Pregnancy-induced pituitary apoplexy: Two lives at stake

Izhar Faisal; Teshi Kaushik; Pragati Ganjoo; Anita Jagetia

doi:10.4103/JOACC.JOACC_53_22

CASE REPORT

Year : 2023 | Volume : 13 | Issue : 1 | Page : 119-121

Pregnancy-induced pituitary apoplexy: Two lives at stake

Izhar Faisal¹, Teshi Kaushik², Pragati Ganjoo³, Anita Jagetia⁴
¹ Department of Anesthesiology, Irene Hospital, New Delhi, India
² Department of Anesthesiology, Emory School of Medicine, Atlanta, USA
³ Department of Anesthesiology and Intensive Care, GB Pant Institute of Postgraduate Medical Education and Research, (GIPMER), New Delhi, India
⁴ Department of Neurosurgery, GB Pant Institute of Postgraduate Medical Education and Research, (GIPMER), New Delhi, India

Date of Submission	17-Aug-2022
Date of Acceptance	28-Aug-2022
Date of Web Publication	09-Mar-2023

Correspondence Address:
Dr. Pragati Ganjoo
Department of Anesthesiology and Intensive Care, GB Pant Institute of Postgraduate Medical Education and Research (GIPMER), Jawahar Lal Nehru Marg, New Delhi - 110 002
India

Source of Support: None, Conflict of Interest: None

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DOI: 10.4103/JOACC.JOACC_53_22

Abstract

Pituitary apoplexy in a pregnant woman is a devastating condition that develops secondary to a massive increase in the size of the pituitary gland and hyperplasia of lactotroph cells caused by high estrogen levels of pregnancy. The resultant sudden hemorrhage or infarction into the pituitary gland or a tumor leads to gland destruction with serious consequences like acute adrenal insufficiency, circulatory shock, neurological deterioration, and visual loss. Prompt handling of complications is necessary to prevent maternal and fetal mortality. Resuscitation is aimed at the early correction of hemodynamic instability, fluid-electrolyte abnormalities, hormone deficiencies, and intracranial hypertension. Urgent decompressive pituitary surgery may be required if the patient has rapidly declining vision and neurological status. Management of such patients is challenging and requires multi-disciplinary collaboration. We describe here the emergency handling of pituitary apoplexy in a pregnant woman.

Keywords: Adrenal insufficiency, apoplexy, critical care, pituitary, pregnancy

How to cite this article:
Faisal I, Kaushik T, Ganjoo P, Jagetia A. Pregnancy-induced pituitary apoplexy: Two lives at stake. J Obstet Anaesth Crit Care 2023;13:119-21

How to cite this URL:
Faisal I, Kaushik T, Ganjoo P, Jagetia A. Pregnancy-induced pituitary apoplexy: Two lives at stake. J Obstet Anaesth Crit Care [serial online] 2023 [cited 2023 Apr 1];13:119-21. Available from: https://www.joacc.com/text.asp?2023/13/1/119/371319

Introduction

Pituitary apoplexy is a potentially life-threatening endocrine emergency caused by hemorrhage or infarction within the pituitary gland, or into a pre-existing adenoma, leading to abrupt gland destruction. Pregnancy is known to induce pituitary apoplexy, albeit rarely. Only 67 such cases are reported over the past 6 decades (1960–2022).^{[1],[2],[3],[4],[5],[6],[7],[8],[9]} Ante-natal apoplexy developed in 60 patients while 7 had apoplexy within 2 h to a week after childbirth; 38 patients had pre-existing adenomas^{[1],[2],[3],[4],[5],[7],[9]}; 32 patients underwent neurosurgery.^{[1],[2],[3],[5],[7],[8],[9]} The high estrogen levels in pregnancy cause lactotroph cell hyperplasia and pituitary enlargement which raises the intracapsular pressure in the sella turcica leading to gland ischemia and/or hemorrhage with consequent rapid swelling and damage; a 120–136% increase in gland size at 3 days post-partum is reported.^[1] Severe complications include pan-hypopituitarism leading to hormone deficiencies, circulatory shock and fluid-electrolyte imbalance, compression of optic chiasma causing vision loss, and a rise in intracranial pressure (ICP) resulting in neurological deficits.^[1],[2],[3] Apoplexy occurring during pregnancy endangers the life of both the mother and fetus, and thus warrants quick and aggressive treatment. Decompressive pituitary surgery is indicated in a rapidly worsening neuro-ophthalmic condition.^[10] Literature on the intensive care and perioperative management of such patients is limited.^{[3],[4],[5],[9]} A case of pregnancy-induced pituitary apoplexy managed with urgent resuscitation and pituitary excision is presented here, along with a brief literature review.

Case Report

A 20-year-old primigravida at 25 weeks of gestation was transferred from the obstetric unit to a neurosurgical emergency with a one-day-old history of sudden and severe headache, repeated bouts of vomiting, decreased vision in both eyes, and drowsiness. She had altered sensorium, heart rate (HR) of 167/min, respiratory rate 28/min, oxygen saturation (SpO₂) 90% on room air, arterial blood pressure (ABP) 64/40 mmHg, central venous pressure (CVP) of 1 mmHg, and abnormal arterial blood gas values (pH: 7.24, pCO₂: 33, pO₂: 60, HCO₃⁻: 17, base deficit: −15, Na⁺: 125, K⁺: 4). She was immediately administered oxygen via face mask, intravenous (IV) sodium bicarbonate (100 meq bolus; 100 meq/12 h infusion), normal saline infusion (2 l/h) and dopamine infusion (5 μg kg^-1 min^-1). Ophthalmological examination showed bitemporal hemianopia and papilledema, and magnetic resonance imaging revealed pituitary apoplexy [Figure 1]. After blood sampling, hydrocortisone (200 mg IV bolus; 4 mg/hour infusion) and mannitol infusion (25 g over 20 mins) were started. The hormonal assay showed low cortisol levels (39.2 nmol/l) and hypothyroidism (T3: 90 ng/dl, T4: 1 μU/dl, TSH: 0.05 μU/ml), and normal growth hormone, luteinizing hormone, follicular stimulating hormone, and prolactin. Oral levothyroxine 100 μg/day was added. In the next 24 h, the patient had rapid, near-total vision loss, and emergency trans-nasal trans-sphenoidal (TNTS) pituitary excision was undertaken after obtaining high-risk consent. Obstetric consultation was sought, and fetal well-being was confirmed. The patient was placed in the TNTS position, and a left lateral pelvic tilt was provided with a table wedge. IV ranitidine (50 mg) and metoclopramide (10 mg) were administered, and hydrocortisone and dopamine infusions continued. Anesthesia was induced using the rapid sequence technique with IV thiopentone (200 mg) and rocuronium (60 mg) and maintained with fentanyl (100 μg IV bolus and 1 μg kg⁻¹hr⁻¹infusion), sevoflurane (2%) and oxygen–nitrous oxide (50:50) mixture; ventilation was controlled. Bi-spectral index and fetal heart rate (FHR) monitors were additionally deployed. A lead abdominal shield was used for irradiation protection of the patient during fluoroscopy. She had one episode of intraoperative hypotension (ABP: 70/40 mmHg) and tachycardia (HR: 130/min) which responded to the rapid saline infusion (500 ml) and increased dopamine (8 μg kg⁻¹min⁻¹); the FHR was stable. The remaining surgical course was unremarkable. Elective postoperative ventilation was continued; dopamine infusion was stopped after 9 h and tracheal extubation was done after 14 h. Oral levothyroxine100 μg/day and hydrocortisone 10 mg 8-hourly therapy was initiated. She developed diabetes insipidus (DI) 23 h after surgery and was treated with IV desmopressin 4–8 μg 8 hourly for 3 days. The histopathology report showed a non-secretory pituitary adenoma. The patient was discharged after 2 weeks on oral replacement medications due to persistent hypothyroidism and low cortisol levels. At 6 weeks, the patient had normal cortisol levels (120 nmol/l), but continued hypothyroidism (T3: 86 ng/l, T4: 1 μU/dl, TSH: 0.1 μU/ml); hydrocortisone was tapered and stopped by the ninth week. She subsequently delivered a healthy baby girl at term. Her thyroid status normalized at 7 weeks post-partum and thyroxine was discontinued. The mother and child are doing well.

Figure 1: A non-enhanced sagittal T1 magnetic resonance imaging of the brain showing an enlarged and heterogeneous pituitary gland, possibly a pituitary tumor, with blooming on gradient images suggestive of internal hemorrhage. The enlarged gland is extending superiorly in the suprasellar region causing compression of the optic chiasm and hypothalamus

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Discussion

Prompt diagnosis and management of apoplexy during pregnancy are crucial for preventing maternal and fetal mortality.^[7] Sudden development of severe headache (94% patients), visual disturbances (61%), and nausea (33%) in a pregnant woman should be viewed with suspicion,^[1] and followed up with quick confirmatory investigations. The patient can present in shock due to adrenal insufficiency, DI, or decreased fluid intake, and is managed with fluid therapy and vasopressor/inotrope drugs to raise the mean ABP, preferably to above 65 mmHg in the parturient. The use of titrated drug doses helps maintain adequate placental blood flow. Cortisol deficiency can cause vasopressor refractory shock and requires IV hydrocortisone (100–200 mg) bolus and infusion (2–4 mg/h), which also helps to control parasellar edema.^[10],[11] Central vasopressin deficiency causes DI with massive fluid loss and requires fluid replacement and desmopressin supplementation in higher doses (up to 16 μg/day) due to the inhibitory effects of placental vasopressin.^[12] Hypothyroidism can cause respiratory depression, bradycardia, and prolonged sedation, and requires thyroxine in higher doses (100–150 μg/day) due to an increased demand during pregnancy.^[12] Hyponatremia occurs from cortisol deficiency leading to altered sensorium and seizures and requires mineralocorticoid replacement with fludrocortisone (0.05–0.2 mg daily)^[12]; we used hydrocortisone and saline therapy as fludrocortisone was not available. IV mannitol (0.25–0.5 mg/kg) for lowering ICP should be used judiciously to avoid maternal and fetal dehydration and hyperosmolarity.^[11] Dopamine agonists do not reduce gland size in non-prolactin secreting tumors, and urgent decompressive pituitary surgery may be the only option to control symptoms rapidly. The preoperative aim is to maximally correct systemic abnormalities within the limited time before surgery. Intraoperative focus is on maintaining stable hemodynamic status and brain conditions, and ensuring fetal well-being; titration of anesthetic drugs, avoidance of vasodilators, readiness with inotropes and/or vasopressors, and FHR monitoring are important measures. Delayed anesthesia recovery due to hypothermia, hyponatremia, hypothyroidism, and raised ICP may necessitate elective postoperative ventilation. Close postoperative monitoring enables early detection and management of fluid-electrolyte imbalance, hemodynamic instability, drowsiness, and seizures. Cortisol and thyroid deficiencies after apoplexy may persist for 4–8 weeks beyond surgery or even longer, as in this case, and require long-term replacement therapies.^[10]

Conclusion

Pituitary apoplexy during pregnancy concurrently jeopardizes two lives, with the fetus being highly susceptible even to minor maternal systemic insults. A rapid resuscitation-diagnosis-treatment response and the need for quick and efficient coordination between the obstetric and neurointensive care teams are thus emphasized.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

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