SAT-496 Acute GI Bleed Associated with Myxedemic Coma: Yes It Still Exists!

Abstract

Introduction: Myxedemic coma is a life-threatening medical emergency. It needs to be treated emergently & carries very high mortality. It involves multi-organ failure at cellular level due to severe thyroid hormone deficiency. Most common clinical presentation involves CVS. With advancement in health care it is now uncommon to see myxedemic coma especially associated with GI Bleed. Here in we present an interesting case of GI bleed associated with myxedemic coma. Case: 84 years old male was discovered in home, minimally responsive. EMS intubated & brought him to ED with agonal respirations, hypotensive & unresponsive, He was admitted to ICU. Past medical history was significant for smoking & hypertension. Physical Exam was significant for dryness of skin, obtundation, hypothermia, tachypnea & BMI >30. Initial Labs revealed anemia with Hemoglobin of 5.1mg/dL, Hematocrit 17.5%, Hyponatremia-134meq/L, Hyperkalemia-K+ levels 5.3meq/L, BUN-84mg/dL & creatinine-4.1mg/dL, His serum TSH levels were 352 mIU/ml with low free T4 and T3 levels at 0.15ng/dl and 1.99pg/ml, respectively. Stool was positive with Blood. IV fluids were given.GI was consulted. He underwent emergent upper GI endoscopy, which found the Dieulafoy’s lesion at cardiac end of stomach & treated with a combination of epinephrine injection, argon laser, & 3 hemo-clips. He had 6 PRBCs transfused. He was started on IV Thyroxine, Liothyronine and Hydrocortisone. His mental status improved, & hemoglobin remained relatively stable. Later on, he decided to move to palliative care & was discharged to hospice. Discussion: Myxedemic coma is a term generally used to denote most severe decompensated hypothyroidism. The typical progression is lethargy evolving into a stupor & eventually into a coma with respiratory failure and hypothermia. It can lead to volume depletion, hyponatremia, & AKI, which can worsen to ATN if prolonged ischemia remains.GI bleed is a rare manifestation of myxedemic coma. Pathophysiology of GI bleed in these patients involves mucosal edema & mucopolysaccharide infiltration. Also, myxedemic coma is associated with neurological changes resulting in slow peristalsis & GI atony. This coupled with coagulopathy associated with decompensated hypothyroidism results in increased risk of bleeding. Dieulfoy’s lesion are rare cause of GI bleed. Stress & ischemic changes are one of the inciting factors for these lesions. These lesions are more common in elderly males & are associated with severe systemic illness similar to our patient. Treatment is usually supportive with goal of identifying the lesions, stopping the bleed & aggressively managing myxedemic coma. We present an interesting case of GI bleed associated with myxedemic coma now relatively uncommon with advancement in healthcare. It provides an excellent learning opportunity for clinicians to consider while managing these patients.