January 23, 2017

Septic Shock: Nothing is Black and White

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Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. 

“Dysregulated host response” begs for an explanation. In order to do that, we need to lay the foundation on what constitutes a normal physiologic response and contrast it to that of a dysregulated host response.

“The normal physiologic response to any localized infection includes activation of host defense mechanisms that result in the influx of activated neutrophils and monocytes, release of inflammatory mediators, local vasodilation, increased endothelial permeability, and activation of coagulation pathways,” reads Coders and CDS: We Are Doing Septic Shock Wrong, an article by Allen Frady. “These response mechanisms occur during sepsis/severe sepsis/septic shock, but on a systemic scale. (This is what a dysregulated host response means, i.e., an overwhelming systemic toxic response to infection.) It leads to diffuse endothelial disruption, vascular permeability, vasodilation, and thrombosis of end-organ capillaries. Endothelial damage itself can further activate inflammatory and coagulation cascades, creating, in effect, a positive feedback loop and leading to further endothelial and end-organ damage.”

Severe sepsis organ failure develops from end-organ damage because of the circulatory blockage from thrombosis of end-organ capillaries (from microcoagulation) and endothelial destruction (from inflammatory mediators), causing tissue hypoxia. With limited amounts of oxygen, glucose is transformed to lactate. When the body’s buffering abilities are overwhelmed, lactic acidosis ensues. Inflammatory mediators further cause accelerated aerobic glycolysis, causing even more lactate production.



The pathology continuum goes from localized infection --> sepsis -->severe sepsis --> septic shock --> death. What distinguishes sepsis from a localized infection is the presence of a life-threatening organ dysfunction. When the organ dysfunction becomes worse and causes organ failure (heart, kidney, respiratory, hepatic, circulatory, etc.) then the patient is categorically in severe sepsis. (Please refer to my article “Organ Dysfunction Versus Organ Failure” for a detailed discussion). Circulatory failure, also known as septic shock, is deemed the worst of the organ failures, and without lifesaving measures, death becomes imminent.

In general, per a piece published on www.medicinenet.com, “shock develops when the circulatory system fails to maintain adequate blood flow, sharply curtailing the delivery of oxygen and nutrients to vital organs. It also compromises the kidneys and so restricts the removal of wastes from the body. Shock can be due to a number of different mechanisms, including not enough blood volume and not enough output of blood by the heart. The signs and symptoms of shock include low blood pressure (hypotension); overbreathing (hyperventilation); a weak, rapid pulse; cold, clammy, grayish-bluish (cyanotic) skin; decreased urine flow (oliguria); and a sense of great anxiety and foreboding, confusion, and sometimes combativeness.” 

At the outset and in certain circumstances, septic shock can be curtailed by prevailing body compensatory mechanisms, and it may not manifest with profound hypotension. In addition, initial IV infusion therapy when the patient presents to the hospital can at times preempt the hypotension. But unless the shock etiology is countermanded, IV fluid therapy alone is not going to be able to hold the pressure and the patient will go into overt shock. When the patient arrives with already profound hypotension, IV fluid therapy alone may not even bring up the blood pressure. Hence, per a May 2016 article titled Septic Shock by author Andre Kalil, “septic shock is also defined by persisting hypotension requiring vasopressors to maintain a mean arterial pressure of 65 mm Hg or higher and a serum lactate level greater than 2 mmol/L (18 mg/dL) despite adequate volume resuscitation.” 

But, alas, things are not going to be that easy in the elderly patient population. If the hypotension and/or altered mental status and/or azotemia is/are corrected within six hours of IV therapy, hypovolemia could be the sole culprit and sepsis can be ruled out (in a patient with a concomitant localized infection, e.g., UTI, cellulitis, etc.)!

As you can see, there is nothing black and white in septic shock (as well as all of medicine, in general) because certain circumstances may change the way diseases manifest. Criterias (e.g., Sofa 1 to 3) may change and be refined, but they may still not fully define sepsis/severe sepsis. Criteria are good in catching a vast amount of patients so we can place them into interventional protocols, effectively decreasing morbidity and mortality. Criteria are not the ultimate, definitive hallmark of a disease, however, because nothing is set in stone. A concurrent condition can account for the patient’s presentation, after study. It then effectively rules out the initial impression. This does not diminish the credibility of treatment protocols and providers, because casting a wide net saves more lives. 

But because of the complexity of diseases and the uniqueness of patient circumstances, it behooves all providers to provide a clear explanation of what is going on with the patient throughout the entire episode of care. It is not enough to document significant diagnoses that affect the full patient complexity; providers need to refine initial impressions/differential diagnoses and revise accordingly as the encounter unfolds and more information becomes available. It is of the utmost importance to explain the underpinnings supporting one’s thoughts on what is going on with the patient. Patient status recorded in the daily notes need to reflect what the current thinking is on what the patient has, based on identified disease criteria, patient progress, and response to treatment.

The working diagnosis should either be confirmed (ruled in) or ruled out or revised, highlighting the reasons; and upon discharge, providers need to document the definitive diagnosis (or at the least, the most probable diagnosis) at that point.
Disclaimer: Every reasonable effort was made to ensure the accuracy of this information at the time it was published. However, due to the nature of industry changes over time we cannot guarantee its validity after the year it was published.
Cesar M Limjoco, MD

Dr. Limjoco has more than 25 years of experience as a consultant with significant expertise in the capture of severity of illness in clinical documentation.  He serves as vice president of clinical services of DCBA, Inc. a position he has held since 2005. Dr. Limjoco is a member of the ICD10monitor editorial board and makes frequent appearances on Talk Ten Tuesdays.