What's the Take Home?

A 47-Year-Old Man Develops Multiorgan Failure

Ronald N. Rubin, MD
Volume 66 - Issue 6 - June 2026

  • Answer: A. Despite the significant mortality risk of the acute illness, with recovery from the acute insult, patients can be expected to have full recovery at 6 months.

    Discussion. The presented patient fulfills Sepsis-3 criteria. A rapid bedside screening tool, qSOFA, includes low blood pressure (systolic BP ≤100 mm Hg); high respiratory rate (≥ 22/min), and altered mentation; this patient meets all three criteria.1,2

    The patient presents with typical findings of infection, specifically that of multilobe pneumococcal pneumonia. This patient now presents with a significant degree of respiratory failure, hypotension, and altered mentation. Thus, he is patient with an infection and a SOFA score increase of 2 points or more such that the clinical and operational diagnosis of sepsis can be made.1 There are no specific blood findings, tissue biopsy, or any other single pathognomonic feature for sepsis so the diagnosis remains a clinical one.

    In the United States, one-third of all in-hospital deaths are associated with sepsis.2 Dissecting this large number into epidemiology reveals that there are 2 dominant factors involved. Pulmonary infection is most common, 40-60% of cases, followed by abdominal (15-30%), and GU (15-30%).2 The usual suspects of causative organisms accordingly follow this list with gram-positive and gram-negative bacteria most common (gram-positive in pneumonia and gram-negatives in gastrointestinal/genitourinary infections [GI/GU]). Viral and fungal organisms are less common. Indeed, sepsis is a serious situation with an estimated acute, 30-day mortality of 20% to 30%, as well as a high longer-term mortality and residual morbidity risk.3

    The precise demographics overlay the epidemiologic list. As would be expected, there are age groupings: bacterial pneumonia coupled with marked increased incidence in elderly patients over 65 years; viral infections matched with pediatric cases below 5 years of age, and fungal infections being coupled again in the elderly populations associated with dialysis, long ICU stays, and indwelling catheters.

    When discussing the pathophysiology of sepsis, perhaps the more appropriate term is “mechanism of disease” because although we are learning the actual mechanisms of sepsis pathophysiology, the core causation remains in the process of discovery. What is known is infection triggers a variety of counterproductive responses in the host patient, including immune dysregulation. An appropriate host immune response to infection, eg, cytokine release, lymphocyte reactions, and marrow efflux of leukocytes, becomes excessive, inappropriate, and counterproductive. This includes lymphocyte apoptosis with lymphopenia and reduced effector functions and overutilization/hypofunctioning of neutrophils. A useful term in the literature for this is immune exhaustion.2

    Another abnormal host response is dysregulated vasculature mechanisms. The normal vascular endothelium that should be smooth and anticoagulant loses its glycocalyx surface barrier such that, metaphorically speaking, the "waxed, smooth finish of a dance floor or basketball court becomes a potholed, irregular and sticky surface.” This results in the now sticky surface contributing to white blood cell count (WBC) and platelets adhering to the vessel wall which lowers the circulating numbers. The disrupted endothelial surface also now becomes far more permeable than normal and leaks fluid into the interstitium with profound third spacing of fluid causing hypotension and shock. From this hypoperfusion comes tissue hypoxia with initiation of anaerobic metabolism and generation of lactic acid which is a significant hallmark finding in sepsis. The hypoperfusion is also causative of the variety of organ failures, eg, acute renal injury, ARDS, and encephalopathy that are part of the sepsis syndrome.1-3

    Regarding diagnosis, a variety of schemes have evolved over the years starting decades ago with the terms “systemic inflammatory response” to the current more simple term of “sepsis” defined as life-threatening organ dysfunction with suspected or confirmed infection and a Phoenix Sepsis score (for pediatrics) of equal or greater than 2, with respiratory, cardiovascular, coagulation, and neurologic symptoms being the most notable.1 We must remember, as we count WBCs, test for lactic acid, and carefully monitor vital signs, is that all current and prior definitions essentially start with suspected or confirmed infection. Indeed, infection triggers the above array of pathophysiologic phenomena whether we can yet precisely explain how or why. Despite our attempts to counter and reverse that pathophysiology, unless we promptly and properly treat and control the infectious trigger, all else will ultimately be futile.

    As for treatment, the detailed therapeutics for patients with sepsis are reserved for the ICU-Critical Care specialists. Nonetheless, there is an orderly plan and more general formulae for therapy grounded in the demographics and pathophysiology of sepsis described earlier that all physicians should have familiarity. As discussed, the triggering event for the sepsis cascade is essentially always (a rare word in medicine but appropriate here) an infection, so proper identification of and therapy for the responsible organism is the first order of business. Until precise identification is confirmed, empiric and broad antimicrobial regimens are indicated. Note the word “antimicrobial” rather than “antibiotic” is used because, as discussed, in the 60-70% of cases wherein a pathogen is identified, the most common are gram-positive and gram-negative bacteria followed by viral and fungal causation with the latter 2 often having strong clues (viral in children and epidemic scenarios such as COVID-19 and fungal in long-term critical care ICU cases).2 The broad coverage should fit the patient and situation.

    The next requirement of therapy is maintenance of adequate tissue perfusion. These patients often have a vasodilatory form of hypotension, which, despite no actual bleeding or obvious other fluid loss, requires volume repletion and support. Recent data support the use of crystalloid, namely lactated Ringer solution, over saline, in generous amounts (30 mL/kg).4,5 ICU care by experienced physicians is indicated to titrate correct fluid amounts and avoid both hypoperfusion and fluid overload in these delicate and unstable situations. There is a role for pressor agents when fluids alone cannot obtain or sustain adequate blood pressures, with norepinephrine the first pressor in line.5

    Finally, there is the decades-old conundrum of the use of pharmacological dose steroids in septic shock (this was being argued as long ago as my residency!). The best available data today suggests stress doses of glucocorticoid (e.g. hydrocortisone) will result in at least less time in shock, on ventilators, and ICU stay, and likely improves all-cause mortality as well.6-8 It must be noted that this entire line of sepsis therapeutics requires prompt decision-making and implementation. Any time delays result in a proportional increase in mortality.9

    Despite the often heroic and timely efforts in the ICU, sepsis carries a very poor prognostic profile, both acutely and longer term.1,10 Sepsis is the most common cause of in-hospital mortality, responsible for about one-third of all in-hospital deaths.1-3 Put another way, in a population of patients diagnosed with sepsis, there is a 20%-30% 30-day mortality.2 Just as striking is the long-term morbidity and mortality in "survivors" of the acute episode. For example, studies have shown in older patients, an increase and worsening of cognitive impairment and new functional impairments such as self-care and dressing of 16.7%.10,11 In younger patients, there is a 40% failure in ability to return to work at 6 months.10,11 Similar losses and decreases in 6-minute walk, health-related quality of life, and increased healthcare usage have been demonstrated at 1,2, and 5 years after a 2-week ICU discharge.10,11 This population had a 40% 1-year mortality after a 2-week ICU stay. For each additional week in the ICU, there was an increase in mortality and multidimensional disability.11

    Patient follow-up. The diagnosis of the acute illness early on was consistent with multilobe pneumococcal pneumonia. However, the systemic toxicity, borderline BP, and incipient multiple organ failure findings (e.g. acute kidney injury and respiratory failure) were consistent with sepsis. He was thus admitted directly to the ICU. Broad spectrum antibiotic coverage was administered pending culture results. He had an adequate response to oxygen delivered via face mask with steady state O2 saturation in the 92% range. Crystalloid fluid in the form of lactated Ringer solution, 30 mL/kg, was administered in 500 mL boluses. These maneuvers resulted in improvement in BP to 115/80 without the use of pressors. Meanwhile, metabolics 12 hours later showed creatinine lowered to 1.9 mg/dL and decreased lactate to 2.1 mmol/L. The following morning the sputum and blood cultures were reported as positive for pneumococcus Type III sensitive to penicillin. Antibiotics were narrowed to penicillin.

    Over the next 3 days, he continued to improve. By morning of day 5, he became afebrile. His temperatures and BP normalized with maintenance fluids. He was able to attain O2 saturations above 94% on nasal cannula oxygen. Creatinine and lactate levels normalized. He continued improving with diminishing pleuritic chest pain, cough and sputum production. Chest films confirmed lessening of the lobar infiltrates and absence of any pleural effusions. He was transferred to floor care with therapy and monitoring for 2 more days and discharged to home on day 7.

    He and his family are aware that tobacco and alcohol contributed to his risk of pneumonia and severe infection. He also knows he is a strong candidate for influenza, RSV, COVID-19, and pneumococcal vaccines at proper intervals in the future.

    What’s the take home? Sepsis is a life-threatening syndrome in which an infection triggers an array of pathophysiologic responses which are counterproductive and/or excessive in nature and noxious to the patient.

    Looking beyond this case, definitions of sepsis have continued to evolve, with Sepsis-3 defining sepsis in adults as life-threatening organ dysfunction caused by a dysregulated host response to infection. Pediatric definitions have also evolved, including the 2024 Phoenix criteria,2 defined as a Phoenix Sepsis score equal or greater than 2; organ dysfunction may include respiratory, cardiovascular, coagulation and neurologic systems.10,11

    The demographics and epidemiology of sepsis correlate with infectious sites, pulmonary is the most common followed by GI and GU; infection being bacterial followed by viral and fungal and the patient populations at risk for these infections being elderly with bacterial pneumonias, pediatric with viral infections and dialysis/transplantation/ICU patients with fungal infections. The pathophysiology is complex but can be somewhat summarized as immune and vascular dysregulation all leading to hectic fevers, lymphopenia due to lymphocyte death cytopenias due to abnormal adhesion of cells to the vascular endothelium with damaged glycocalyx barrier loss and hypotension due to vasodilation and vascular leak again related to the breakdown of the vascular endothelium barrier. The hypotension results in diminished tissue perfusion with triggering of anaerobic metabolism and the lactic acidosis which is a hallmark diagnostic finding in sepsis.

    The keystone of therapeutics is identifying and addressing the infectious trigger and utilizing appropriate antimicrobials and drainage of infection as indicated. Adjuvant therapies include supporting adequate tissue perfusion with lactated Ringer solution in generous amounts; adding pressors to combat the vasodilation seen in sepsis cases with hypotension and addition of high-dose corticosteroids when there is inadequate response to the listed maneuvers.

    Sepsis is a very serious life-threatening situation with a 20%-30% acute 30-day mortality and is the leading cause of in-hospital deaths in the United States. Furthermore, even when the acute event is survived patients have a high degree of residual mortality risk, morbidity such as mental acuity deterioration in the elderly and inability to return to work in younger patients.

    Those of us not directly involved in the ICU care and measures discussed but significantly involved in the overall care of these patients prior to, during, and after a sepsis ICU hospitalization need to be aware of these statistics to help patients and families with decision-making.

    AUTHOR
    Ronald N. Rubin MD1,2

    AFFILIATIONS
    1Lewis Katz School of Medicine at Temple University, Philadelphia, PA
    2Department of Medicine, Temple University Hospital, Philadelphia, PA

    CITATION
    Rubin RN. A 47-Year-Old Man Develops Multiorgan Failure. Consultant. 2026;67(6):doi: 10.25270/con.2026.05.000003

    DISCLOSURES
    The author reports no relevant financial relationships.

    CORRESPONDENCE:
    Ronald N. Rubin, MD, Temple University Hospital, 3401 N. Broad Street, Philadelphia, PA 19140 (blooddocrnr@yahoo.com)

    References

    1. Schlapbach LJ, Watson RS, Sorce LR, et al. International consensus criteria for pediatric sepsis and septic shock. JAMA. 2024;331(8):665-674.
    2. Meyer NJ, Prescott HC. Sepsis and septic shock. N Engl J Med. 2024;391(22):2133-2146.
    3. Meyer N, Harhay MO, Small DS, et al. Temporal trends in incidence, sepsis-related mortality, and hospital-based acute care after sepsis. Crit Care Med. 2018;46(3):354-360.
    4. Semler MW, Self WH, Wanderer JP, et al. Balanced crystalloids versus saline in critically ill adults. N Engl J Med. 2018;378(9):829-839.
    5. Evans L, Rhodes A, Alhazzani W, et al. Surviving Sepsis Campaign: international guidelines for management of sepsis and septic shock 2021. Crit Care Med. 2021;49(11):e1063-e1143.
    6. Venkatesh B, Finfer S, Cohen J, et al. Adjunctive glucocorticoid therapy in patients with septic shock. N Engl J Med. 2018;378(9):797-808.
    7. Annane D, Renault A, Brun-Buisson C, et al. Hydrocortisone plus fludrocortisone for adults with septic shock. N Engl J Med. 2018;378(9):809-818.
    8. Fang F, Zhang Y, Tang J, et al. Association of corticosteroid treatment with outcomes in adult patients with sepsis: a systematic review and meta-analysis. JAMA Intern Med. 2019;179(2):213-223.  
    9. Seymour CW, Gesten F, Prescott HC, et al. Time to treatment and mortality during mandated emergency care for sepsis. N Engl J Med. 2017;376(23):2235-2244.
    10. Prescott HC, Angus DC. Enhancing recovery from sepsis: a review. JAMA. 2018;319(1):62-75.
    11. Herridge MS, Azoulay É. Outcomes after critical illness. N Engl J Med. 2023;388(10):913-924.

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