Genesis of Antibiotic Resistance LV: Validity Contexture of Mixing Length Hypothesis Turbulence Modelling (MLH ‐ TM) in an exacerbated mortality rate of Early Resuscitation Protocol ‐ Early Goal‐Directed Therapy (ERP‐EGDT) for sepsis.
Authors: Rodriguez Denise , Cerrillo Veronica , Botello Cynthia , Carmona Lucero , Kannan Subburaj 
Published: April 2020

To decipher the validity of Prantel’s Mixing Length Theory (MLH‐TM) in ERP‐EGDT for sepsis with comorbidity (CC) Capillary Leakage Syndrome ( CLS), also called as Vascular Leak Syndrome ( VLS); Systemic Capillary Leak Syndrome ( SCLS); Sepsis Induced Coagulopathy ( SIC); Sepsis‐induced Disseminated Intravascular Coagulation syndrome ( DIC)) a hypothesis that MLH could be of the valid diagnostic tool in clinical stratification of symptoms pertaining to sepsis with comorbidity, in real‐time scale to determine the onset of “Critical Closing Pressure” (CCP), and consequent collapse of vasculature is presented. Per contexture of the aforementioned objectives, NCT01663701 was chosen because of the case selection criteria and clinical case presentation, to the point data analysis, accessibility of data sets in the public domain and follow‐up care of both primary outcome of in‐hospital mortality and secondary efficacy outcome including 28‐day mortality and time to death. As per MLH, that a lump of fluid particles in one layer of the fluid flow, retains its original momentum at a specific location prior to the transition. During the transition from laminar viscous sublayer to buffer layer to turbulent zone, the turbulent velocity component and viscosity of the lump is dependent on a turbulent fluctuation. The universal velocity distribution law for smooth pipes: laminar viscous sublayer, buffer zone, and the turbulent zone is correlated with intact capillary bed. As indicated, this profile and eq:10.45 to 10.47, for rough pipe where protrusion extending outside of the laminar viscous sublayer, is correlated with dysfunctional vascular endothelium scramming the turbulent zone, escalating an adverse pressure gradient (ISBN: 9780070667624; 2008). It is known that such an adverse pressure gradient can plausibly induce an alteration in antibiotic resistance gene repertoire (ARGR) expression profile augmenting a selection pressure on AR persisters. Diagnostic index such as platelet aggregation, activation of the coagulation cascade and endothelial cell damage in sepsis‐induced coagulopathy originating from comorbidities are known to promote DIC and subsequent loss of capillary bed by glycocalyx shedding (J.Clin.Med.2019, 8,728; Crit.Care (2019) 23:259). Taken together, loss of vascular autoregulation and loss of the intravascular net filtration pressure (~25mmHg) gradient in the capillary bed revives MLH as imperative. It is our interpretation that subsequent to ERP‐EGDT, within the four hour period of admitting to ER/ICU/medical ward, a decrease in arterial pressure leading to increase the resistance with a gradual collapse of capillary bed, due to reduced distending pressure below a critical level (≤ 20mmHg) referred to as Critical closing pressure exacerbating the mortality rate in ERP‐EGDT for sepsis. With the turbulence modeling, in particular, the time scale, knowledge on its viscosity profile of fluid bolus along the damaged endotheliam (rough wall boundary layer), would benefit patient care by mitigating the mortality rate.Support or Funding InformationSupported by the professional development funds by SWTJC to Subburaj Kannan