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.
Updated on: May 18, 2017
Original story posted on: May 16, 2017
Demystifying the Pathogenesis of Sepsis
By Wilbur Lo, MD, CDIP, CCA, AHIMA-Approved ICD-10-CM/PCS TrainerOriginal story posted on: May 16, 2017
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 is Chief Medical and CDI Officer for cdiWorks, a Physician CDI consulting company. A US-trained Physician, Dr. Lo obtained his medical degree from the University of Toledo College of Medicine and completed a Residency in Anatomic and Clinical Pathology at Allegheny University Hospitals.
During his Postdoctoral Fellowship at Vanderbilt University Medical Center, Dr. Lo conducted research in Renal Pathology and published in a peer-reviewed journal, Kidney International.
At present, Dr. Lo is Lead Physician CDI consultant for a hospital in New York City. Outside the US, Dr. Lo has served as Physician CDI content and curriculum expert for AHIMA and AHIMA World Congress. Dr. Lo has extensive domestic and international CDI experience, with respect to MS-DRG, APR-DRG, IR-DRG and AR-DRG payment models.
