INTRODUCTION: A 40 year old male with no significant past medical history presented with complaints of three weeks of progressively worsening fatigue, myalgias and an episode of hematemesis. He was in his usual state of health until three weeks prior to admission when he noticed progressively worsening fatigue. Two weeks prior to admission, he had dry cough associated with pleuritic chest pain. He denied chills or rigors and was unsure about fever. A 20 to 25 pounds weight loss with decreased appetite was also noted. One time he vomited bright red blood while coughing. He was born and raised in India and moved to the US in 1991. He had a history of prior alcohol use and was employed at a gas station.
CASE PRESENTATION: In the ER, he was hypoxic, tachypneic with accessory muscle use and tachycardic. Examination revealed diffuse rhonchi on auscultation. Additionally, he had palpable hepatomegaly and 1+ pitting pedal edema bilaterally. Dentition was poor. Chest x-ray showed a diffuse, symmetrical infiltration. Prior x-ray was normal. ABG -on 100% O2 was 7.38/ 33/65/19; The A-a gradient was 600 with p/f ratio of 65. He was intubated and started on Ceftriaxone and Azithromycin after blood and sputum cultures were drawn for presumed community acquired pneumonia complicated by ARDSLabs showed a hematocrit of 24.5, INR of 14, sodium of 118, chloride 88, bicarbonate of 19, alkaline phosphatase 218, ALT 61, total bilirubin 3.9 and a lactate of 3.7. Following intubation, he remained in refractory shock and was subsequently started on Norepinephrine. During the hospitalization, HIV, DFA, PCP, urine legionella antigen and blood and fungal cultures were negative. Viral serologies were consistent with a cleared hepatitis B infection. He underwent bronchoscopy that showed 1+ acid fast bacilli and was started on a four drug regimen for tuberculosis. Septic shock improved and he was extubated after four days. A DNA probe for mycobacterium tuberculosis was positive.
DISCUSSION: Our immunocompetent patient developed septic shock from a pulmonary tubercular infection which necessitated vasopressor and ventilatory support. As he had been living in a non-endemic region for many years, this was most likely a reactivation of a primary Ghon focus. Reactivation disease typically follows a more benign course and his X-ray was highly suggestive of a military pattern. The PaO2:FiO2 ratio is diagnostic of ARDS.
CONCLUSIONS: Septic shock from military tuberculosis has been described previously. Only a few case reports of septic ARDS from tuberculosis at hospital presentation has been described in the literature.
Reference #1 Ahuja SS, Ahuja SK, Phelps KR et al. Hemodynamic confirmation of septic shock in disseminated tuberculosis. Crit Care Med. 1992;20(6):901
DISCLOSURE: The following authors have nothing to disclose: Manmeet Singh, William McGee
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