Oral Board Case: Management of Sepsis

How do you distinguish sepsis from septic shock in this patient, and why does it matter?

Expected answer

Sepsis is life-threatening organ dysfunction from a dysregulated host response to infection. Septic shock is a subset with persistent hypotension requiring vasopressors to maintain MAP ≥65 mmHg AND a lactate >2.0 mmol/L despite adequate fluid resuscitation. The distinction matters because septic shock carries substantially higher mortality, mandates vasopressors and ICU admission, and signals failed initial resuscitation. This patient's hypotension, lactate elevation, and confusion already place him at least in sepsis with concern for shock.

What are your first steps in the immediate management of this patient?

Expected answer

Resuscitation comes before any imaging. Establish IV access (two large-bore, plus arterial/central access as needed), draw blood cultures and lactate, give 30 mL/kg crystalloid for hypotension or lactate >4, and start broad-spectrum empiric antibiotics within 1 hour. Place on continuous monitoring and pulse oximetry. Obtain cultures BEFORE antibiotics if it does not delay them. This is the sepsis bundle: cultures, lactate, fluids, antibiotics.

What is the likely source of infection here, and how do you work it up?

Expected answer

Given the recent UTI and diabetes, a urinary source (pyelonephritis, emphysematous pyelonephritis, or an obstructing infected stone) is most likely. I'd send a urinalysis and urine culture, blood cultures, and once he is resuscitated obtain a CT of the abdomen/pelvis to look for obstruction, abscess, emphysematous change, or perinephric collection requiring drainage. Diabetics are also at risk for occult deep infections like necrotizing soft tissue infection, so a thorough skin and soft tissue exam is mandatory.

You give 30 mL/kg crystalloid and the patient remains hypotensive with MAP 55. What now?

Expected answer

This is refractory hypotension defining septic shock. Start a vasopressor; norepinephrine is first-line, titrated to MAP ≥65 mmHg. Before and during pressors, reassess volume status and perfusion with dynamic measures—passive leg raise, fluid challenge, bedside echo, or CVP/ScvO2—rather than giving fluid blindly. Recheck lactate to assess clearance. If still hypotensive add vasopressin, and consider stress-dose steroids for refractory shock.

How do you choose and time empiric antibiotics?

Expected answer

Broad-spectrum IV antibiotics should be started within 1 hour of recognizing sepsis. For a urinary source in a diabetic I'd cover gram-negatives including resistant Enterobacteriaceae and Pseudomonas (e.g., a beta-lactam such as piperacillin-tazobactam or a carbapenem), considering local antibiogram and prior cultures. I narrow/de-escalate once culture and sensitivity data return. Typical duration is 7–10 days, longer if there's an undrainable source, bacteremia, slow response, or immunocompromise.

What is the role of source control and what defines an emergency intervention?

Expected answer

Antibiotics alone cannot cure a controllable anatomic source. Patients needing emergent source control—an obstructed infected urinary system, abscess, or necrotizing infection—must be identified early and intervened upon as soon as the patient is medically stable enough. For an obstructing infected stone with pyonephrosis, urgent decompression with a ureteral stent or percutaneous nephrostomy is required. Necrotizing soft tissue infection demands emergent surgical debridement. Source control should not be unduly delayed waiting for full physiologic normalization.

The patient develops hypoxemia and ARDS requiring intubation. How do you ventilate him?

Expected answer

Use lung-protective ventilation: low tidal volumes of 6 mL/kg predicted body weight with plateau pressure ≤30 cmH2O, which showed an absolute mortality reduction in sepsis-induced ARDS. Apply appropriate PEEP, permit permissive hypercapnia, and target adequate oxygenation. Minimize sedation, use spontaneous breathing trials and a weaning protocol when ready, and avoid neuromuscular blockade unless there is severe ARDS—and if used, ensure adequate concurrent sedation and analgesia.

What ongoing supportive ICU measures do you institute?

Expected answer

Glucose control (especially important in this diabetic), DVT prophylaxis, stress ulcer prophylaxis, and transfusion only for hemoglobin <7.0 g/dL in the absence of myocardial ischemia, active hemorrhage, or severe hypoxemia. I'd trend lactate and perfusion markers, monitor renal function and urine output, daily reassess for de-escalation of antibiotics and pressors, and have early goals-of-care and prognosis discussions with the patient and family.

How do you assess whether your resuscitation is working?

Expected answer

Reassess clinically and with objective measures: improving MAP ≥65, decreasing pressor requirement, restored urine output, improving mental status and capillary refill, and lactate clearance on serial measurement. Dynamic indices (passive leg raise, stroke volume variation, echo) gauge continued fluid responsiveness so I avoid both under- and over-resuscitation, since excessive fluid worsens edema and outcomes.