Thread by @fernandbteich

1/ My patient has tachycardia, fevers and lactic acidosis. Does he/she have sepsis? Heffner et. al found that, up to 18% of patients with SIRS, initially diagnosed as sepsis, had a non-septic SIRS also known as "sepsis mimicker". #Tweetorial

2/ A 30-ish y.o. patient with history of type 1 diabetes mellitus, essential hypertension & asthma presented to the ED with a 2-day history of dry cough. No dyspnea, chest pain, documented fevers, sweats, rhinorrhea or sore throat. Mentions 30-lb wt loss + fatigue last 6 months.

3/ Patient stopped working due to fatigue. Diabetes is well controlled (A1c 7.5%). Patient smokes cigarettes, drinks socially and denies using drugs. No vaping.
On presentation: BP 150/110, HR 134, RR 20, SpO2 98%, Tm 99.5F.

4/ Few initial thoughts:
- Cough is acute (foreground). Wt loss + fatigue are chronic (background).
- Is cough the culmination of a chronic disease or a superimposed phenomenon?
- Wt loss + decent oral intake suggests calorie expenditure > calorie intake a.k.a. hypermetabolism.

5/ Quick exam: thin-appearing, does not look sick, tachycardic/regular, CTAB, tender in RUQ of abdomen, no skin rash.

6/ Initial labs: WBC 8.2, Hgb 13.3, Plts 348, BMP unremarkable, albumin 3.7, protein 9.6, ALP 312, AST 65, ALT 49, bili 0.3, INR 1.2, Ca 10.4, ketones normal, lactic acid 2.9-->3.3-->4.8, ESR 126, CRP 4.3, HIV-, TSH 1.9, UA w/ 2+ protein. Highlights?

7/ CXR to the left, compared to old one from 2017. Seems overall more hazy. Poorly penetrated by x-rays? No clear alveolar infiltrates. Hilar prominence?

8/ Haziness is real indeed. CT shows tree-in-bud and faint ground glass opacities. Mention of reactive hilar and mediastinal lymphadenopathies. Is this septic pneumonia? But how to explain chronic weight loss?🤔

9/ The plot thickens. CT of the abdomen reveals hepatosplenomegaly. Spleen and liver full of innumerable hypoenhancing nodules. This is what @MedEdPGH would call the "rabbit hole". Chase the most esoteric finding in presentation.

10/ Time for a quick PR:
30-ish y.o. with history of T1DM and HTN presenting with acute dry cough and a background of wt loss & fatigue. Found to have tachycardia, inflammation, lactic acidosis and cholestatic liver injury. CT with hepatosplenomegaly and small hypodense lesions.

11/ Given patient’s significant tachycardia, ⬆️inflammatory markers and lactic acidosis, a tentative no-miss diagnosis of sepsis was made in the ED.
Patient was treated with 4L of IV fluids and was started on broad spectrum antibiotics.

11(cont'd)/ He was never febrile. He did not look sick. He did not have a significant leukocytosis or leukopenia.
Despite this treatment, patient’s tachycardia persisted and his HR was up to mid-120s twelve hours later.
Not your typical sepsis illness script, eh?

12/ Now that antibiotics are in, we can sit down and try to interpret these lung, liver & spleen lesions.
Differentials include lymphoma, TB, atypical mycobacteriosis, endemic mycoses, sarcoidosis, amyloidosis. If immunosuppressed, can add nocardiosis, aspergillosis, cryptococcus

13/ More labs: Blasto Ag, Histo Ag/Ab, Crypto Ag, IGRA all negative. Respiratory viral panel negative. COVID-19 negative. Monospot negative. Sputum culture growing scan amounts of S. agalactiae. ANA, ds-DNA, ANCAs negative. Can't diagnose with a serum biomarker? Sample tissue.

14/ A bronchoscopy was done and revealed:
- Cobblestoning of the mucosa, notably in RLL (see representative image).
- Enlarged subcarinal lymph node status post FNA.
- BAL RUL anterior segment, microbrushing and transbronchial biopsies RLL superior segment.

15/ Path revealed:
Non-necrotizing granulomas.
AFB and GMS were negative.
No evidence of malignancy seen.

16/ A diagnosis of disseminated sarcoidosis with multi-organ involvement mimicking severe sepsis was made.
Significant cholestatic liver injury attributed to liver infiltration. Lactic acidosis due to poor lactic acid clearance(?), cytokine-induced mitochondrial dysfunction(?).

17/ Patient was started on high dose steroids with rapid improvement in hemodynamics, clearance of lactic acid and ⬇️ in ALP.
Antibiotics were discontinued. No solid ground to call this syndrome "sepsis" was found.

18/ Teaching points:
- Non-septic SIRS or "sepsis mimickers" or "sterile inflammatory disorders" cause up to 20% of hospital SIRS presentations.
- While sepsis (SIRS + infection) is a no-miss diagnosis, one must entertain alternative diagnosis when things are not adding up.

18 (cont'd)/
Think of a non-septic SIRS when you have atypical features in presentation (Faget’s sign, lack of a source of infection & microbiological documentation within 24h, well-appearing and not feeling the fevers, lack of defervescence or change in hemodynamics despite AB

19/ Some patients will still have late-confirmed sepsis (difficult-to-grow bugs, infection confirmed by serology).

Thanks for tuning in. I leave you with a refresher schema from @CPSolvers on sarcoidosis: