A 49-year-old previously healthy male from rural India (Burdwan, West Bengal) was brought to the emergency department with two episodes of generalized motor tonic-clonic seizures and confusion in the last 24 hours. After hemodynamic stabilization, his wife was called for detailed history taking. According to her, he complained of sluggishness of movements, generalized weakness, decreased appetite, increased thirst, increased daily urinary output, extreme loss of libido, and hoarseness of voice for the last six months. He had four hospitalizations for hyponatremic encephalopathy-like episodes in the previous four months. Past medical history was significant for a snakebite envenomation (identified as Russell’s viper by the emergency medical officer) 29 years back (in July 1993) needing hospitalization and infusion of anti-snake venom but no hemodialysis or ventilatory support. Otherwise, there was no other medical, traumatic, surgical, or recent medication history. He has been vaccinated against SARS-CoV-2 and has never contracted the disease in the last three years. He had normal growth and sexual development and was a father of two healthy adults. Cognitive functions could not be tested as he was confused and drowsy with intermittent incoherent talks and bizarre behavior. He was afebrile with a normal respiratory rate and oxygen saturation but had tachycardia (114 bpm) and low systolic blood pressure (86 mmHg). Capillary blood glucose level was low (36 mg/dl). He was rapidly resuscitated with the infusion of intravenous thiamine and D50 solutions, but his consciousness level did not improve. Pertinent laboratory investigations were ordered, keeping the working diagnosis of metabolic encephalopathy due to glycopenia, hyponatremia, or prolonged post-ictal confused state (or non-convulsive status epilepticus). Complete blood cell count and renal and hepatic function tests were normal. Serum electrolytes revealed normal potassium, calcium, and magnesium levels but low sodium i.e., hyponatremia (116 mmol/L). During initial therapy, blood pressure, hypoglycemia, and sodium levels responded poorly to intravenous dextrose and normal saline infusions, for which vasopressor (norepinephrine) and 3% NaCl were added for maintenance of systolic blood pressure and sodium concentration, respectively. Suspecting an underlying hypopituitarism, relevant pituitary hormonal assays were ordered revealing an extremely low 8 A.M. serum cortisol level (1.0 μg/dL; biological reference range, 4.82–19.5 μg/dL), inappropriately low 8 A.M. plasma adrenocorticotropic hormone level (12.4 pg/mL; biological reference: 0.1–46.0 pg/mL), low free T3 (1.51 pg/mL; biological reference range 2.50–4.30), low free T4 (0.21 ng/dL; biological reference range 0.93–1.70), and inappropriately normal thyroid-stimulating hormone (2.542 μIU/mL; biological reference: 0.27–4.20 μIU/mL). Serum total testosterone level was low (0.8 ng/dL; biological reference range: 280–800 ng/dL), along with low insulin-like growth factor-1 (IGF-1) less than 15 ng/mL (reference: 57–241 ng/mL). Luteinizing hormone was 0.86 mIU/mL (biological reference interval: 1.7–8.6 mIU/mL), follicle-stimulating hormone was 2.14 mIU/mL (biological reference interval: 1.50–12.40 mIU/mL) and prolactin was 11.2 ng/mL (reference: 4.6–21.4 ng/mL). The clinical and laboratory findings showed that the most tentative diagnosis was secondary adrenal insufficiency. Contrast-enhanced magnetic resonance imaging of the brain and pituitary demonstrated a thin and flat pituitary gland located on the floor of sella turcica with prominent cerebral spinal fluid space (), compatible with empty sella syndrome. Intravenous hydrocortisone 100 mg three times a day was started from the third day of admission, followed by the addition of oral levothyroxine (50 mcg/day) from the eighth day of admission. Hyponatremia got smoothly corrected, and recurrent episodes of hypoglycemia abated as blood glucose levels stabilized after treating hypocortisolism. On day nine of admission, he was shifted to oral hydrocortisone (30 mg/day). However, symptoms of excessive thirst and polyuria had increased. Urinalysis revealed no proteinuria or glycosuria, and the pH was 6.0. A 24-hour urine collection (without any fluid restriction) confirmed polyuria (3.6 liters/24 hours). The urinary excretions of uric acid, phosphate, calcium, citrate, and oxalate were also within normal limits. The serum osmolality was 302 mOsm/kg, but urine osmolality was 182 mOsm/kg. Serum copeptin levels could not be checked due to their unavailability in India. Hence, an inpatient modified water deprivation test confirmed the presence of central diabetes insipidus. The bone density scan revealed severe vertebral osteoporosis (normal vitamin D level). An intramuscular testosterone enanthate injection (200 mg every three weeks) was initiated for hypogonadotropic hypogonadism. Meanwhile, for central diabetes insipidus, intranasal desmopressin, 10 μg twice daily (once at bedtime), was added alongside hydrocortisone, levothyroxine, calcium carbonate, and calcitriol. After six months of follow-up, there was a significant improvement in symptoms and general well-being. The impact of hormone replacement on his sexual life needs to be seen in further follow-ups.