Updated on: May 18, 2017

Demystifying the Pathogenesis of Sepsis

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Original story posted on: May 16, 2017
I want to begin with a coding scenario: sepsis and pneumonia are documented, and the coder captures these conditions and assigns MS-DRG 871 and APR-DRG 720 with severity of illness (SOI) 2. 

Sepsis presents challenges for coders as well as clinicians. I want to provide insight into the complex molecular and cellular processes involved in the pathogenesis of sepsis.

Assume that a chest X-ray identifies infiltrates in the left lower lobe of the lung. Sputum gram stain reveals dark blue and purple clusters of spherical bacteria. These are gram-positive bacteria with cell walls comprised of thick layers of peptidoglycan that absorb crystal violet dye, resist decolorization by ethanol or acetone, and do not counterstain with safranin.

Culture and sensitivity reveals methicillin-resistant Staphylococcus aureus (MRSA). MRSA has a mecA gene that encodes penicillin-binding protein 2a, which does not bind to the β-lactam ring in methicillin, other penicillins, and cephalosporins. This implies multi-drug resistance because MRSA is able to cross-link peptidoglycan for cell wall synthesis and survive in the presence of β-lactam antibiotics.

MRSA is virulent. Coagulase clots plasma, coats the bacterial cell wall, and prevents phagocytosis; hyaluronidase breaks down hyaluronic acid in the extracellular matrix; staphylokinase dissolves fibrins. Together, these enzymes pave a path for MRSA to spread through tissue, enter the bloodstream, and cause bacteremia.

So, how does MRSA bacteremia lead to sepsis?

MRSA has specific gram-positive, pathogen-associated molecular patterns (PAMPs) derived from peptidoglycan and lipoteichoic acid components of the cell wall. PAMPs are recognized by pattern recognition receptors (PRRs) located on the surface of macrophages. PRRs include toll-like receptors (TLRs) which process PAMPs, and via NF-κB transcription factor, induce the formation of coagulation factors and proinflammatory cytokines (e.g., TNF-α, IL-1, IL-6 & IL-12 and IFN-γ). In a parallel fashion, the anti-inflammatory cytokines (e.g., TGF-β, IL-4 & IL-10) are produced by macrophages and lymphocytes to balance the proinflammatory cytokines.

The imbalance between the proinflammatory and anti-inflammatory cascades leads to vasodilation, vascular permeability, hypotension, microthrombi deposition, and multi-organ failure, all reflected in SOFA and qSOFA scores for sepsis.
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.
Wilbur Lo, MD, CDIP, CCA, AHIMA-Approved ICD-10-CM/PCS Trainer

Dr. Wilbur Lo, MD, CDIP, CCA, AHIMA-Approved ICD-10-CM/PCS Trainer, is a clinical documentation improvement (CDI) content and curriculum expert for AHIMA World Congress and a physician CDI consultant for Jzanus in New York City.

He published a feature article in Journal of AHIMA, “Document Like This, Not That- CDI Insights from the Physician and CDI Specialist Perspective” and has facilitated numerous CDI Workshops for Physicians, Clinical Information Specialists, Coders and HIM Professionals in UAE, Philippines, Qatar and Kingdom of Saudi Arabia.  In 2017, he served as Co-Chair of the AHIMA CDI Summit Program Committee and member of the AHIMA CDI Task Force.

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