In developed countries, studies have revealed varying prevalence rates of Sheehan's syndrome (SHS) among women, ranging from 0.0051% (1) to 3.1% (2). There were also studies showing that the prevalence of SHS ranged from 1% to 2% among women who experienced hypotension due to blood loss of 1–2 L (3, 4). Contrastingly, in undeveloped nations, the prevalence varies from 3.1% to 27.6% (5–7). The diagnostic journey for SHS patients spans a considerable duration of 7–19 years from symptom onset to definitive diagnosis (8). Sheehan's syndrome arises from ischemic necrosis of the anterior pituitary gland triggered by postpartum hemorrhage (8), leading to pituitary hormone dysfunction, including insufficient secretion of growth hormone, thyroid stimulating hormone, gonadotropin, prolactin, and adrenocorticotropin (ACTH) (7, 9). Predominant symptoms are associated with dysfunction of the gonads, thyroid, and adrenal cortex due to insufficient secretion of gonadotropins, thyroid stimulating hormones, and ACTH, respectively. The latter is the most prominent and sometimes life-threatening. Supplementing various deficient hormones is the primary treatment for SHS.

Glucocorticoids, pivotal adrenal cortex hormones, play crucial roles in regulating glucose metabolism, blood pressure, and electrolyte balance. Deficiency in glucocorticoids can lead to hypoglycemia, hypotension, and electrolyte disturbances. Lifetime glucocorticoid replacement therapy stands as a cornerstone in managing SHS patients. Fluctuations in neuroendocrine system activity necessitate adjustments in glucocorticoid supplementation, while metabolic disruptions from other etiologies also dictate dosage alterations. Inadequate comprehension of these dynamics among healthcare professionals may impact the prognosis of SHS patients and predispose them to risks. Surgical treatments, including interventional procedures, represent significant stressors in medical care. Failure to administer preoperative stress doses of glucocorticoids to SHS patients can engender serious consequences. To our knowledge, this article represents the first documented case of severe hyponatremia in an SHS patient following percutaneous coronary intervention (PCI).

A 70-year-old female patient presented with paroxysmal exertional chest tightness persisting for one month, alleviated by a few minutes of rest. Forty years ago, the patient suffered from postpartum hemorrhage, without blood transfusion, subsequently developing lactation failure and amenorrhea. Five years later, she was diagnosed with SHS at the Affiliated Hospital of Shandong University. Management included 5 mg of prednisone acetate in the morning for secondary adrenal insufficiency, and 50 ug of levothyroxine for secondary hypothyroidism. Apart from medication adherence, the patient lacked awareness regarding adrenal insufficiency. The patient had a decade-long history of hypertension, controlled with 5 mg of telmisartan and 5 mg of amlodipine daily. This patient had a weight of 46 kl, a height of 1.57 m, and a BMI of 18.66 kg/m². Upon hospital admission, her vital signs were stable with a blood pressure of 122/58 mmHg, and a heart rate of 65 beats per minute. Physical examination revealed no pulmonary rales, cardiac murmurs, lower limb edema. Laboratory finding indicated elevated blood troponin I (0.5487 ng/ml, 0–0.0175 ng/ml), normal blood sodium (141.5 mmol/L, 137 mmol/L–147 mmol/L), and elevated fasting total cholesterol (6.28 mmol/L, 3 mmol/L–5.7 mmol/L). Thyroid function tests revealed low level of free thyroxine (FT4) (6.77 pmol/L, 7.98 pmol/L–16.02 pmol/L), with normal levels of free triiodothyronine (FT3) and thyroid stimulating hormone. Electrocardiogram indicated sinus bradycardia. We diagnosed the patient with acute non-ST segment elevation myocardial infarction (NSTEMI) and performed percutaneous coronary angiography (CAG) and intravascular ultrasound (IVUS) examination. We found that the stenosis degree was 40%, 80%, and 60%, 98%, and almost completely occluded, respectively, in the left main trunk (LM), the proximal and middle segments of the left anterior descending branch (LAD), the proximal segments of the left circumflex branch (LCX), and the middle segment of the right coronary artery (RCA) (Figures 1A–C). The minimum lumen area at the distal stenosis of the LM was 4.51 mm² (Figure 1E), the plaque load at the most severe stenosis of the proximal LAD was 80%, with a minimum lumen area of 2.88 mm² (Figure 1F). Due to the patient's refusal to undergo coronary artery bypass grafting, two stents were inserted in the middle segment of the RCA (Figure 1D). The intervention lasted for 2 h, including coronary angiography, bilateral intravascular ultrasound examination, patient involvement in treatment decision-making based on examination results, and subsequent coronary intervention treatment, utilizing 130 ml of iodixanol. The patient did not experience any chest discomfort, but was nervous and had a blood pressure rise to 190/100 mmHg, managed with sublingual nifedipine tablets and intravenous isosorbide nitrate. Following percutaneous intervention (PCI), the patient experienced a sequence of symptoms from the 12th to the 50th h, including nausea and loss of appetite, profuse sweating, mild limb twitching, and drowsiness in sequence (Table 1). Limb twitching persisited for 18 h from the 38th to the 56th h post-PCI. On the 24th h post-PCI, the patient was diagnosed with hyponatremia (Table 1), and 2%−3% sodium chloride was intermittently administered intravenously. Despite increased sodium chloride supplementation, symptoms persisted until administration of hydrocortisone, leading to symptom resolution and rapid improvement in blood sodium levels (Table 1). By the 62nd h post-PCI, symptoms of hyponatremia completely resolved, with blood sodium level increasing from 114.2 mmol/L to 132 mmol/L (Table 1). At the 86th h post-PCI, blood sodium level returned to normal. After 40 h, blood tests revealed low levels of cortisol (2.76 ug/dl, 6.7ug/dl–22.6 ug/dl), ACTH (4.26 pg/ml, 10.1 pg/ml–57.6 pg/ml), FT3 (3.41 pmol/L, 3.53 pmol/L−7.37 pmol/L), and FT4 (7.12 pmol/L, 7.98 pmol/L–16.02 pmol/L). Following discharge, the patient continued oral medication with 2.5 mg prednisone acetate and 50 ug levothyroxine sodium daily, as well as dual antiplatelet drugs, statins, and antihypertensive agents. During the next nine-month follow-up period, the patient did not experience ischemic symptoms or hyponatremia.

The deficiency of glucocorticoids caused by secondary adrenal insufficiency is the primary mechanism for severe hyponatremia in this patient with SHS. The stress induced by PCI exacerbates glucocorticoid deficiency. The contrast agent further contributes to dilutional hyponatremia. The preoperative stress dose of glucocorticoid is crucial to avoid this complication. Glucocorticoids were crucial in correcting severe hyponatremia in this SHS patient with secondary adrenal insufficiency. Shortening the duration of PCI and minimizing the dosage of contrast agents may be beneficial for preventing severe hyponatremia. Meanwhile, it is also crucial for this SHS patient to receive interdisciplinary management involving endocrinologists before and after the procedure. Additionally, SHS may serve as a potential risk factor for CAD.