Episode Details

Date: July 9, 2026 Reference: The ARISE FLUIDS Investigators. Vasopressors or Fluids in Early Septic Shock. NEJM June 2026.  Guest Skeptic: Dr. Aaron Skolnik is an Assistant Professor of Emergency Medicine at the Mayo Clinic Alix School of Medicine and Vice Chair of Critical Care Medicine at Mayo Clinic Arizona.  He is board-certified in Emergency Medicine, Medical Toxicology, Addiction Medicine, Internal Medicine-Critical Care, and Neurocritical Care.  Aaron is a full-time multidisciplinary intensivist and enjoys serving as the medical student clerkship director for critical care. Case: A 69-year-old man presents by EMS to the emergency department (ED) with fever, productive cough, confusion, and weakness. He has hypertension, type 2 diabetes, and mild chronic kidney disease. His initial vitals are Temperature 38.8°C, heart rate 118 bpm, blood pressure 82/48 mmHg, respiratory rate 28 bpm, SpO₂ 90% on room air, and Glasgow Coma Scale (GCS) score of 14. He looks mottled, has delayed capillary refill, crackles at the right base, and dry mucous membranes. A chest x-ray suggests right lower-lobe pneumonia. Labs show white blood cell count (WBC) 17,000, creatinine 1.8 mg/dL, and lactate 3.4 mmol/L. Blood cultures are drawn, broad-spectrum antibiotics are started, and he receives 1 litre of balanced crystalloid. Thirty minutes later, his mean arterial pressure (MAP) remains around 60 mmHg. The resident asks: “Should we give more fluid to get to 30 mL/kg, or start norepinephrine now?” Background: Sepsis remains one of the highest-stakes and humbling diagnoses in emergency medicine. It is not as simple as infection plus abnormal vitals. Sepsis-3 reframed sepsis as life-threatening organ dysfunction caused by a dysregulated host response to infection, moving away from the older SIRS-based definition and retiring the term severe sepsis. Septic shock is now generally understood as sepsis with persistent hypotension requiring vasopressors to maintain a MAP of at least 65 mmHg, with lactate greater than 2 mmol/L despite adequate volume resuscitation. For emergency physicians, the challenge is that sepsis is still largely a clinical diagnosis without a gold standard test. Systemic Inflammatory Response Syndrome (SIRS) is sensitive (true-positive) but not specific (true-negative). qSOFA may predict mortality, but it is not sensitive enough to rule out sepsis in the ED. Lactate is useful for risk stratification, but it's not a magic wand, and procalcitonin is not accurate enough to rule in or rule out bacterial infection. The SGEM has repeatedly emphasized that sepsis screening tools, biomarkers, and bundles should be used with healthy skepticism rather than blind obedience.     Treatment in the ED usually starts with the basics: recognize the patient may be septic, obtain cultures when appropriate without delaying care, give early appropriate antimicrobials, seek source control, and support perfusion. The resuscitation controversy has evolved over two decades. Early goal-directed therapy (EGDT) gave way to usual-care trials that challenged protocolized central venous pressure and ScvO₂ targets. Fixed fluid mandates have been questioned, and many clinicians now worry about both under-resuscitation and fluid overload. As SGEM has argued, whether rigid bundles based on low-certainty evidence improve patient-oriented outcomes (POO).     That leaves a very practical bedside question: after an initial litre or two, should we keep pouring in crystalloid, or should we start vasopressors earlier? Fluids can improve preload and perfusion, but excessive fluid administration may worsen pulmonary edema, tissue edema, and organ dysfunction. Vasopressors can restore vascular tone and perfusion pressure, but raise concerns about ischemia, monitoring, IV access, and intensive care unit (ICU) resource use. This is exactly the kind of EM question that deserves a patient-oriented answer. As we say on the SGEM, they are called guidelines, not GODlines. Clini