key: cord-1043201-lbouywhm
authors: Damani, Jalal
title: DISSEMINATED INTRAVASCULAR COAGULOPATHY FROM WARM AUTOIMMUNE HEMOLYTIC ANEMIA IN A PATIENT WITH COVID-19
date: 2020-10-31
journal: Chest
DOI: 10.1016/j.chest.2020.08.388
sha: a82089c6dea96ae64f3de89861a4b1e8bcdbd33f
doc_id: 1043201
cord_uid: lbouywhm

nan

JALAL DAMANI INTRODUCTION: As the world faces many deaths from COVID-19 due to multi-organ dysfunction (MOD), the underlying mechanism for mortality continues to be investigated. Some propose cytokine storm while others postulate uncontrolled endothelial damage as the cause for MOD. There may be an additional novel mechanism involving auto-antibodies made after novel coronovirus infection which is then directed against RBCs causing autoimmune hemolytic anemia (AIHA) and subsequently MOD. We present one such case that was witnessed early in the pandemic in the united states.

A 67 year old female with a history of breast cancer in remission presented to the hospital with tachypnea. She was immediately intubated due to her persistent hypoxia. Patient was found to have wheezes. Patient's labs revealed severe renal failure with uremia, hyperkalemia, uricemia and hyperphosphatemia. Patient had persistent lactic acidosis despite fluid resuscitation and elevated blood pressure. She also had indirect hyperbilirubinemia, elevated LDH and creatinine kinase. Her urine analysis revealed hemoglobinuria. She was severely anemic with marked nucleated RBCs and without any signs of gross bleeding. Her anemia was refractory to blood transfusions. Her ABG showed metabolic acidosis and respiratory acidosis along with hypoxemic respiratory failure. Additionally, patient continued to drop her platelets and coagulation factors which were consistent with Disseminated intravascular coagulopathy (DIC). Patient was found to have warm autoantibody with broad specificity. Patient continued to be acidemic even after hemodialysis and ended up having cardiac arrest and subsequently passing. Patient was infected with the novel coronovirus and also had left sided peripheral infiltrates as seen on her chest x-ray. Patient's blood cultures were negative. DISCUSSION: Patient survived less than 12 hours in the ICU, however, gave significant insight into a possible mechanism by which COVID-19 can harm people. She had presented with metabolic encephalopathy from renal failure, respiratory failure from SARS-COV2, severe AIHA, and DIC. Patient had no current disease that would explain the constellation of abnormalities witnessed other than COVID-19. Our patient with SARS-COV2 died from refractory AIHA leading to MOD and DIC. Our case brings forth a unique mechanism by which COVID-19 impacts mortality and therefore warrants further research to evaluate this connection between COVID-19 and AIHA. Once such a connection is established then treatments such as steroids, immunoglobulin therapy and even plasma exchange can be entertained that may help patients with critical COVID-19 who otherwise despite anti-viral, anti-IL6, and convalescent plasma therapy are still dying.

CONCLUSIONS: Our patient who suffered from COVID-19 also had warm antibody induced AIHA which caused refractory acidemia and subsequent MOD with DIC causing her demise.

Concise review: Autoimmune Hemolytic Anemia