauma CT incidental sellar mass; subtle acromegalic features	MRI: 22-mm enhancing sellar–suprasellar macroadenoma	Elevated GH and IGF-1; other hormones normal	Trauma-associated recognition of functional incidentaloma	Endoscopic TSS resection	Hormones normalized; no recurrence at 24 months
Ward, 201819	63/M	Closed head trauma; within 48 h developed AMS, fever, tachycardia, hypotension	MRI: hemorrhagic necrotic pituitary mass; sphenoid mucosal thickening	Panhypopituitarism	Closed head injury → apoplexy in known macroadenoma	Steroids + thyroid replacement; urgent endoscopic TSS	Mental status improved; vision returned to baseline
Bao, 200720	79/M	Severe headache, nausea/vomiting, neck stiffness after fall	CT/MRI: sellar–suprasellar mass + suprasellar SAH; MRA negative	Hypopituitarism	Fall → apoplexy in incidental adenoma complicated by SAH	Conservative treatment	Tumor regressed; well at 18 months
Uchiyama, 199921	60/F	Severe headache/nausea; rapid bilateral vision loss (delayed)	MRI: dumbbell sellar–suprasellar macroadenoma with fresh intratumoral hemorrhage	Not specified	Fall with occipital fracture → apoplexy in asymptomatic macroadenoma	Hydrocortisone + urgent TSS (12 h) + staged completion TSS	Vision near baseline by 1 week; no chronic hormone replacement reported
Uchiyama, 199921 (case 2)	66/M	Disorientation; at 15 h developed bilateral blurred vision → rapid severe loss + lethargy	CT/MRI: frontal contusion + enlarging sellar tumor with hemorrhage	Not specified	Fall from height with occipital fracture + frontal contusion → apoplexy	Left frontotemporal craniectomy + partial tumor removal	Vision improved; moderate disability at 4 months; tumor regressed
Holness, 198322	39/M	Immediate severe vision loss; no meningism	CT/angiography: intrasellar/suprasellar hematoma with chiasmal compression; ACA displaced	Mild prolactin elevation; low testosterone	Minor closed head trauma → apoplexy in silent adenoma	Steroids + frontal craniotomy + hematoma drainage; radiotherapy	Partial right eye recovery; no left recovery at 3 months

Note: This table is an illustrative selection and not a systematic review.

Abbreviations: ACA, anterior cerebral artery; ACTH, adrenocorticotropic hormone; AMS, altered mental status; CN, cranial nerve; CT, computed tomography; CSF, cerebrospinal fluid; DI, diabetes insipidus; FU, follow-up; GCS, Glasgow Coma Scale; GH, growth hormone; ICH, intracerebral hemorrhage; IGF-1, insulin-like growth factor-1; LOC, loss of consciousness; MRA, magnetic resonance angiography; MRI, magnetic resonance imaging; NFPA, non-functioning pituitary adenoma; SAH, subarachnoid hemorrhage; TBI, traumatic brain injury; TSH, thyroid-stimulating hormone; TSS, transsphenoidal surgery; HM, hand-movement vision.

Left ptosis had been present for 10 days before trauma, supporting pre-existing or subacute left cranial nerve III dysfunction related to the sellar lesion or cavernous sinus involvement. Isolated oculomotor palsy with ptosis has been reported in pituitary apoplexy.^16,23,24 By contrast, the fixed, dilated right pupil at presentation was more compatible with acute compressive cranial nerve III dysfunction from epidural hematoma-related intracranial mass effect.^25,26 A complete neuro-ophthalmological examination was not possible at admission because of limited cooperation; therefore, these anatomical attributions are presented as the most clinically compatible explanations rather than definitive proof.

Head trauma has been reported in temporal association with hemorrhage or infarction in pre-existing pituitary adenomas.^15,16,22 However, the current case cannot establish causality. Because left ptosis preceded the crash and no pre-event imaging was available, apoplexy may have preceded the trauma, trauma may have precipitated or aggravated an evolving hemorrhagic event, or the two events may have been coincidental. MRI is the preferred imaging modality when pituitary apoplexy is suspected, but its signal characteristics provide only an approximate estimate of hemorrhage age.^8,9,12

The endocrine profile was more consistent with pituitary dysfunction than with stalk-effect hyperprolactinemia. Unlike a stalk-effect pattern, which generally causes increased prolactin,^27,28 this patient had low prolactin together with central hypothyroidism and reduced gonadotropins. Because testosterone was unavailable, the gonadal-axis abnormality is described as gonadotropin deficiency rather than confirmed hypogonadotropic hypogonadism. Morning cortisol was within the laboratory reference interval, whereas ACTH was low-normal to borderline low. A single morning cortisol value during acute illness does not fully exclude secondary adrenal insufficiency; therefore, after endocrinology consultation, stress-dose hydrocortisone was administered before surgery and through the immediate postoperative period and was subsequently tapered.^9,12,14

The pathology report did not describe hemorrhage, necrosis, or hemosiderin deposition in the submitted sections; however, the operative field contained chronic motor oil-like blood and fragmented dark clot, providing direct evidence of chronic and subacute intratumoral bleeding. Histopathology confirmed a low-proliferative gonadotroph pituitary neuroendocrine tumor with a Ki-67 labeling index below 1%. The discrepancy between the operative and microscopic findings may reflect sampling of nonhemorrhagic tumor fragments and is reported explicitly rather than interpreting the pathological sample as excluding apoplexy.

In trauma patients, sellar-protocol MRI should not delay treatment of an immediately life-threatening intracranial lesion. It should be considered after stabilization when cranial nerve findings, visual symptoms, or endocrine abnormalities are not adequately explained by the traumatic lesion. This selective approach is more practical than routine early sellar MRI for all patients with head trauma.

Conclusions

Coexisting epidural hematoma and pituitary apoplexy can produce overlapping but anatomically distinct neurological signs and competing treatment priorities. In this patient, the life-threatening epidural hematoma required immediate evacuation; persistent pre-injury left ptosis, endocrine abnormalities, sellar MRI findings, and intraoperative chronic/subacute blood subsequently supported pituitary apoplexy in a gonadotroph pituitary neuroendocrine tumor. The temporal relationship to trauma remains uncertain. After stabilization of the traumatic lesion, targeted sellar imaging and early endocrine consultation are appropriate when cranial nerve, visual, or hormonal findings remain unexplained.

Funding Statement

There is no funding to report.

Data Sharing Statement

All data generated or analyzed during this study are included in this published article.

Consent for Publication

Written informed consent was obtained from the patient for publication of the case details and accompanying images.

Disclosure

The authors declare that they have no competing interests.