Infectious Disease · Sepsis and Septic Shock
The facts most likely to be tested
Septic shock is defined as sepsis with persistent hypotension requiring vasopressors to maintain a mean arterial pressure (MAP) ≥ 65 mmHg despite adequate fluid resuscitation.
The primary hemodynamic profile of septic shock includes decreased systemic vascular resistance (SVR), increased cardiac output (CO), and decreased pulmonary capillary wedge pressure (PCWP).
Early management requires intravenous fluid resuscitation with 30 mL/kg of crystalloid within the first three hours to restore tissue perfusion.
Norepinephrine is the first-line vasopressor of choice for patients who remain hypotensive after initial fluid resuscitation.
Serum lactate levels serve as a critical marker of tissue hypoperfusion and are used to guide the adequacy of resuscitation efforts.
Broad-spectrum intravenous antibiotics must be administered within one hour of recognition, ideally after obtaining blood cultures.
Patients with septic shock often exhibit wide pulse pressure and bounding peripheral pulses due to profound vasodilation in the early stages.
Vignette unlocked
A 68-year-old male is brought to the emergency department with a fever of 102.4°F and confusion. Physical examination reveals flushed skin, bounding pulses, and a blood pressure of 82/40 mmHg. Laboratory studies show a serum lactate of 4.2 mmol/L and a white blood cell count of 18,000/µL. Despite the administration of 2 liters of normal saline, his blood pressure remains 85/45 mmHg. The patient has a history of a recent urinary tract infection.
What is the most appropriate next step in the management of this patient's hypotension?
Initiation of norepinephrine infusion
The patient meets criteria for septic shock (hypotension requiring vasopressors despite fluid resuscitation), necessitating the initiation of norepinephrine as the first-line vasopressor.
Full handout
High yield triage
Etiology / Epidemiology
Common in immunocompromised, elderly, and post-surgical patients; triggered by systemic infection.
Clinical Manifestations
Presents with warm shock, wide pulse pressure, and bounding pulses.
Diagnosis
Diagnosis requires qSOFA score ≥ 2 or SIRS criteria plus confirmed infection.
Treatment
Immediate IV crystalloids (30mL/kg) and norepinephrine for refractory hypotension.
Prognosis
High mortality; multi-organ failure is the primary cause of death.
Full handout
Epidemiology & Etiology
Septic shock is the most common form of distributive shock, typically caused by Gram-negative bacteria (e.g., E. coli) or Gram-positive cocci (e.g., S. aureus). High-risk populations include those with indwelling catheters, recent instrumentation, or chronic comorbidities like diabetes.
Pertinent Anatomy
Systemic vasodilation occurs primarily in the arteriolar and venular beds, leading to a massive increase in capacitance. This anatomical shift results in venous pooling and decreased venous return to the heart.
Pathophysiology
Infection triggers a massive release of pro-inflammatory cytokines (TNF-alpha, IL-1), causing widespread endothelial dysfunction. This leads to profound vasodilation and increased capillary permeability, resulting in third-spacing of fluids. The heart initially compensates with high cardiac output, but eventually fails due to myocardial depression.
Clinical Manifestations
Patients exhibit warm shock with flushed skin and bounding pulses early in the course. Look for tachycardia, tachypnea, and altered mental status. Hypotension (MAP < 65 mmHg) despite adequate fluid resuscitation is the hallmark of septic shock. Watch for oliguria as a sign of end-organ hypoperfusion.
Diagnosis
The Gold standard for diagnosis is the identification of a source of infection combined with persistent hypotension requiring vasopressors to maintain a MAP ≥ 65 mmHg. Serum lactate > 2 mmol/L is a critical marker of tissue hypoperfusion. Obtain blood cultures prior to antibiotic administration.
Treatment
Initiate IV crystalloids (30mL/kg) within the first hour. If hypotension persists, norepinephrine is the first-line vasopressor. Administer broad-spectrum antibiotics within 1 hour of recognition. Avoid corticosteroids unless the patient is refractory to vasopressors.
Prognosis
Mortality increases significantly with each hour of delayed antibiotic administration. Multi-organ dysfunction syndrome (MODS) is the most common complication. Monitor central venous oxygen saturation (ScvO2) to guide resuscitation.
Differential Diagnosis
Hypovolemic shock: cold extremities and low JVP
Cardiogenic shock: elevated JVP and pulmonary edema
Neurogenic shock: bradycardia and loss of sympathetic tone
Anaphylactic shock: history of allergen exposure and urticaria
Adrenal crisis: refractory hypotension despite vasopressors