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In short, you can avoid sepsis denials when documentation in the patient encounter shows a clear delineation of a non-systemic infection. This is the only ironclad defense that will withstand any and all scrutiny. Sepsis clinical parameters are good for capturing and preempting even early sepsis cases, but unless the full clinical picture before and during the inpatient encounter is consistent with sepsis, it will just be another “he said, she said” state of affairs.

Many folks lament the fact that their sepsis capture dropped when they went from using Sepsis 1.0 to 3.0 criteria. Were hospitals placed in a position of enduring negative cash flow unjustly? Or did many get away with sepsis admissions because of criteria that was not meant to be used for billing purposes, but to ensure that casting a wide net would result in better outcomes (even if not all cases turned out to be sepsis)?

Some would even justify the practice of billing for sepsis based on meeting criteria because the hospitals are not getting enough reimbursement for resource utilization. “Hospitals get only a percentage of the cost of actual healthcare delivery!” is a commonly heard refrain. Many would even justify it by saying that they are just taking advantage of what the rules allow. No wonder rules and regulations began mushrooming – and then we started to complain that they are impeding quality of care.

But insurance was never meant to fully recompense actual expenditures. Otherwise, all of us would have to pay more to our Medicare payroll garnishment and/or private health insurance. It is not a feasible business model, because it would mean many lower- to middle-income households would not be able to afford food, clothing, and shelter.

It isn’t a good business model to focus primarily on service volume. This is the reason behind value-based purchasing, the Medicare Access and CHIP (Children’s Health Insurance Program) Reauthorization Act (MACRA), and other quality measures. Gone are the days of focusing on the number of admissions or patient encounters. It does not really help to admit patients to inpatient care when there is no medical necessity for it. We are just increasing risk for patients and limiting resources to those who are truly in need of inpatient care. The idea is to admit those that truly will benefit from inpatient care (outweighing the risks that come with hospitalization, like hospital-acquired conditions and infections) and discharge them appropriately when it is safe. This, in turn, will improve healthcare for everyone.

So, what is needed to differentiate local/regional infectious conditions from true sepsis? It all comes down to the narrative. A good H&P will truly capture severity of illness in the depiction of the patient’s signs and symptoms. Marry that with a good explanation of the significance of the workup findings. Continue that with an accounting of the patient’s course of hospitalization. If all of the preceding criteria (i.e., history of present illness, workup evaluation, course of treatment) is consistent with a picture of sepsis, it will withstand scrutiny. If it does not rise above what is expected from the localized or regional condition, then it is not sepsis. Plain and simple!

Clinical parameters change, but if the patient narrative is consistent with the patient’s condition, then positive billing outcomes can be expected. Parameters are helpful guidelines to direct you to the right conclusion, but they are not infallible. The patient narrative needs to show evidence that the patient’s condition has started down an alarming course that will lead to organ failure(s), and ultimately, death. This is what true sepsis is.

From a practical level, ask yourself: what is it that this patient has? If it is a specific infection (e.g., UTI, pneumonia, acute pyelonephritis, ascending cholangitis, bacterial endocarditis, etc.), does the patient findings (history of present illness, physician exam findings, laboratory results) go beyond what you normally expect in a local infection? These may include mental status changes, pre-renal azotemia, transaminasemia, tachycardia, tachypnea, lactic acidosis, or hypotension. Can these findings be explained by some other etiology? For example, another condition that the patient has (e.g., hypovolemia, heart failure, arrhythmia, diabetes,COPD exacerbation) or is the patient on some medication that is known to cause said effects (e.g., sedatives, tranquilizers, medications that cause hypotension). How did the symptoms respond to the sepsis protocol (which includes IV hydration)? Did the patient’s symptoms resolve rapidly, within hours (4-6) of hydration? Were the patient’s sepsis antibacterial medications (e.g., Zosyn, Vancocin, Avelox, Flagyl, etc.) discontinued or changed prior to its intended duration? Did the discontinuation of the patient’s other medications for their co-morbid conditions resolve the symptoms?

These are some of the important questions that need to be answered before one can come to the true conclusion of sepsis. It’s all about the clinical truth!


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