Septicemia or Sepsis

Consider the following scenario: A 25-year-old female presents to the ED with RLQ pain, onset three days ago. She reports that the pain is aggravated by palpation. She had just returned from a visit out of the country when she developed nausea with vomiting and fever.

On admission, the patient presented with fever and tachycardia and was placed on sepsis protocol. Workup showed leukocytosis and normal lactic acid. CT of abdomen demonstrated right pyelonephritis. Blood culture grew gram-negative bacteremia, identified as E. coli. She was started on IV hydration and Zosyn. Symptoms resolved in less than 24 hours. Patient was discharged 48 hours after admission. Documentation in the health record was consistent with “sepsis secondary to pyelonephritis.” Did the patient really have sepsis?

The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) recommends that “sepsis should be defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. For clinical operationalization, organ dysfunction can be represented by an increase in the Sequential (Sepsis-related) Organ Failure Assessment (SOFA) score of 2 points or more, which is associated with anin-hospital mortality greater than 10 percent.”

The patient in the case study had an infection – acute pyelonephritis – and scored 3 out of 4 in the SIRS criteria (fever, tachycardia and leukocytosis), but zero on the SOFA score. Her blood grew Escherichia coli. Is this sepsis?

In order to answer the question, one needs to be able to differentiate between the localized infection (i.e., acute pyelonephritis) and sepsis. So, what are the features of acute pyelonephritis?

Clinical and Laboratory Findings in Patients withAcute Pyelonephritis

In the above table, physical examination findings include fever of greater than >100.4 F and tachycardia. Note that these are all part of SIRS criteria. In addition, the table shows laboratory tests with “positive blood culture in 15 to 30 percent of cases.”

Approximately 12-20 percent of patients have cultures that are positive for infection. Bacteremia has not been associated with a poor outcome unless sepsis or another significant comorbidity is present,” which leads one to ask the question, what then would a patient with acute pyelonephritis manifest when sepsis sets in?

Positive blood cultures do not always make for a diagnosis of sepsis. It may be integral to the localized infection. You will see this as a common finding in urinary tract infections (including acute pyelonephritis), pneumonia, cellulitis, ascending cholangitis, bacterial endocarditis, lymphangitis, epididymitis, and infected vascular catheters, as well as other infections. And vice versa, negative blood cultures do not rule out sepsis. Independent studies have shown that only 30 to 60 percent of patients with sepsis have positive blood cultures.

Then why is it that many physicians have historically depended on blood cultures to make the diagnosis? The reason is that long before the complex systemic inflammatory response syndrome (SIRS) and counter-inflammatory response syndrome (CARS) cascade was discovered, providers seeing patients with severe sepsis (i.e., with organ failure) tended to have positive blood cultures. It became an easy crutch to hang on as it pertained to the diagnosis of sepsis.

What is really crucial to diagnosing sepsis is the presence of manifestation(s) that are beyond what one would expect in the localized infection; hence, indicating end-organ dysfunction (sepsis) – leading to organ failure (severe sepsis) Please refer to my article Organ Dysfunction vs Organ Failure online at https://www.linkedin.com/pulse/organ-dysfunction-vs-failure-cesar-m-limjoco-m-d-.

Going back to the case study above, the patient did not present with any features that would have signified end-organ dysfunction or failure. If the patient presented with hypotension on admission, that could have indicated organ dysfunction. If it persisted and required vasopressors to prop up the blood pressure, it would have signified septic shock. Lactic acidosis (with no other possible etiologies of lactatemia) would have indicated sepsis. Altered mental status in this otherwise healthy adult with no comorbid conditions would also have indicated metabolic encephalopathy in severe sepsis. Other end organ failures, e.g., liver, kidney, ARDS, etc., would also have signified severe sepsis. Sepsis and severe sepsis patients would have taken longer to recover from such a more critical, systemic event.

All things considered, the above picture was only consistent with the diagnosis of acute pyelonephritis in an otherwise young, healthy patient with great response to hydration and antibiotics – so much so that the course of events acceded to a quick amelioration of symptoms and discharge in 48 hours.

In the diagnosis of sepsis/severe sepsis, it is imperative that the root causes of the initial findings be discerned, and it is also essential to observe how the patient’s hospital course unfolds. It is crucial to admit patients for whom sepsis is suspected and place them on sepsis protocol, but then it behooves a provider to take them off sepsis protocol when it becomes clear that the patient’s presentation is discovered to be not indicative of sepsis.

Documentation then needs to reflect that sepsis was ruled out, and the local infection or factors that explain the patient’s clinical picture must be identified. Clinical truth should always be the main objective in documenting the patient’s narrative, and it should be based on the complete clinical picture – from the time of onset to resolution of the patient’s condition.