An Elderly Man with Fatal Respiratory Failure after Eating a Poisonous Mushroom Podostroma cornu-damae
A 73-year-old man presented with nausea, vomiting, diarrhea, dry mouth, and hot flushes 3 hours after eating boiled wild mushrooms. He visited a primary clinic, where his blood pressure was 70/50 mmHg. Laboratory findings showed azotemia and leukocytosis, and he was referred to the emergency department of our hospital. His wife also experienced nausea and vomiting that resolved spontaneously. He had a history of cigarette smoking (35 packs/yr). His medical history was insignificant, and he had not been on any medication (including over-the-counter medication) and was denied contact with any sick persons, use of illicit drugs, exposure to animals, and recent travel outside Seoul.\nOn admission, his blood pressure was 106/51 mm Hg, heart rate was 115 beats/min, respiratory rate was 24/min, and body temperature was 37.1℃. He looked acutely ill but was mentally alert. Laboratory tests revealed the following: white blood cell (WBC) count, 34,670/µL (absolute neutrophil count [ANC], 32,243/µL); hemoglobin (Hb), 17.0 g/dL; platelet count, 322,000/µL; blood urea nitrogen, 47.9 mg/dL; serum creatinine, 1.6 mg/dL (reference, 0.6-1.1 mg/dL); total protein, 6.2 g/dL; albumin, 3.7 g/dL; aspartate aminotransferase (AST), 34 IU/L (reference, 5-40 IU/L); alanine aminotransferase (ALT), 19 IU/L (reference, 5-40 IU/L); lactic dehydrogenase (LDH), 313 IU/L (reference, 145-250 IU/L); creatine kinase (CK), 213 IU/L (reference, 38-160 IU/L); serum Na/K/Cl, 140/4.9/108 mEq/L; total CO2, 17.1 mmol/L; serum glucose, 180 mg/dL; HbA1c, 7.3%; C-reactive protein (CRP), 159 mg/dL (reference, 0.0-8.0 mg/dL); and prothrombin time (PT) international normalized ratio (INR), 1.24. After receiving 2 L/min of oxygen via nasal prongs, blood gas analysis revealed the following: pH, 7.351; PCO2, 30.1 mmHg; PO2, 65.4 mmHg; HCO3, 18.2 mmol/L; and SaO2, 91.8%. Chest radiography showed slight blunting of the left costophrenic angle (). Urinalysis revealed no proteinuria or hematuria. After admission, he received a large amount of fluid (9 L over 24 hours), and his clinical condition improved as vomiting and diarrhea had subsided until day 3 of hospitalization.\nOn day 4, he developed sudden shortness of breath, coughing, and severe respiratory distress. His laboratory examinations were more aggravated as follows: WBC count, 2,840/µL (ANC 2,720/µL); platelet count, 57,000/L; PT INR, 1.16; activated partial thromboplastin time (aPTT), 38.0 seconds; fibrin degradation product >20 µg/mL (reference, 0.0-5.0 µg/mL); plasma D-dimer, 6.56 µg/mL (reference, 0.0-0.5 µg/mL); CRP, 185 mg/L; AST, 82 IU/L; ALT, 50 IU/L; total bilirubin, 0.6 mg/dL; and serum creatinine, 1.6 mg/dL. Chest radiography revealed new widespread consolidations in the whole left lung (). A subsequent computed tomographic (CT)-scan showed extensive consolidations in the left lung and multiple consolidations from the sublobular to subsegmental areas in the right lung, as well as a small amount of pleural effusion in both lungs (). However, the CT scan did not show any intra-abdominal infection foci or abnormal findings to explain the severe pneumonia sepsis. Bronchoscopy showed no evidence of endobronchial lesions. He received mechanical ventilation and continuous renal replacement therapy (CRRT) owing to severe hypoxemic respiratory failure, a PaO2/FiO2<200 mm Hg, and acute oliguric kidney failure. However, he developed refractory shock and his condition rapidly deteriorated. We suspected a possible fulminant course of necrotizing pneumonia and considered surgical intervention and thus consulted the thoracic department. He underwent left pneumonectomy because the gross appearance of the lung inflammation suggested impending pulmonary gangrene. Skin lesions such as miliaria, bullae, and erythroderma were found on the chest wall, face, and upper extremities (not shown). Lung histology revealed varying stages of inflammation with areas of extensive hemorrhagic necrosis (), massive inflammatory cell infiltration and edema in the alveolar space and interstitium (), type II pneumocyte hyperplasia and prominent proliferation of young fibroblasts (), and the formation of a hyaline membrane along the alveolar wall ().\nHe subsequently suffered from rhabdomyolysis, kidney failure, hepatic failure, pancytopenia, disseminated intravascular coagulopathy, and prolonged shock. On day 7, his body temperature was 39.4℃, and his laboratory examinations were more aggravated as follows: WBC count, 120/µL (ANC, 80/µL); platelet count, 32,000/µL; PT INR, 1.50; aPTT, 41.7 seconds; fibrin degradation product>20 µg/mL (reference, 0.0-5.0 µg/mL); plasma D-dimer, 4.95 µg/mL (reference, 0.0-0.5 µg/mL); CRP, 250 mg/L; AST, 122 IU/L; ALT, 54 IU/L; total bilirubin, 5.0 mg/dL; serum creatinine, 2.0 mg/dL; LDH, 500 IU/L; CK, 4,997 IU/L; and serum myoglobin>1,000 ng/mL (reference, 10-92 ng/mL). A peripheral blood smear showed severe pancytopenia mimicking aplastic anemia. Treatment comprising fluid resuscitation with crystalloid and inotropics was performed. Although causative infectious pathogens were not identified from bronchial washing or blood and lung tissues, broad-spectrum antibiotics such as carbapenem, vancomycin, and respiratory quinolone were administrated. Despite the administration of granulocyte colony stimulating factor (GCSF), transfusion of platelet concentrates and packed red blood cells, high doses of inotropics (including norepinephrine, dopamine, and dobutamine), as well as lung protective ventilation strategy and CRRT, he did not recover from multiorgan failure and died on day 13 of hospitalization.\nThe wild mushroom specimen in question was sent to a team of expert mycologists, at the National Academy of Agricultural Science in Korea, were it was determined to be P. cornu-damae ().