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sepsis & septic shock

life-threatening organ dysfunction from a dysregulated host response to infection, with septic shock defined by vasopressor-dependent hypotension and elevated lactate despite fluids

infectious diseasescommonemergency

About This Page

This is a clinician-written, evidence-based summary aligned to the USMLE Step 2 CK Content Outline. It is intended for medical students preparing for USMLE Step 2 CK. Management reflects current ACC/AHA, USPSTF, and APA guidelines. Always cross-reference with UpToDate, institutional protocols, and clinical judgment.

The Bottom Line

  • Sepsis = suspected infection plus life-threatening organ dysfunction; septic shock = vasopressors needed to maintain MAP >=65 and lactate >2 after adequate fluids
  • Recognize early: fever or hypothermia, tachycardia, tachypnea, hypotension, altered mentation, oliguria, elevated lactate
  • Obtain blood cultures before antibiotics if this does not delay therapy; give broad-spectrum antibiotics rapidly, ideally within 1 hour for shock or high likelihood sepsis
  • Initial fluid resuscitation: balanced crystalloid, commonly 30 mL/kg for sepsis-induced hypoperfusion or septic shock
  • First-line vasopressor is norepinephrine; add vasopressin or epinephrine if refractory
  • Source control matters: drain abscess, remove infected catheter, debride necrotizing infection, relieve obstruction

Overview

Sepsis is a medical emergency caused by a dysregulated host response to infection leading to organ dysfunction. The Sepsis-3 definition uses an acute SOFA score increase of 2 or more points, while bedside screening often uses qSOFA or SIRS to prompt escalation. Septic shock is the subset with profound circulatory and metabolic abnormalities: persistent vasopressor requirement to maintain MAP at least 65 mmHg and lactate greater than 2 mmol/L despite adequate fluid resuscitation.

Epidemiology

Sepsis is a leading cause of hospital mortality in the United States and is common among older adults, immunocompromised patients, patients with indwelling devices, and those with pneumonia, urinary infection, intra-abdominal infection, skin/soft tissue infection, meningitis, or catheter infection. Mortality rises with delayed antibiotics, persistent hypotension, elevated lactate, multi-organ failure, and inadequate source control.

Clinical Features

Symptoms
Fever, chills, rigors, or hypothermia in older or immunocompromised patients
Altered mental status, confusion, lethargy, or agitation
Dyspnea, tachypnea, or respiratory failure
Oliguria, dizziness, syncope, or profound weakness from hypoperfusion
Localizing symptoms: cough, dysuria, abdominal pain, wound pain, meningismus, catheter pain
Purpura, rapidly progressive pain, or severe soft tissue pain suggests invasive infection or DIC
Signs
Hypotension, narrow pulse pressure late, or bounding pulses/warm extremities early in distributive shock
Tachycardia and tachypnea
Cool mottled skin, delayed capillary refill, cyanosis, or weak pulses in late shock
Focal infection signs: crackles, CVA tenderness, peritonitis, cellulitis, meningismus, catheter erythema
Petechiae, purpura fulminans, bleeding, or jaundice indicates severe disease

Investigations

First-line
Serum lactateElevated lactate indicates tissue hypoperfusion and increased mortality; repeat if initially elevated
Blood cultures x2 before antibioticsDraw from separate sites before antibiotics if this does not delay treatment
CBC, CMP, coagulation profile, bilirubin, creatinine, glucoseAssess organ dysfunction, DIC, renal/hepatic injury, and metabolic complications
Urinalysis/urine culture, sputum culture, wound cultures as indicatedTarget likely source; do not delay empiric therapy in shock
Second-line
Chest X-rayCommon first imaging test when respiratory source possible; may show pneumonia or ARDS
CT abdomen/pelvis or site-specific imagingFor intra-abdominal abscess, obstruction, perforation, pyelonephritis, necrotizing infection, or unclear source
ProcalcitoninMay support discontinuation decisions in some settings but should not replace clinical judgment or delay antibiotics
Specialist
Echocardiography or invasive monitoringIf shock etiology is unclear or refractory; evaluate cardiogenic component, volume responsiveness, and cardiac output
Lumbar punctureIf meningitis suspected after stabilizing airway/circulation; give antibiotics first if LP delayed
1
First hour priorities
  • Assess airway, breathing, circulation; give oxygen and establish two large-bore IVs
  • Measure lactate and repeat if elevated
  • Obtain blood cultures before antibiotics if no meaningful delay
  • Give broad-spectrum antibiotics immediately for septic shock or high likelihood sepsis
  • Start crystalloid resuscitation for hypotension or lactate elevation
2
Antibiotics
  • Choose empiric therapy based on source, severity, prior cultures, local resistance, immune status, and healthcare exposure
  • Cover MRSA, Pseudomonas, anaerobes, or fungi only when risk factors exist
  • De-escalate when cultures and clinical course identify the pathogen
  • Shorter courses are preferred when source control is adequate and the patient improves
3
Hemodynamics
  • Initial fluid: balanced crystalloid; 30 mL/kg is a common initial target for septic shock or sepsis-induced hypoperfusion
  • First-line vasopressor: norepinephrine to target MAP >=65 mmHg
  • Add vasopressin or epinephrine for refractory shock; use dobutamine if persistent hypoperfusion with cardiac dysfunction
  • Hydrocortisone 200 mg/day if shock remains vasopressor-dependent despite fluids and vasopressors
4
Source control and supportive care
  • Drain abscess, remove infected hardware/catheters when possible, debride necrotizing tissue, relieve obstruction
  • Use lung-protective ventilation for ARDS
  • Glucose target often 140-180 mg/dL in ICU; provide VTE and stress ulcer prophylaxis when indicated
  • Transfuse RBCs generally at hemoglobin <7 g/dL unless active ischemia, severe hypoxemia, or bleeding

Complications

  • Septic shock: Persistent vasodilatory shock with cellular metabolic dysfunction
  • ARDS: Diffuse inflammatory lung injury requiring lung-protective ventilation
  • AKI: Hypoperfusion, nephrotoxins, and inflammatory injury
  • DIC: Thrombosis and bleeding with low platelets, prolonged PT/PTT, low fibrinogen, high D-dimer
  • Multi-organ dysfunction: Encephalopathy, hepatic injury, ileus, myocardial depression
USMLE Step 2 CK Exam Tips
  • 1Septic shock definition requires vasopressors for MAP >=65 plus lactate >2 despite fluids
  • 2Do not wait for cultures to return before antibiotics in shock; cultures first only if this will not delay therapy
  • 3Norepinephrine is first-line vasopressor in septic shock
  • 4Sepsis-induced hypoperfusion classically gets 30 mL/kg crystalloid, then dynamic reassessment
  • 5Necrotizing fasciitis or abscess requires source control; antibiotics alone are not enough
  • 6Persistent hypotension despite fluids and norepinephrine = add vasopressin or give stress-dose hydrocortisone if refractory
  • 7Elevated lactate is a marker of hypoperfusion and mortality even if blood pressure initially looks acceptable
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Verified Sources & References

Surviving Sepsis Campaign Guidelines 2021
CDC Hospital Sepsis Program Core Elements
Sepsis-3 Consensus Definitions (JAMA 2016)