Abstract Introduction Steroid-responsive encephalopathy associated (SREAT) with autoimmune thyroiditis or Hashimoto’s encephalopathy (HE), is a rare and often controversial diagnosis defined by encephalopathy with thyroid autoantibodies after exclusion of alternative causes. Recognition is especially challenging in critically ill patients, where thyroid antibodies and encephalopathy frequently coexist nonspecifically. Case A 26-year-old woman with congenital heart block and heavy alcohol use was admitted after 4 weeks of progressive confusion, word-findings difficulty, cold intolerance, weight gain, edema, vomiting and diarrhea. She presented in shock from severe urosepsis and was found to have autoimmune hypothyroidism (TSH 87 µIU/mL, free T4 0.4 ng/dL, anti-TPO 169 IU/mL and levothyroxine was started. Her inpatient course was complicated by severe systolic heart failure with shock, and progressive renal failure. Despite initiation and up titration of levothyroxine, hemodynamic stabilization, and thiamine repletion, she remained brady psychic with her mental status deteriorating to stupor with nonverbal episodes and diffuse hyperalgesia. EEG showed abundant triphasic waves with diffuse slowing and no seizures; brain MRI was deferred due to pacemaker incompatibility. CSF analysis revealed protein 54.8 mg/dL, glucose 70 mg/dL, WBC 4/µL, with negative cultures and viral/fungal studies.Renal failure progressed, requiring dialysis, without neurologic improvement. After exclusion of infectious, structural, and metabolic etiologies, SREAT /HE was suspected. High-dose IV methylprednisolone (1 g × 3 days), followed by taper, led to striking improvement within 72 hours: spontaneous speech returned, command following resumed. Her strength improved while the diffuse dysesthesias subsided. She subsequently completed six weeks of rehabilitation for critical illness myopathy. At six months, she had returned to cognitive baseline, was dialysis-independent, and had recovered normal ejection fraction (60%) with only mild distal neuropathy. Discussion No single clinical, laboratory, or imaging feature is pathognomonic for SREAT/ HE, and anti-thyroid antibodies or triphasic EEG patterns lack specificity in critical illness; diagnosis rests on synthesis and exclusion. Rapid neurologic improvement within 72 hours of pulse steroids—after no improvement on thyroid hormone—supports a steroid-responsive autoimmune encephalopathy rather than isolated hypothyroid encephalopathy or ICU delirium. Negative CSF infectious studies, non-inflammatory myocardial histology, and concordant multiorgan recovery strengthen this inference. A closely supervised therapeutic steroid trial may be appropriate when suspicion remains high after thorough evaluation. This abstract is funded by: None
Bhandiwad et al. (Fri,) studied this question.