Functional pituitary macroadenomas, although rare,1 present a unique challenge for anesthesiologists. These tumors, arising from the anterior pituitary gland, exhibit an expansive growth pattern (often exceeding 10 mm in diameter) and have the potential for endocrine dysregulation. Their functional nature further complicates the perioperative management, as these adenomas can manifest with an array of hormonal abnormalities, such as acromegaly, Cushing’s disease, and prolactinomas. The interplay of hormonal disturbances, coupled with the mass effect of the tumor itself, necessitates a complex approach to anesthesia delivery, encompassing comprehensive preoperative evaluation, tailored intraoperative strategies, and vigilant postoperative care. This case report aims to highlight the challenges faced by anesthesiologists when navigating the perioperative care of patients with functional pituitary macroadenomas. We will explore the preoperative assessment, anesthetic strategies, and postoperative considerations crucial for optimizing patient outcomes in the face of these neuroendocrine tumors. We hope to contribute to the collective knowledge base, fostering a deeper understanding of the multifaceted nature of anesthetic management in the context of functional pituitary macroadenomas.
A 23-year-old male with no significant past medical history presented with daily headaches for about one year and loss of peripheral vision for approximately six months. He is 5’11” and weighs 102 kg with a BMI of 31.5. Physical exam showed coarse facial features with an abnormally enlarged jaw when compared to previous pictures of the patient. Workup revealed a large pituitary mass (5.5 x 5.4 x 5.7 cm), with extension into the suprasellar region. Trans-sphenoidal biopsy showed a growth hormone secreting pituitary adenoma and the patient was scheduled for craniotomy for excision of the tumor. Preoperative laboratory work was significant for growth hormone (73.70), insulin-like GF1 (1,165), prolactin (19.17), HbA1C (6.4) and glucose (350 mg/dL) which was being treated with insulin.
General anesthesia was induced with intravenous lidocaine, fentanyl, and propofol. Muscle relaxation was achieved with succinylcholine. Mask ventilation was moderately difficult due to his prognathism. Intubation was easy with the use of a Macgrath videoscope despite the patient’s enlarged tongue and epiglottis. A radial arterial line was placed for close blood pressure monitoring and possible arterial blood gasses tests during the case. A femoral central venous line was placed due to difficult IV access. A partial selective scalp block was performed with 10 mL of 0.5% bupivacaine after the surgical incision was marked to aid with analgesia throughout the case. Intraoperative neuromonitoring was performed during the case for somatosensory (SSEP) and motor evoked potentials (MEP). Anesthesia was maintained with propofol and remifentanil infusions to facilitate neuromonitoring. The oxygen saturation of the patient during the case stayed between 90-93% in spite of all attempts to improve it including high FiO2 and PEEP. Arterial blood gas during the case showed a PaCO2 of 47 mmHg (EtCO2 was 35 mmHg) and a PaO2 of 108 mmHg despite an FiO2 of 0.5. The patient remained hyperglycemic intra-operatively even with insulin therapy. Rest of the surgery was uneventful. After extubation, the patient was transported to the neuro intensive care unit and remained hypertensive despite hydralazine, labetalol, and narcotics for pain control. Later that same evening, the patient was re-intubated due to respiratory distress. He remained on a ventilator overnight and was extubated the following morning. The rest of his hospital stay was uneventful and was discharged home a few days later.
Anesthetic Challenges & Discussion:
Pituitary adenomas are categorized based on primary cell origin and type of hormone secreted.1 If the adenoma does not secrete a sufficient level of hormones to be detectable in the blood or to result in clinical manifestations, it is considered non-functioning. Prolactinomas comprise 40% to 57% of all adenomas, followed by non-functioning adenomas (28% to 37%), growth hormone–secreting adenomas (11% to 13%), and adrenocorticotropic hormone (ACTH)–secreting adenomas (1% to 2%). Pituitary adenomas that secrete follicle-stimulating hormone (FSH), luteinizing hormone (LH), or thyroid-stimulating hormone (TSH) are rare.1
Preoperative: Giant secreting pituitary adenomas pose several perioperative challenges. Preoperatively, abnormal hormonal secretions can lead to significant anatomical, physiological and metabolic changes in the body affecting multiple organs and tissues. These include acromegaly (excessive growth hormone secretion leading to soft tissue and connective tissue overgrowth, difficult airway, peripheral neuropathy, glucose intolerance, ischemic cardiomyopathy, ventilation-perfusion mismatch, skeletal muscle weakness), Cushing’s syndrome (excessive adrenocorticotropic hormone secretion leading to difficult airway, abnormal glucose metabolism, fragile skin, muscle weakness). Mechanical pressure on the visual tracts due to the location of the tumor often results in vision changes. A thorough preoperative work up of the patient including radiological studies and hormone and metabolic laboratory workup is mandatory in diagnosing the type of tumor and the extent of hormonal and physiological derangement.
Intraoperative: Many of these patients present potential for difficult airway due to acromegaly and alternative airway management options such as a video laryngoscope and other equipment along with experienced personnel should be available. The airway changes commonly seen are the following.
- Skeletal overgrowth leading to large mandible and prognathism.
- Soft tissue overgrowth of lips and tongue leading to difficulty in placing an anesthesia face mask.
- Enlargement of tongue and epiglottis leading to difficult mask ventilation and visualization of vocal cords.
- Increased distance between the lips and the vocal cords due to enlarged mandible.
- Narrowed glottic opening due to enlargement of vocal cords and subglottic narrowing may necessitate smaller sized endotracheal tubes than predicted.
- Enlargement of nasal turbinates may make placing nasal tubes difficult.
- Stretching caused by overgrowth of laryngeal tissues may lead to hoarseness and paralysis of recurrent laryngeal nerves.
Other intraoperative complications may include diabetes insipidus (due to damage to posterior pituitary gland during surgery leading to deficiency of vasopressin or ADH), surgical site bleeding or cerebrospinal fluid leak.
Invasive intraoperative monitoring with an arterial line is recommended to closely monitor blood pressure due to the commonly preexisting uncontrolled hypertension and the complicated craniotomy surgery procedure with potential blood loss. Many of these patients may have inadequate collateral blood circulation from the ulnar arteries due to the presence of carpal tunnel syndrome and other soft tissue abnormalities. Due to soft tissue changes from acromegaly, IV access may be difficult and a large bore central venous access may be necessary. Acromegaly related preexisting sleep apnea and increased ventilation-perfusion mismatch may cause perioperative ventilatory complications. The low intraoperative oxygen saturation in our case may be explained by undiagnosed pre-existing acromegaly-related pulmonary changes.2 Blood loss should be closely monitored. Scalp block, along with intraoperative narcotics are analgesic options in these cases. Intraoperative neuromonitoring may be done depending on the size and location of the tumor. In such cases, intravenous anesthetic infusions using propofol and remifentanil are good choices.
Postoperative: Immediately post-surgery, urine output monitoring and sodium levels are vital.3 Patients may either develop the syndrome of inappropriate antidiuretic hormone secretion (SIADH) or, conversely, diabetes insipidus and necessitate desmopressin administration. The adrenal function should be monitored and treated appropriately immediately postoperatively.3
Our patient needed postoperative reintubation most likely due to a combination of factors including prolonged surgery and anesthetic, large size of the tumor and consequent extensive brain tissue manipulation and edema, preexisting physiologic and pathologic changes of secreting giant pituitary adenoma which make these patients susceptible for postoperative ventilatory complications. Preexisting pulmonary conditions such as sleep apnea, post-surgical brain edema from significant surgical brain dissection and retraction, postoperative pneumocephalus, long duration of surgery, large dose of anesthetics could be some of the contributing factors. Close monitoring of these patients in the immediate postoperative period and neuro recovery assessment and possible postoperative ventilatory support after surgery may be necessary.
Positive pressure mask ventilation after trans-sphenoidal surgery is contraindicated due to potential for causing pneumocephalus. Our patient underwent trans-sphenoidal tumor biopsy two weeks before this craniotomy. Therefore, for the postoperative reintubation, he was preoxygenated with 100% oxygen and rapid sequence intubation was performed in the ICU uneventfully. Postoperative imaging should ideally be done a minimum of 3 months after surgery as the fat and gel foam packing can take that long to be resorbed.4
Figure 1. MRI with and without contrast. Large, heterogeneously enhancing mass lesion involving the sella and extending into the suprasellar region with multiplanar foci of intralesional hemorrhage within. The mass invades the bilateral cavernous sinuses and encases and narrows the bilateral terminal internal carotid arteries and proximal bilateral ACA and right MCA without loss of flow void. It displaces the cisternal segments of the optic nerves superiorly and encases them. The optic chiasm is also superiorly displaced and compressed. The mass also involves the hypothalamic region. There is prominent expansion of the sella into the sphenoid sinus. It extends into the suprasellar cistern with extension into the perimesencephalic, prepontine interpeduncular cisterns with mass effect upon the brainstem. It also partially encases the basilar artery and proximal posterior cerebral arteries without loss of flow-void. There is mass effect upon the bilateral basal frontal and medial temporal lobes without evidence of edema or invasion.
- Lake MG, Krook LS, Cruz SV. Pituitary adenomas: an overview. Am Fam Physician. 2013 Sep 1;88(5):319-27. PMID: 24010395.
- Camilo GB, Guimarães FS, Silva DP, Mogami R, Kasuki L, Gadelha MR, Melo PL, Lopes AJ. Pulmonary function testing and chest tomography in patients with acromegaly. Multidiscip Respir Med. 2013 Nov 13;8(1):70. doi: 10.1186/2049-6958-8-70. PMID: 24219873; PMCID: PMC3831601.
- Adigun OO, Nguyen M, Fox TJ, Anastasopoulou C. Acromegaly. 2023 Feb 2. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan–. PMID: 28613738.
- Marquez Y, Tuchman A, Zada G. Surgery and radiosurgery for acromegaly: a review of indications, operative techniques, outcomes, and complications. Int J Endocrinol. 2012;2012:386401.
MRI w & w/o contrast
Large, heterogeneously enhancing mass lesion involving the sella and extending into the suprasellar region with multiplanar foci of intralesional hemorrhage within. The mass invades the bilateral cavernous sinuses and encases and narrows the bilateral terminal internal carotid arteries and proximal bilateral ACA and right MCA without loss of flow void. It displaces the cisternal segments of the optic nerves superiorly and encases them. The optic chiasm is also superiorly displaced and compressed. The mass also involves the hypothalamic region. There is prominent expansion of the sella into the sphenoid sinus. It extends into the suprasellar cistern with extension into the perimesencephalic, prepontine interpeduncular cisterns with mass effect upon the brainstem. It also partially encases the basilar artery and proximal posterior cerebral arteries without loss of flow-void. There is mass effect upon the bilateral basal frontal and medial temporal lobes without evidence of edema or invasion. This could represent a pituitary macroadenoma. Meningioma is less likely given the presence of mild diffusion restriction, absence of dural tail