67 year old man presented to the emergency room with syncope and melena. He was recently diagnosed with cirrhosis by biopsy. His cirrhosis was attributed to NASH.
For several weeks, he noted intermittent black stools, which became constant. He was admitted for fall after he passed out while having a bowel movement. While he denied any abdominal pain, he did admit that he felt that his abdomen was distended. He also had nausea, but denied emesis, hematemesis, and hematochezia. He denied NSAID, alcohol or illicit drug use. His medications on admission were prednisone, Lasix, spironolactone, ursodiol and vitamin E.
On initial examination, he was hypotensive (88/31), pulse rate 89 beats/min; He was ill appearing with icterus and jaundice. He was noted to have a distended abdomen with tenderness on palpation. A rectal exam yielded heme positive stool.
Initial laboratory studies revealed a leukocytosis, anemia, thrombocytopenia, hyperuremia, acute kidney injury, electrolyte abnormalities, transaminitis, hyperbilirubinemia.
The patient was admitted for acute GI bleed. He was resuscitated with normal saline. He was started on a PPI infusion and spontaneous bacterial peritonitis (SBP) prophylaxis. His hemoglobin remained stable. The next morning, the differential diagnosis was broadened to include sepsis. His antibiotics were broadened and blood cultures were obtained.
Later, the patient decompensated and was transferred to the ICU. His blood pressure plummeted to 69/39. His hemoglobin dropped to 7.8. The patient received a bolus of saline, and multiple blood products. He was unable to maintain adequate blood pressures on 4 pressers. Additionally, a diagnostic paracentesis did not reveal SBP. A bedside upper endoscopy was performed and revealed a duodenal ulcer containing adherent clot and severe pallor in gastric body.
Despite aggressive resuscitation efforts, he declined further. He developed disseminated intravascular coagulopathy, marked lactic acidosis and worsening acute kidney injury. In the late afternoon, the decision to focus on comfort care was made. The patient expired shortly thereafter. The initial blood cultures revealed Cryptococcus neoformans.
Cryptococcus neoformans is an encapsulated fungi emerging as more virulent pathogens. The most frequently immunosuppressive states other than AIDS that predispose to cryptococcal disease are cirrhosis (36.4%) as seen in this case, diabetes, and autoimmune disorders. Cryptococcus can affect any organ system. While GI involvement is rare there are several reported cases. In the GI tract, Cryptococcus can present with ulcerated lesions in the stomach or intestines. GI involvement is most frequently seen in patients with AIDS or cirrhosis. Biopsies have shown atrophic mucosa with neutrophil and eosinophil inflammatory response in the lamina propia, and cryptococcal granulatomus disease. Unfortunately, in this case, biopsies were not taken due to tenuous state of the patient at the time of the EGD.
Disseminated Cryptococcus is associated with a high rate of mortality. In the retrospective study of patient with disseminated Cryptococcus without AIDS, cirrhosis was most highly associated with mortality at 63%.
A rare presentation of disseminated cryptococcal infection includes GI involvement with Gastric and duodenal ulcers. GI involvement is most frequently seen in Cirrhotic patients. Patients with cirrhosis can be at higher risk for disseminated cryptococcus infections and are at a high risk of mortality.
To cite this abstract:McGann LK. A Rare Presentation of Disseminated Cryptococcus. Abstract published at Hospital Medicine 2016, March 6-9, San Diego, Calif. Abstract 676. Journal of Hospital Medicine. 2016; 11 (suppl 1). https://www.shmabstracts.com/abstract/a-rare-presentation-of-disseminated-cryptococcus/. Accessed January 29, 2020.