Genesis of Antibiotic Resistance (AR) LXXIV: Turbulence Modeling of Simplified Severe Sepsis Protocol‐2 (SSSP‐2), NCT01663701: Mechanism of Torque on E‐Cpx Thrusted Leucocyte(s)‐Platelet(s)‐Erythrocyte(s) Aggregates’ (LPE) drag on capillary lumen ace Elicit Irreversible Occlusion‐CCP‐Coma, Impediments for in vivo Simulation

Abstract

Clinical Observation: NCT01663701, (PMID:28973227) observed that within 6 hours of ERP, sepsis protocol cohort encountered 86 pts GCS score 13-15, with in-hospital (ihm) mortality 36pts; 7 pts GCS score 9-12, with ihm 4; 11 pts GCS score 3-8 with ihm, 10, (ref table 3, p1239, ibid), SAPS3 score 55 (ref Table 1p1237, ibid), with primary outcome of SSSP-2 cohort mortality 48%(51 deaths) vs standard care 33%(34 deaths), number needed to harm 6.6, secondary outcome 28 day mortality SSSP cohort 67% vs Standard care 45% contradict, EGDT trial (PMID: 11794169), ProCESS NCT00510835 (PMID:24635773), EGDT-ARISE-ANZICS: NCT00975793 (PMID: 25272316), EGDT - ProMISe, ISRCTN36307479 (PMID: 25776532), restricted fluid resuscitation FEAST, ISRCTN69856593(PMID: 21615299). Pathophys. Interpretation: SpO2 <92%, SBP 50 to 75 mmHg in children aged <12 months, 60 to 75mmHg in children 1 to 5 years, and 70 to 85 mmHg in children >5years), signs of shock at the point of demise - severe tachycardia or bradycardia plus one of prolonged capillary refill time >2 seconds, PaO2 <90%, Blantyre Coma Score ≤2, Ifhypoxia was also present then this mode of the predominant clinical mode of death (TCE) (verbatim) (PMID:23496872; PMID:31775837; PMID:31196803). Our goal is to postulate a plausible hemodynamic aberration leading to mortality with a specific objective(s) focusing on the time frame, from 0 hr. ER, admission to 6 hrs. and possibly 28-day mortality utilizing turbulence modeling (CFD/Fluid Mechanics ). Geometry: Governing equations: To determine the flow rate of LPE, Darcy's law: Q=kA∆P/μl, -Eq3.27, where Q=discharge flow rate, k=permeability, A= cross-section of the media (blood), ∆P=pressure drop, μ=viscosity, L=length, derived eq 3.28 – 3.34; (p104-105, ISBN 9780128024089); for determining Torque of LPE: τ=r x F, where force, F, that acts on a particle at the position, r (p250 eq;7.6 (ISBN 9780521198110). Clinical data vs CFD: Our simulation efforts were muddled due to the lack of knowledge on pathophysiological parameters originating from CC or MCC, DDx for sepsis cohort of NCT01663701, may indicate that geographically variable DaCCI, MAS, sHLH SARS, DIC of bacterial origin w/o TBI/trauma, vascular thrombosis, (PMID: 32835247), SCLS or CLS/VLS, are confounding limiting factors for accurately assigning the fluid profile, particle mass, length, time, velocity profile, viscosity profile, hematocrit, the concentration of coagulation factors vs anticoagulants in the circulation in CFD mesh generation while compelled that EEG of sepsis cohort would only be the conclusive to determine the laminar to turbulence transition (Ack: Assignments of HMX-Fund. Phys, HMS, 07/ 9 – 08/21, 2020 completed by Subburaj Kannan, MD., Ph.D.). However, we are pursuing the hypothesis that the LPE aggregates, alongside AR clinical persisters in the cerebrovascular capillary bed with intrinsic torque of LPE aside drag of LE, vortices would rupture capillary bed eliciting CCP in an anisotropic mode with the abrupt collapse of starling forces consequent comatose.