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Review article
peer-reviewed

Symptomatic Cerebral Vasospasm After Transsphenoidal Tumor Resection: Two Case Reports and Systematic Literature Review



Abstract

Cerebral vasospasm is a rare life-threatening complication of transsphenoidal surgery (TSS). We report our experience with two cases of symptomatic vasospasm after endoscopic TSS, alongside a systematic review of published cases. Two patients who underwent endoscopic TSS for resection of a tuberculum sella meningioma (case 1) and pituitary adenoma (case 2) developed symptomatic vasospasm. Clinical variables, including demographics, histopathology, the extent of subarachnoid hemorrhage (SAH), diabetes insipidus (DI), day of vasospasm, vasospasm symptoms, vessels involved, management, and clinical outcome, were retrospectively extracted. We subsequently reviewed published cases of symptomatic post-TSS vasospasm. Including our two cases, we identified 34 reported cases of TSS complicated by symptomatic vasospasm. Female patients accounted for 20 (58.8%) of 34 cases. The average age was 48.1 ± 12.9 years. The majority of patients exhibited postoperative SAH (70.6%). The average delay to vasospasm presentation was 8.5 ± 3.6 days. The majority of patients exhibited vasospasm in multiple vessels, typically involving the anterior circulation. Hemodynamic augmentation with hemodilution, hypertension, and hypervolemia was the most common treatment. Death occurred in six (17.6%) of 34 patients. Common deficits included residual extremity weakness (17.6%), pituitary insufficiency (8.8%), and cognitive deficits (8.8%). Symptomatic vasospasm is a rare, potentially fatal complication of TSS. The most consistent risk factor is SAH. Early diagnosis requires a high index of suspicion when confronted with intractable DI, acute mental status change, or focal deficits in the days after TSS. Morbidity and death are significant risks in patients with this complication.

Introduction & Background

Transsphenoidal surgery (TSS) is a relatively safe and very effective approach for reaching parasellar and suprasellar tumors. Cerebral vasospasm is an extremely rare, life-threatening complication of TSS that can be difficult to diagnose because of its delayed presentation and heterogeneous course [1]. The symptomatic onset of vasospasm typically occurs 5 to 10 days after surgery, mimicking the time course of vasospasm observed in the setting of aneurysmal subarachnoid hemorrhage (SAH) [2-4]. Clinically, vasospasm presents with signs and symptoms associated with ischemia in the territory of the implicated vessel(s).

Although the mechanism of post-TSS vasospasm is uncertain, postoperative SAH seems to be the most consistent risk factor. SAH has been observed in the majority of post-TSS vasospasm cases (84.6%) and is presumed to have a pathophysiological role, although vasospasm in the absence of SAH has been described [5-8]. Vasospasm is thought to be an infrequent contributor to the overall spectrum of ischemic complications after TSS, which includes direct injury to the internal carotid artery (ICA) and compression secondary to apoplexy [9]. However, the treatment of this idiosyncratic condition lacks evidence-based guidelines, and even with intensive care, the mortality rate associated with post-TSS vasospasm is approximately 30% [4,5,10].

Compared to the typical complications of pituitary tumor resection (e.g., diabetes insipidus [DI], pituitary insufficiency, cerebrospinal fluid [CSF] leak, meningitis, vision deficits), reports of symptomatic vasospasm after TSS are sparse [1,4-6,9,11-19]. As a consequence, very little is understood about the prevalence, etiology, and management of this condition. We report here our experience with two cases of symptomatic vasospasm and delayed cerebral ischemia after endoscopic TSS for resection of a tuberculum sella meningioma (case 1) and a pituitary adenoma (case 2). We also summarize our review of published cases to highlight the common presenting features, timing, clinical course, and management strategies.

Review

Institutional miniseries

During the year of 2019, two patients who underwent endoscopic TSS for pituitary tumor resection at the Indiana University Department of Neurological Surgery developed symptomatic vasospasm within two weeks of surgery. The medical records for these patients were accessed retrospectively, and the following clinical variables were extracted from each patient’s chart: demographics (age and sex), presenting symptoms, tumor extension, histopathological diagnosis, the documented occurrence of CSF leak, identification of postoperative SAH, postoperative DI, postoperative day (POD) of vasospasm diagnosis, clinical signs and symptoms during vasospasm, diagnostic modality used to confirm vasospasm, the vessels involved, management strategy, and outcome at discharge or last follow-up.

Institutional review board/ethics committee approval and patient consent were neither required nor sought for this study.

Literature review

We searched the literature for all published cases of symptomatic vasospasm after TSS for sellar or suprasellar tumor resection. An initial set of articles was obtained by querying the Medline/PubMed database with the following search terms (similar to those used by Mansouri et al.): [“pituitary”] and [“vasospasm” or “spasm” or “delayed cerebral ischemia”] and [“resection” or “surgery” or “transsphenoidal” or “TSS” or “ETSS”] [4]. Additional articles were obtained by cross-checking references and hand searching in Medline/PubMed and Google Scholar. Articles published in a language other than English were discarded. Cases in which vasospasm was preceded by pituitary apoplexy were also excluded because of the established risk of cerebral vasospasm in patients with this disorder [4]. The literature search was performed by two independent authors (H.C.B. and S.B.T.), and inconsistencies were resolved by discussion with the senior author (A.C.G.). After screening each abstract for relevance, full-length articles were reviewed for the clinical variables listed earlier.

Statistical reporting

Descriptive statistics (means and standard deviations) are used to report group-level continuous data from the literature search. Categorical variables (e.g., presence of SAH) were reported as percentages. Variables that could not be readily categorized (e.g., symptoms during vasospasm) are presented individually.

Case 1

A 36-year-old right-handed woman presented with a mild right homonymous hemianopsia. MRI revealed a large suprasellar mass with prepontine cisternal extension, encasement of the left proximal posterior cerebral artery (PCA), and partial encasement of the bilateral supraclinoid ICA and A1 segments (Figure 1A). She underwent endoscopic TSS, which resulted in a gross-total resection of a large tuberculum sella meningioma. A lumbar drain was used during the surgery for CSF drainage and continued postoperatively. The optic nerves were decompressed during the operation, but no significant dissection of the nerves was required. Allograft was used for closure. No obvious CSF leak or excessive bleeding was noted during the operation.

Shortly after surgery, the patient developed DI and a significant worsening of her vision. CT of her head revealed intraventricular hemorrhage (IVH) within the fourth ventricle, which prompted the initiation of dexamethasone (Figure 1B). On POD 3, she developed a nasal CSF leak, which was treated with CSF diversion via the lumbar drain. Her DI and pain remained difficult to manage, but her vision began to improve. The lumbar drain was discontinued, and she was transferred out of the intensive care unit (ICU) on POD 6. On POD 7, she was transferred back to the ICU for correction of severe hyponatremia (sodium level, 116 mEq/L) with intravenous hypertonic saline, oral salt replacement, and fludrocortisone.

On POD 13, the patient developed acute dysarthria, anxiety, right-arm apraxia, and gait instability, which spontaneously resolved over several hours. On POD 16, she had altered mental status and right hemiparesis, which prompted emergent imaging. CT of her head revealed an acute infarct of the left frontal lobe. CT angiography (CTA) of her head suggested delayed cerebral vasospasm (Figure 1C and D). Digital subtraction angiography revealed severe vasospasm in the paraclinoid left ICA, which resolved with balloon angioplasty, and mild-to-moderate left A1 and proximal left M2 vasospasm, which required super-selective intra-arterial papaverine administration (Figure 1E). Therapeutic hypertension (systolic blood pressure goal, >180 mm Hg) was initiated. Nimodipine was avoided because of the difficulty maintaining therapeutic hypertension. MRI revealed acute infarcts of the bilateral anterior cerebral artery (ACA) and left middle cerebral artery (MCA) distributions (Figures 1F and G). Transcranial Doppler (TCD) ultrasonography continued to reveal evidence for MCA vasospasm on POD 17, which prompted the initiation of vasopressors. Over the next week, she remained in the ICU and underwent daily monitoring with TCD ultrasonography. By POD 27, the patient had regained full strength and returned to her cognitive baseline. At discharge, her only lasting deficits were right-hand clumsiness and preexisting visual field deficits.

Case 2

A 55-year-old man presented with a three-month history of vision loss, erectile dysfunction, and diminished libido. MRI revealed a pituitary adenoma (Figure 2A). He underwent endoscopic TSS, which was complicated by an intraoperative CSF leak. His preoperative lumbar drain was left in place after surgery for CSF diversion. The patient developed DI on POD 1, and CT of his head performed at this time revealed SAH in the basal cisterns (Figure 2B). He was started on prophylactic therapy with intravenous fluids, nimodipine, levetiracetam, and atorvastatin.

On POD 7, the patient developed altered mental status and acute lethargy. TCD ultrasonography results were consistent with bilateral MCA vasospasm. Therapeutic hypertension was initiated with a systolic blood pressure goal of >180 mm Hg. His clinical course fluctuated over the next few days in accordance with his hemodynamic status. On POD 12, CTA of his head confirmed vasospasm in the bilateral supraclinoid ICAs, MCAs, and A1 segments (Figure 2C). On POD 14, the patient was brought to the interventional radiology suite for intra-arterial nicardipine administration (Figure 2D). After endovascular treatment, no evidence of clinical or subclinical vasospasm was found, and the patient was weaned off of intravenous fluids. TCD ultrasonography results gradually normalized, and the patient was discharged from the hospital on POD 21 without any deficits. 

Literature review results

Including our two institutional cases, our literature search identified 21 articles describing 34 cases of TSS complicated by symptomatic vasospasm (Table 1). Of these cases, 13 (38.2%) overlap with the recent literature review performed by Eseonu et al., whereas the remaining cases, to our knowledge, have not been presented in this format [5]. Female patients accounted for 58.8% of the patients in these cases, and the overall mean age at the time of surgery was 48.1 ± 12.9 years (range, 19-74 years). Common presenting signs and symptoms before surgery included headache, fatigue, visual disturbance, amenorrhea, sexual dysfunction, and hypopituitarism. The most prevalent pathologies were pituitary adenoma (70.6%) and craniopharyngioma (11.8%).

Case Age (y) Sex Presenting symptom(s) Tumor type Tumor extension CSF leak SAH/postop hemorrhage Vasospasm (POD) Diagnostic modality Management Outcome
Camp et al et al. [20] 33 F Amenorrhea, galactorrhea Pituitary adenoma Large sellar Yes No 6 Cerebral angiography Triple H, antibiotics Death
Hyde-Rowan et al. [21] 30 F Galactorrhea, headache, blurred vision Pituitary adenoma NR No Yes (1.4 L EBL, SAH on POD 2) 5 Cerebral angiography Conservative Death
Cervoni et al. [22] 51 M NR Pituitary adenoma Suprasellar NR Yes (SAH, POD 4) NR TCD Triple H, nimodipine Complete recovery
Friedman et al. [23] 41 M Acromegaly Pituitary adenoma NR No No 10 Cerebral angiography  Balloon angioplasty Complete recovery
Nishioka et al. [24] 41 M Decreased libido, vision changes Pituitary adenoma Suprasellar No Yes 12 Cerebral angiography  IA papaverine, triple H, thromboxane A2 antagonist Stable hypopituitarism
Kasliwal et al. [14] 34 F Amenorrhea, galactorrhea, headache, vision changes Pituitary adenoma Suprasellar Yes Yes (hematoma) 13 Cerebral angiography, TCD Hypervolemia Death
Popugaev et al. [25] 45 M NR Pituitary adenoma Suprasellar Yes Yes (SAH on POD 4) 4 TCD, cerebral angiography IV antibiotics GOS 4
52 F NR Pituitary adenoma Suprasellar NR No 4 TCD IV antibiotics GOS 5
Zada et al. [13] 59 M Bitemporal hemianopsia, hypogonadism Pituitary adenoma Suprasellar, floor of third ventricle, encasing ACAs NR Yes (SAH and hematoma on POD 2) 2 Cerebral angiography, CTA IA verapamil (3×) Short-term memory and stable visual field deficits
66 M Visual blurring, hypogonadism Pituitary adenoma Suprasellar, right frontal lobe invasion NR Yes (hematoma on POD 5) 8 Cerebral angiography, MRA IA verapamil Death
36 F Headache, vision change, hypopituitarism Pituitary adenoma Suprasellar NR Yes (SAH on POD 0) 9 CTA Triple H, IA verapamil (4×) Stable hypopituitarism
Puri et al. [1] 59 M NR Pituitary adenoma Suprasellar, floor of third ventricle No Yes 5 Cerebral angiography IA verapamil, triple H, nimodipine Cognitive and visual deficits, mild weakness
36 F Vision changes Pituitary adenoma Suprasellar No Yes 9 CTA IA papaverine, triple H, nimodipine Stable hypopituitarism
66 M Headaches, hypogonadism Pituitary adenoma Suprasellar, right frontal lobe invasion Yes Yes 8 Cerebral angiography Triple H, nimodipine, IA verapamil Death
Kim et al. [11] 51 M Vision changes Pituitary adenoma Suprasellar No Yes 9 Cerebral angiography Triple H, nimodipine Complete recovery
74 M Vision changes, headaches Pituitary adenoma Suprasellar No Yes 9 Cerebral angiography IA papaverine, triple H, nimodipine Complete recovery
65 F Vision changes Pituitary adenoma Suprasellar No Yes 7 Cerebral angiography IA papaverine, triple H, nimodipine Minor residual weakness
51 F Vision changes Pituitary adenoma Suprasellar No Yes 9 Cerebral angiography IA papaverine, triple H, nimodipine Complete recovery
Page et al. [8] 44 F Headaches, vision changes, nausea Pituitary adenoma Suprasellar No No 3 TCD, CTA Nimodipine, triple H Tracheostomy, gastrostomy, long-term rehabilitation
Eseonu et al. [5] 43 F Headache, fatigue, vision changes Pituitary adenoma Suprasellar Yes Yes (tumor bed hemorrhage) 12 MRA, TCD Hypertension, euvolemia, phenylephrine, nimodipine Complete recovery
Nash et al. [18] 48 F NR Craniopharyngioma NR No No 11 MRI, MRA Hypertension, nimodipine Complete recovery
49 F Vision changes Craniopharyngioma NR No No 5 CTA, cerebral angiography Hypertension, hypervolemia, balloon angioplasty, nimodipine Mild residual dysphagia
Bierer et al. [17] 54 M Vision changes Meningioma Suprasellar Yes No 11 MRA Antibiotics Subtle personality changes and impaired short-term memory
Bougaci and Paquis [15] 60 M Vision changes, hypopituitarism Pituitary adenoma Suprasellar, bilateral cavernous sinuses No Yes (SAH and suprasellar hematoma on POD 0) 9 Cerebral angiography Balloon angioplasty Complete recovery
Osterhage et al. [9] 52 M Homonymous hemianopsia Pituitary adenoma Suprasellar No Yes (SAH) 8 Cerebral angiography, TCD, CTA IA nimodipine Complete recovery
55 F Headaches, DI Rathke's cyst Suprasellar No Yes (prepontine) 13 Cerebral angiography, TCD, CTA IA nimodipine, aspirin Impaired left hand motor skills, CN III palsy, hypopituitarism
42 F Headaches, dizziness, DI Rathke cleft cyst/ granulation tissue NR No Yes (hematoma [prepontine]) 12 Cerebral angiography, TCD, CTA IA nimodipine Complete recovery
56 F Hydrocephalus, chiasmal syndrome, gait and speech disturbances Craniopharyngioma Suprasellar Yes Yes (SAH, IVH) 2 Cerebral angiography, TCD, CTA IA nimodipine Death
Suero Molina et al. [16] 23 F Hypopituitarism Pituitary adenoma Suprasellar Yes Yes 8 Cerebral angiography, CTA IA and IV nimodipine, hypertension Slight facial droop
Karimnejad et al. [2] 19 F Headache, nausea, vomiting, fatigue, vision change Lymphocytic hypophysitis Suprasellar No No 9 MRI, MRA Nimodipine, triple H, IA nicardipine Global aphasia, right hemiplegia
Ricarte et al. [6] 67 F NR Craniopharyngioma Suprasellar NR No 16 TCD, CTA Nimodipine, hypertension Mild paresis
Aggarwal et al. [7] 41 F Headache, amenorrhea, vision change Craniopharyngioma Suprasellar NR No 9 DSA, CTA IA milrinone, systemic milrinone Complete recovery
Current study 36 F Right-sided visual field cut Tuberculum sella meningioma Pre-pontine cistern Yes Yes 16 Cerebral angiography, CTA Hypertension, hypervolemia, nimodipine, IA papaverine, balloon angioplasty Slow gait and right-hand clumsiness
55 M Vision changes, sexual dysfunction Pituitary adenoma Sellar Yes Yes 7 TCD IA nicardipine Complete recovery

The majority of patients exhibited postoperative SAH or intracranial hematoma (70.6%). The timing of postoperative SAH was not consistently documented among these reports. CSF leak (29.4%) and postoperative DI (17.6%) were reported less commonly, although they were observed in both of the patients treated at our institution.

The average onset of symptomatic vasospasm was POD 8.5 ± 3.6 (range, POD 2-16). The clinical presentation of vasospasm was extremely variable across patients, with many patients exhibiting some combination of altered mental status, lethargy, and/or focal neurological deficits referable to the territory of the compromised vessel(s) (Table 1). Imaging modalities used to diagnose vasospasm included digital subtraction angiography (DSA), CTA, MRI/MRA, and TCD ultrasonography. In many patients, multiple modalities were used to confirm the diagnosis, identify the implicated vessels, and monitor for resolution or recurrence. DSA was often performed for both diagnostic and interventional purposes (see below).

The vessel(s) involved at the initial diagnosis of vasospasm was discerned in 94.1% of the cases; vasospasm in the remaining cases was described as “diffuse” [13,25]. The majority of patients exhibited vasospasm in multiple cerebral vessels, usually involving the anterior circulation (Table 2). In 40.6% of the patients, vasospasm was identified in segments of the ICA, MCA, and ACA simultaneously. The ACA was the most frequently implicated vessel, exhibiting spasm in 78.1%, with most cases involving the proximal segment. The supraclinoid segment was involved most frequently in patients with spasm of the ICA. The basilar arteries (12.5%), PCA (6.3%), and posterior communicating artery (3.1%) were rarely involved.

Study ICA MCA ACA PCA PComm Basilar
Current study X X X      
Current study X X X      
Aggarwal et al. [7] X X X      
Zada et al. [13] X X X      
Puri et al. [1] X X X      
Puri et al. [1] X X X      
Puri et al. [1] X X X      
Nishioka et al. [24] X X X      
Kim et al. [11] X X X      
Nash et al. [18] X X X      
Bougaci and Paquis [15] X X X      
Osterhage et al. [9] X X X      
Suero Molina et al. [16] X X X      
Karimnejad et al. [2] X X X      
Hyde-Rowan et al. [21] X          
Friedman et al. [23] X          
Kasliwal et al. [14] X          
Eseonu et al. [5] X          
Popugaev et al. [25]   X        
Osterhage et al. [9]   X        
Cervoni et al. [22]   X X      
Page et al. [8]   X X      
Nash et al. [18]   X X      
Ricarte et al. [6]   X X      
Bierer et al. [17]   X X     X
Osterhage et al. [9]   X X X   X
Zada et al. [13]     X X    
Kim et al. [11]     X      
Kim et al. [11]     X      
Kim et al. [11]     X      
Camp et al. [20] X       X  
Osterhage et al. [9] X   X     X
Popugaev et al. [25] Diffuse
Zada et al. [13] Diffuse

A variety of treatment strategies were described in the literature (see Table 1). Hemodynamic augmentation with hemodilution, hypertension, and hypervolemia (triple-H therapy) was very common but not universal among the cases. In patients who underwent intra-arterial therapy, the most frequently used agents were papaverine, verapamil, nimodipine, and milrinone. It was notable that 14.7% of the patients underwent endovascular balloon angioplasty. Systemic antibiotics were used in two cases for which post-TSS meningitis (not SAH) was the presumed cause of vasospasm [25].

In terms of outcomes, death of the patient was reported in six (17.6%) cases. At the other extreme, for 41.2% of the patients, complete resolution, a Glasgow Outcome Scale score of 5, or no deficits were reported. Common deficits included residual extremity weakness (17.6%), pituitary insufficiency (8.8%), and cognitive deficits such as aphasia and memory impairment (8.8%). We found no consistency in the follow-up durations or outcome variables documented among the studies.

Discussion

Symptomatic vasospasm is a potentially deadly complication of TSS. The first reported case of angiogram-confirmed vasospasm after TSS emerged in 1980, and only a handful of cases have been reported in the years since then [20]. In this study, we add two cases recently encountered at our institution to the literature, which now includes (to the best of our knowledge) a total of 34 cases.

Prevalence of symptomatic vasospasm after TSS

Rates of post-TSS vasospasm are unknown, but existing evidence suggests that the phenomenon is extremely rare. In the most compelling study on this topic, Osterhage et al. retrospectively examined just under 2,000 consecutive microscopic TSS cases treated at their center over an eight-year period [9]. They identified symptomatic vasospasm as a postoperative complication in only four (0.2%) patients, two with a Rathke cleft cyst, one with a suprasellar craniopharyngioma, and one with a giant nonfunctioning pituitary adenoma. In all four cases, SAH preceded the onset of vasospasm. Despite the rigor and size of this retrospective analysis, the possibility that a certain number of vasospasm cases went undetected should be considered when interpreting their observed prevalence.

SAH is the major risk factor for symptomatic post-TSS vasospasm

Authors of the most recent literature review of post-TSS cerebral vasospasm evaluated 13 cases and found that SAH preceded the onset of symptomatic vasospasm in the majority (84.6%) of the patients [5]. The results of this study and others suggest a prominent role of subarachnoid blood in triggering a vasospastic response. In its own right, significant SAH is a rare complication of TSS that occurs in just 1% to 2% of cases [9,26]. There are limited data by which to ascertain how often SAH leads to the even rarer phenomenon of symptomatic vasospasm. However, Kim et al. found that 26.7% of patients who developed post-TSS SAH went on to exhibit angiogram-confirmed symptomatic vasospasm [11]

The pathophysiology of post-TSS vasospasm remains uncertain. Many authors have drawn mechanistic parallels to the more common occurrence of vasospasm after aneurysmal SAH. In this setting, vasospasm is frequently attributed to the effects of blood breakdown products [27]. Delayed vasospasm after open tumor resection has also been documented, especially after skull base tumor resection [28,29]. The etiology of this complication has not been elucidated, but studies have identified sphenoid wing tumor location, a diagnosis of meningioma, postoperative bacterial meningitis, and SAH as risk factors [10]. Manipulation of vessels during tumor resection is more common and more traumatic when the tumor encases the vessels, and as such, vascular encasement is a proposed risk factor for vasospasm [30,31]. Vascular tone alteration via vessel manipulation during tumor resection has also been proposed as a mechanism for postoperative vasospasm via the impairment of vasodilation [32]. Tumors have also been known to release vasogenic molecules such as calcium and lipids, which can induce vasospasm [32,33].

Sellar tumors confer a larger risk of postoperative vasospasm because of their spatial relationship to the circle of Willis. In addition to the proposed etiologies of vasospasm after tumor resection, hypothalamic injury or electrolyte disturbance can contribute to the risk of vasospasm after TSS [1,5,10,34]. Other proposed risk factors for postresection vasospasm are pituitary apoplexy, intraoperative CSF leak, basal cistern tumor extension, hyponatremia, and postoperative syndrome of inappropriate antidiuretic hormone [35]. Hypothalamic dysfunction can also induce vasospasm by triggering a sympathetic discharge and catecholamine release [36,37]. DI and the resultant electrolyte disruptions can also make a patient more susceptible to vasospasm [38]. During craniopharyngioma or dermoid cyst resection, vasospasm can be caused by cystic fluid spillage, as seen in practice [39] and in in vivo rat studies, in which cystic fluid injected into rats resulted in femoral artery vasospasm [40]. In our cases, early mild vasospasm most likely led to intractable DI because of the resultant ischemia of the pituitary stalk and adjacent neurovascular structures.

Surveillance and treatment strategies for post-TSS vasospasm vary

It has been proposed that treatment for vasospasm after TSS should be similar to that for vasospasm after aneurysmal SAH, which includes euvolemia/hypervolemia, permissive hypertension, prevention of hyponatremia, seizure prevention, and endovascular treatment, if necessary [3]. Given that this condition is relatively uncommon after tumor resection, especially transsphenoidal resection, systematic screening and treatment protocols have not been established at most institutions, including our own. Our literature review found an impressive heterogeneity of treatment strategies, including hemodynamic augmentation, systemic pharmacotherapy, intra-arterial antispasmodic medications/vasodilation, and angioplasty. There is a similar paucity of literature surrounding the issue of postoperative surveillance. Considering the potentially devastating consequences of undetected vasospasm, the index of suspicion should always remain high in the setting of acute neurologic deterioration in the face of an unchanged or nondiagnostic CT scan. Further complicating this matter is the assumption that neurologic deterioration caused by an expanding hematoma or syndrome of the inappropriate antidiuretic hormone could be treated with stricter blood pressure parameters and volume restriction, which can exacerbate vasospasm. This exacerbation can be a significant factor in poor final outcomes and should be strongly avoided.

Death is common in the setting of post-TSS vasospasm

Given the limitations of our retrospective literature review, we were unable to perform a rigorous examination of clinical outcomes over a consistent follow-up period with standardized outcome variables. However, the results of our review corroborate previous findings that suggested that death frequently occurs in the setting of post-TSS vasospasm [4,5,10]. The mortality rate observed in our analysis (17.6%) is lower than the 30.8% mortality rate documented in the review by Eseonu et al. [5]. There seems to be a temporal pattern in the reported deaths within our review; five of six cases involving death were published before 2013. Several non-mutually exclusive explanations might contribute to this pattern, including (1) increased awareness of this rare complication; (2) superior diagnostic capabilities, surveillance, and treatment options; and (3) changes in publishing trends, resulting in fewer accounts of unfavorable outcomes.

Conclusions

Symptomatic vasospasm is a rare complication of transsphenoidal tumor resection. We evaluated a total of 34 reported cases to better understand the time course, presentation, treatment approaches, and outcomes of post-TSS vasospasm. Our results confirm that there is very limited evidence in the literature with which to make clinical decisions, leading to significant institutional or case-by-case heterogeneity. Despite intensive care, high morbidity and mortality rates are relatively common in the setting of this poorly understood complication.


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Review article
peer-reviewed

Symptomatic Cerebral Vasospasm After Transsphenoidal Tumor Resection: Two Case Reports and Systematic Literature Review


Author Information

Hailey C. Budnick

Neurological Surgery, Indiana University, Indianapolis, USA

Samuel Tomlinson

Neurological Surgery, School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, USA

Jesse Savage

Neurological Surgery, Indiana University, Indianapolis, USA

Aaron Cohen-Gadol Corresponding Author

Neurological Surgery, Indiana University, Indianapolis, USA


Ethics Statement and Conflict of Interest Disclosures

Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work.

Acknowledgements

We are grateful to the two patients included in this study, as well as the medical professionals who participated in their care.


Review article
peer-reviewed

Symptomatic Cerebral Vasospasm After Transsphenoidal Tumor Resection: Two Case Reports and Systematic Literature Review


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