NCT01663701 SSSP‐2 (PMID: 28973227) noted that within 6 hours of ERP, among sepsis protocol cohort 11 patients sustained GCS score 3-8 with in-hospital mortality 10 patients, with a median jugular vein pressure (JVP) of ~ 2 cm H20 below the clavicle or -2cm H20 implicit of hypovolemia, (ref table 3, p1239, ibid). Here, we present a plausible physiological sequel of the patient(s) from the time of presentation to the emergency dept. and 6 hours after ERP, and the onset of comatose followed with mortality. The geometry for this analysis are following: PMN 8-15μm, eosinophils ~15 μm, basophils ~12-15 μm, monocytes ~14-25 μm, lymphocytes (T, B & NK cells) ~8-15 μm, platelets ~2-3 μm, erythrocytes ~ 7.7 ± 0.7 μm ; capillaries (med. size) internal diameter 6 μm, wall thickness, 1 μm, length ~0.1cm, ~blood viscosity 0.03 cm/s (human) (p48, 63: ISBN 9780128024089). Elements: Fahraeus Effect, the hematocrit in true capillaries (Hctv) is lower compare to that of blood entering (due to cell-free layer formation (p95-96, Fig3.8. ibid) vs discharge hematocrit (HctD) and Fahraeus-Lindqvist effect where the apparent viscosity of (μapp) blood is the function of capillary diameter for a range of 10μm ≤ D ≤ 300μm. For the thoroughfare channel, to venules, the viscosity will be reversed as it increases in viscosity (μrel) (Fig 3.10, p98 ibid). Platelet and RBC morphological deformity as shown in Fig 1, panel a; fig 6 a-c, turning, crossing, and riding of platelet and tracer particle deflections in presence of a tumbling RBC; streamlines around a tank-treading RBC Fig 9 panel a-c, platelet crossing, rolling; from PMID: 24231958; Fig 1, of PMID: 17208982; PMID: 24896133; PMID: 17851167; Fig 3 and 5 for skewed hematocrit, PMID: 31933711, would likely to be rapid in vivo., extrapolated to sepsis cohort in NCT01663701. It is suggested that the LPE either forms or part of the bluff body at the junction of precapillary sphincters & thoroughfare channel / true capillaries impede the vasomotion into the arterial end of capillary bed, which may lead terminal arteriole directly connecting metarteriole to venules (bypassing true capillaries, thoroughfare channel) causing vascular shunt with no blood flow in capillary bed en masse. As a result NFP for filtration and net reabsorption pressure is impaired. It is envisioned that LPE anchoring on the scruffy (Awol?) glycocalyx on the endothelial surface of arteries will generate torque Ref Eq-1 (PMCID: PMC5437748, PMID: 28529430 and PMID: 8304490), increase in Kolmogorov length - scale (l) ratio eq. 3.1a, Time-scale ratio (t) eq 3.1b, Velocity-scale ratio (v) eq 3.1c, p43(ISBN:9780131274983) for bluff bodies/large eddies, causing cyclical, relaxation, creep and hysteresis, impairing viscoelasticity, rupturing the capillary bed en masse, resulting in irreversible traumatic brain injury (CVA!). It is implicit that under such conditions onset of CCP in true capillaries. Such a scenario would likely be the contributing factor for the investiture of comatose in turn mortality.