Sepsis and septic shock

Why examiners ask this

Septic shock is the examiner's favorite way to test whether you understand distributive physiology rather than just a checklist: a patient who is warm, vasodilated and hypovolemic at the same time, who needs an operation to control the source, and who will not tolerate a standard induction. It stresses judgment (how much fluid, when to start pressors, whether to delay for source control) and adaptability when the pressure collapses on induction. It also opens the door to steroids, lactate, and the choice between norepinephrine and vasopressin.

The 60-second answer

Decision points and the "why"

• Antibiotics before the OR, not after — within one hour of recognition, after cultures if that costs no time; the operation controls the source but the antibiotics treat the bacteremia that follows manipulation of pus. I never let the trip to the OR become the reason antibiotics were missed.
• Fluid: 30 mL/kg as a starting point, then reassess — the Surviving Sepsis Campaign suggests it, a weak recommendation,¹ but the patient with a stiff heart or ARDS tells me to stop earlier. I use pulse-pressure variation, a passive leg raise or a bedside echo of the IVC and ventricle, because static CVP does not predict fluid responsiveness. Balanced crystalloid over saline, because hyperchloremic acidosis worsens renal outcomes.
• Norepinephrine first, early — it restores the vascular tone that the sepsis destroyed, and waiting until the patient is "full" prolongs hypotension. I start it peripherally when the line is good and move it centrally when I can.¹ Dopamine is out because it roughly doubles arrhythmias compared with norepinephrine;¹ phenylephrine is a bridge, not a plan.
• Vasopressin at 0.03 units/min when norepinephrine reaches 0.25–0.5 mcg/kg/min — relative vasopressin deficiency is part of the disease, and adding it is suggested over escalating norepinephrine.¹ Epinephrine is my third drug; with a depressed ventricle and persistent hypoperfusion I add dobutamine or switch to epinephrine.¹
• Hydrocortisone 200 mg/day for an ongoing pressor requirement — it shortens shock duration; I start it once norepinephrine or epinephrine has been at least 0.25 mcg/kg/min for 4 hours,¹ not as a reflex for every septic patient.
• Induction — reduced-dose ketamine 0.5–1 mg/kg or etomidate 0.2 mg/kg, with norepinephrine running and a push-dose pressor drawn up, because the venodilation and myocardial depression of a full propofol induction will produce a cardiac arrest in a patient living on sympathetic tone. I accept the single-dose etomidate adrenal effect because the alternative is hypotension now.
• Lactate as a trend — I resuscitate to bring an elevated lactate down,¹ and a single value tells me the severity. Septic shock is a vasopressor requirement to hold a MAP of 65 with a lactate above 2 mmol/L despite adequate fluid.²

The complication they will inject

After induction the blood pressure falls to 55/30 and stays there despite a norepinephrine bolus. I call for help, go to 100% oxygen, confirm the tube and the end-tidal CO2, and treat with push-dose epinephrine 10–20 mcg while the infusion rate climbs. I check the arterial line is not the problem, give a 500 mL bolus if the ventricle looks empty, and I look at the heart with the echo probe: an empty hyperdynamic ventricle gets fluid and more norepinephrine; a dilated, poorly contracting ventricle is septic cardiomyopathy and gets epinephrine or dobutamine added. I add vasopressin and give hydrocortisone 100 mg now. If the pressure has not responded to any catecholamine, I consider the other causes examiners hide in sepsis: tension pneumothorax from the line, adrenal crisis, anaphylaxis to the antibiotic just given, and an acidosis below pH 7.1 blunting the pressors. I tell the surgeon that source control is the treatment and we continue once the pressure holds.

Pitfalls that cost points

• Delaying the operation "until resuscitated" when the abscess is the reason the patient is dying.
• Quoting 30 mL/kg and stopping there, with no plan for assessing whether the patient wants more.
• Starting pressors only through a central line after a 20-minute struggle to place it.
• A full-dose propofol induction with no pressor running.
• Treating the mean arterial pressure and never looking at lactate, urine output or the ventricle.

Rapid-why

Q: Why norepinephrine and not phenylephrine as the first pressor? A: Norepinephrine adds beta-1 inotropy to alpha vasoconstriction; phenylephrine alone raises afterload on a ventricle that is already depressed and can lower cardiac output.

Q: Why does a septic patient need so much fluid? A: Venodilation enlarges the capacitance bed and capillary leak moves fluid into the interstitium; the stressed volume that returns to the heart falls even though total body water rises.

Q: Why avoid saline? A: Large volumes produce hyperchloremic metabolic acidosis and renal vasoconstriction; balanced solutions lowered major adverse kidney events in the SMART trial (14.3% vs 15.4%).³

Q: Why hydrocortisone and not dexamethasone? A: Hydrocortisone has mineralocorticoid activity and matches physiologic cortisol; the dose of 200 mg/day replaces what a stressed adrenal gland is failing to produce.

Numbers to know

Links

• Vasopressors and inotropes: choosing and titrating, Fluid management: crystalloid, colloid, goal-directed, Arterial blood gas and acid-base interpretation, Intraoperative hypotension: differential and management, Adrenal insufficiency and stress-dose steroids
• Atlas: Volume status, IVC and fluid responsiveness; Ventricular function and wall motion
• Surviving Sepsis Campaign international guidelines (2021 adult update)