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 and a serum lactate > 2 mmol/L despite adequate fluid resuscitation.
The initial management of septic shock requires the rapid administration of 30 mL/kg of intravenous crystalloid fluids within the first three hours.
Norepinephrine is the first-line vasopressor of choice for patients who remain hypotensive after initial fluid resuscitation.
Broad-spectrum intravenous antibiotics must be administered within one hour of recognition, ideally after obtaining blood cultures if this does not delay antibiotic delivery.
Vasopressin is the preferred second-line agent to add to norepinephrine if the patient remains refractory to initial vasopressor therapy.
Low-dose intravenous corticosteroids (e.g., hydrocortisone) are indicated for patients with septic shock who are hemodynamically unstable despite adequate fluid and vasopressor therapy.
The qSOFA score (quick Sequential Organ Failure Assessment) utilizes altered mental status, respiratory rate ≥ 22/min, and systolic blood pressure ≤ 100 mmHg to identify patients at high risk for poor outcomes.
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A 68-year-old male is brought to the emergency department with a 2-day history of fever, chills, and productive cough. On examination, the patient is lethargic, has a temperature of 39.2°C (102.6°F), a respiratory rate of 28/min, and a blood pressure of 88/52 mmHg. Laboratory studies reveal a serum lactate of 4.2 mmol/L and a leukocytosis with a left shift. Despite the administration of 2 liters of normal saline, his blood pressure remains 86/50 mmHg.
What is the most appropriate next step in the management of this patient?
Initiate norepinephrine infusion
The patient meets the criteria for septic shock (hypotension requiring vasopressors despite fluid resuscitation and elevated lactate); therefore, the next step is to start a first-line vasopressor.
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Etiology / Epidemiology
Systemic infection leading to distributive shock. High risk in immunocompromised, elderly, and post-surgical patients.
Clinical Manifestations
Hypotension requiring vasopressors despite fluid resuscitation. Warm shock early, cold shock late.
Diagnosis
Serum lactate > 2 mmol/L and persistent hypotension despite adequate fluid resuscitation.
Treatment
Early broad-spectrum antibiotics and norepinephrine as the first-line vasopressor.
Prognosis
High mortality; monitor mean arterial pressure (MAP) ≥ 65 mmHg to ensure organ perfusion.
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Epidemiology & Etiology
Commonly caused by Gram-negative bacilli (e.g., E. coli) or Gram-positive cocci (e.g., S. aureus). Primary sources include pneumonia, intra-abdominal infections, and urinary tract infections. Immunocompromised status and indwelling medical devices are major risk factors.
Pertinent Anatomy
Systemic vasodilation occurs due to loss of vascular tone in the peripheral arterioles. This leads to a decrease in systemic vascular resistance (SVR), causing blood to pool in the periphery and reducing venous return to the heart.
Pathophysiology
Infection triggers a massive release of pro-inflammatory cytokines, leading to widespread endothelial damage and capillary leak. This results in distributive shock characterized by maldistribution of blood flow and impaired cellular oxygen utilization. The body initially compensates with increased cardiac output, but eventually, myocardial depression leads to cold shock.
Clinical Manifestations
Patients present with hypotension, tachycardia, and altered mental status. Early stages show warm shock with bounding pulses and flushed skin, while late stages show mottled skin and peripheral cyanosis. Refractory hypotension despite 30 mL/kg of crystalloid fluid is the hallmark of shock.
Diagnosis
Diagnosis requires serum lactate > 2 mmol/L and the need for vasopressors to maintain MAP ≥ 65 mmHg. Obtain blood cultures prior to antibiotic administration. Use the qSOFA score (respiratory rate ≥ 22, altered mentation, systolic BP ≤ 100) for rapid bedside screening.
Treatment
Initiate IV fluids (30 mL/kg crystalloid) within the first hour. Administer broad-spectrum antibiotics immediately after cultures. If hypotension persists, start norepinephrine as the first-line vasopressor. Avoid corticosteroids unless the patient is refractory to vasopressors.
Prognosis
Mortality increases significantly with delayed intervention. Monitor urine output (> 0.5 mL/kg/hr) as a surrogate for end-organ perfusion. Multiple organ dysfunction syndrome (MODS) is the most common cause of death.
Differential Diagnosis
Hypovolemic shock: low central venous pressure and dry mucous membranes
Cardiogenic shock: elevated pulmonary capillary wedge pressure and pulmonary edema
Anaphylactic shock: presence of urticaria, wheezing, and angioedema
Neurogenic shock: bradycardia and loss of sympathetic tone following spinal injury
Adrenal crisis: refractory hypotension with history of chronic steroid use