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Nursing Diagnosis for Sepsis: 5 Sample Care Plans & Interventions

Mike Linares, MSN RN headshot
By Mike Linares MSN, RN | Updated June 10, 2026 · Editorial Standards
Updated June 10, 2026 Medically Reviewed by: Mackenzie Butler, DNP, MSN, RN-BC
Mackenzie Butler, DNP, MSN, RN-BC
Medically Reviewed by:
Mackenzie Butler, DNP, MSN, RN-BC
Sepsis nursing care plan with a cartoon virus on a yellow background

Choosing the right nursing diagnosis for sepsis — and acting on it before the patient slides into septic shock — is one of the highest-stakes assignments in nursing school and one of the most time-sensitive bedside decisions in clinical practice. Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection; early recognition, timely antimicrobials, hemodynamic support, and source control are central to sepsis outcomes.

This sepsis nursing care plan walks through what to assess, the NANDA-I-aligned nursing diagnoses for sepsis you’ll see most often, and 5 sample care plans modeled on the current Sepsis-3 framework and Surviving Sepsis Campaign 2026 principles, with reminders to follow facility protocols and provider orders.

It’s written for nursing students, new grads, and any RN who wants a refresher grounded in the Sepsis-3 definitions (Singer et al. 2016), the Surviving Sepsis Campaign 2026 adult guideline, NICE NG253 / NG254 / NG255 (UK, by population), and CDC sepsis data. Always verify against the most current published edition.

Guideline basis. Sepsis-3 definitions (Singer et al., 2016); Surviving Sepsis Campaign 2026 adult guideline; NICE NG253 (adults 16+ not pregnant), NG254 (under 16s), NG255 (pregnant / recently pregnant) – published November 19, 2025. Facility protocol is required for bedside use. Applies to adult patients unless otherwise stated.

Scope note. This is an educational care plan for nursing students and new graduates. It is not a substitute for facility sepsis protocols, provider orders, or specialist clinical judgment. Sepsis recognition, antimicrobial selection, fluid resuscitation, vasopressor initiation, and ICU escalation are time-sensitive and depend on the patient and your institution — always follow current local policy.

Quick answer. The five most common nursing diagnoses for sepsis are Ineffective Tissue Perfusion (the canonical high-priority diagnosis), Impaired Gas Exchange (sepsis-induced ARDS), Risk for Shock, Hyperthermia, and Acute Confusion (sepsis-associated encephalopathy). Choose the diagnosis based on the patient’s actual assessment findings.

Patient findingBest-fit nursing diagnosis
Hypotension, lactate elevation, mottled skin, decreased urine outputIneffective Tissue Perfusion (high priority)
SpO₂ low, PaO₂/FiO₂ ≤ 300, bilateral infiltrates, increased work of breathingImpaired Gas Exchange
Sepsis with worsening hemodynamic warning signs but no vasopressor yetRisk for Shock
T > 38.3 °C with chills, rigors, tachycardiaHyperthermia
New confusion, agitation, delirium, decreased GCSAcute Confusion (sepsis-associated encephalopathy)

Common mistakes to avoid. Don’t use qSOFA alone as the sepsis screen — SSC 2026 recommends facility-approved tools (NEWS2, MEWS, SIRS, or organizational pathway). Don’t rely on SIRS-only definitions — Sepsis-3 (2016) defined sepsis as organ dysfunction, not just inflammatory response. Don’t apply a fixed MAP target rigidly to every patient — SSC 2026 generally uses an initial MAP target around 65 mm Hg, with 60–65 mm Hg sometimes appropriate for adults ≥ 65 and provider-specified targets for some patients. Do not delay vasopressors solely to wait for central access when shock is present and an appropriate peripheral IV is available — peripheral norepinephrine initiation is acceptable per SSC 2026 while central access is being secured. Don’t interpret lactate alone as proof of hypoperfusion — trend it alongside the full clinical picture. Verify exact NANDA-I labels against the licensed 2024–2026 text.

Table of contents

What is sepsis?

Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection. That’s the formal Sepsis-3 definition (Singer et al., JAMA 2016) — and it’s not just an inflammatory response (the older SIRS-based definition). It’s the inflammatory cascade going badly wrong, damaging the patient’s own tissues, vasculature, and organs.

The CDC reports approximately 1.7 million adult sepsis hospitalizations annually in the U.S., and sepsis contributes to over a third of hospital deaths. Most cases originate in the community before admission, and the most common sources are the lungs, urinary tract, abdomen, and skin and soft tissue.

Sepsis-3 definitions

The Sepsis-3 framework (Singer et al., 2016) replaced the older “severe sepsis” / SIRS-based definitions. Three tiers:

TermSepsis-3 definition
InfectionInvasion of normally sterile tissue by microorganisms
SepsisLife-threatening organ dysfunction caused by a dysregulated host response to infection — operationally a SOFA score increase ≥ 2 from baseline
Septic shockSepsis + vasopressor requirement to maintain MAP ≥ 65 mm Hg + lactate > 2 mmol/L despite adequate fluid resuscitation

The older term “septicemia” is no longer used in formal definitions. It used to mean “bacteria in the bloodstream causing illness,” but it’s been replaced by bacteremia (organisms in blood) and sepsis (organ dysfunction from infection).

Sepsis vs septic shock

The distinction matters at the bedside because septic shock has a higher mortality (~ 40%) than sepsis without shock (~ 10%):

MarkerSepsisSeptic shock
MechanismDysregulated host response to infection → organ dysfunctionSepsis + circulatory failure
HemodynamicsMay have hypotension responsive to fluidsPersistent hypotension requiring vasopressors
MAP target≥ 65 mm Hg with fluids≥ 65 mm Hg with vasopressors after adequate fluids
LactateMay be elevated> 2 mmol/L despite adequate fluid resuscitation
Mortality~ 10%~ 40%

Causes and risk factors

The most common sources of sepsis (by frequency):

  • Pneumonia — single most common source overall (see our pneumonia care plan)
  • Urinary tract infection — frequent in older adults and patients with Foley catheters
  • Intra-abdominal infections — perforated viscus, cholangitis, peritonitis
  • Skin and soft tissue — cellulitis, necrotizing soft-tissue infection, wound infection
  • Bloodstream / line-associated — CLABSI, endocarditis
  • CNS — meningitis (less common but high mortality)

Risk factors

  • Age ≥ 65 or pediatric (extremes of age)
  • Immunosuppression — chemotherapy, biologics, chronic steroids, HIV, transplant
  • Chronic conditions — diabetes (impaired neutrophil function), CKD, cirrhosis, COPD, heart failure
  • Indwelling devices — central lines, Foleys, ventilators, drains, prosthetic joints, ports
  • Recent hospitalization or surgery
  • Malnutrition
  • Recent antibiotic exposure (drives resistant organisms and C. difficile)
  • Social factors — substance use, homelessness

Pathophysiology

Sepsis is what happens when the immune response that’s supposed to contain an infection turns destructive. Four key processes drive the clinical picture:

  1. Cytokine storm — pro-inflammatory mediators (TNF-α, IL-1, IL-6) flood the circulation
  2. Distributive shock — endothelial dysfunction + nitric-oxide-mediated vasodilation drop systemic vascular resistance; relative hypovolemia even with normal absolute volume
  3. Capillary leak — endothelial junctions loosen → intravascular fluid moves to the interstitium → worsens functional hypovolemia and causes edema
  4. Microvascular dysfunction — sluggish capillary flow + microthrombi from activated coagulation impair tissue oxygen delivery even when the macroscopic hemodynamics look acceptable

Result: tissues hypoperfuse, lactate rises, organs fail.

Signs and symptoms

The data below is what to consider, not what every patient with sepsis will have. Older adults and the immunocompromised may present atypically — confusion, falls, decreased PO intake — without fever or classic findings. Hypothermia in an older adult or critically ill patient is a sepsis red flag.

Subjective

  • Fever, chills, rigors — or feeling unusually cold
  • Generalized weakness, fatigue, “feel terrible”
  • Confusion, agitation, or behavior change reported by family
  • Decreased urine output
  • Source-specific complaints (productive cough, dysuria, abdominal pain, wound drainage)

Objective

  • Temperature > 38.3 °C or < 36 °C (hypothermia matters)
  • Heart rate > 90 (often > 110 in shock)
  • Respiratory rate ≥ 22
  • SBP ≤ 100 mm Hg; MAP < 65 mm Hg
  • SpO₂ low, increased work of breathing
  • Altered mental status (new confusion is a major red flag)
  • Mottled skin, prolonged capillary refill, cool extremities (in distributive shock the periphery may initially feel warm — “warm shock” — before progressing to cold)
  • Decreased urine output (< 0.5 mL/kg/hr)
  • Lactate elevation (> 2 mmol/L concerning; ≥ 4 high-risk)
  • Leukocytosis or leukopenia, left shift, bands

Sepsis screening (SSC 2026)

Use your facility-approved sepsis screening tool: NEWS2, MEWS, SIRS, or your organization’s pathway. qSOFA should not be used alone as a screening tool per SSC 2026.

ToolWhat it captures
NEWS2Composite score from RR, SpO₂, O₂ requirement, SBP, HR, AVPU, and T — UK NHS standard
MEWSSimilar composite to NEWS2; more common in some US facilities
SIRST > 38 or < 36, HR > 90, RR > 20 or PaCO₂ < 32, WBC > 12K or < 4K or > 10% bands. Sensitive but not specific — not a stand-alone sepsis definition since Sepsis-3 (2016).
qSOFARR ≥ 22, altered mental status, SBP ≤ 100. Supports escalation but should not be the sole screening tool.
SOFAComprehensive organ-dysfunction score — used for formal sepsis diagnosis (≥ 2 increase from baseline)

Bedside escalation cues

  • RR ≥ 22
  • Altered mental status
  • SBP ≤ 100 mm Hg
  • Lactate > 2 mmol/L
  • Source of infection present (or strongly suspected)

If two or more of these are present alongside known or suspected infection, activate the facility sepsis pathway.

Diagnostic studies

TestWhat it tells you
Lactate> 2 mmol/L concerning; ≥ 4 mmol/L high-risk. Not specific for hypoperfusion — interpret with perfusion exam, hemodynamics, liver disease, seizures, beta-agonists, metformin, severe exertion. Trending matters.
CBC with differentialWBC up or down; left shift (bands); thrombocytopenia → DIC concern
BMP / CMPCreatinine, BUN, electrolytes for AKI; liver enzymes; glucose dysregulation
Blood cultures × 2 (separate sites)Before antibiotics when feasible — don’t delay therapy in severe disease
Source-specific culturesUrine, sputum, wound, CSF as indicated
ProcalcitoninDo not use procalcitonin to decide whether to start antimicrobials in suspected sepsis. When duration is unclear and source control is adequate, procalcitonin plus clinical evaluation may support antimicrobial discontinuation decisions.
ABGpH, PaO₂, PaCO₂, base deficit; metabolic acidosis from lactate
Coagulation panelPT/INR, aPTT, fibrinogen, D-dimer, platelets — assess for DIC
CXR / CT chestPneumonia or ARDS workup
CT abdomen / CT angioSource identification — abscess, perforation, mesenteric ischemia
Ultrasound (point-of-care)Volume status (IVC), cardiac function, lung B-lines (pulmonary edema), abscess identification
UrinalysisUTI screen

Reference ranges vary by lab — check facility normals.

Hour-1 Bundle vs Sepsis Six

Two clinical bundles drive the time-critical sepsis response. They share core elements; the Surviving Sepsis Campaign is an international guideline, and Sepsis Six is a UK bedside tool.

Hour-1 Bundle (Surviving Sepsis Campaign bundle implementation framework)

  1. Measure lactate; re-measure if initial > 2 mmol/L
  2. Obtain blood cultures × 2 before antibiotics when feasible
  3. Administer broad-spectrum antimicrobials — immediately, ideally within 1 hour, for septic shock or high-likelihood sepsis without shock. For possible sepsis without shock, perform a rapid time-limited evaluation and give antimicrobials within 3 hours from when sepsis was first suspected if concern persists (per provider order and facility policy).
  4. Begin 30 mL/kg balanced crystalloid within the first 3 hours for sepsis-induced hypoperfusion or septic shock, with reassessment of fluid responsiveness
  5. Apply vasopressors for MAP < 65 mm Hg unresponsive to fluids — peripheral norepinephrine acceptable short-term while central access is being secured
  6. Pursue source control early — abscess drainage, infected device removal, surgical source control as indicated

The Hour-1 framework traces to the SSC bundle implementation tool; the full SSC 2026 adult guideline contains 129 statements with 46 new recommendations. Timing windows start at sepsis recognition, not arrival.

Sepsis Six (UK bedside tool)

The Sepsis Six is a UK sepsis-recognition and response mnemonic used to support rapid bedside action; it should be aligned with current NICE guidance (NG253 / NG254 / NG255) and local policy.

  1. Give oxygen to maintain SpO₂ within an individualized target (94–98% for most adults; 88–92% for hypercapnic-risk)
  2. Take blood cultures
  3. Give IV antibiotics
  4. Give IV fluids
  5. Measure lactate (and hemoglobin)
  6. Measure accurate hourly urine output

Both frameworks expect the same care; the labels differ by region.

Antibiotic timing and source control

Antibiotic principles (verify with facility protocol):

  • Septic shock or high-likelihood sepsis without shock — administer antimicrobials immediately, ideally within 1 hour of recognition per SSC 2026
  • Possible sepsis without shock — perform a rapid time-limited evaluation; if concern for infection persists, give antimicrobials within 3 hours from when sepsis was first suspected (per provider order and facility policy)
  • Empiric broad-spectrum coverage based on suspected source, prior cultures, recent antibiotic exposure, and local antibiogram
  • Collect cultures × 2 before antibiotics when feasible — but don’t delay therapy in severely ill patients
  • De-escalate by 48–72 hours based on culture results and clinical course
  • Duration is individualized by source, pathogen, immune status, source control, and clinical response. With adequate source control and clinical improvement, SSC 2026 generally favors shorter rather than unnecessarily prolonged antimicrobial courses; longer courses for select pathogens, immunocompromised patients, or persistent source

Source control is one of the core SSC 2026 principles. Many sepsis cases will not resolve until the source is physically controlled:

  • Abscess → drainage (interventional radiology or surgical)
  • Infected vascular device → removal
  • Necrotizing soft-tissue infection → emergent surgical debridement
  • Empyema → chest tube
  • Obstructed urinary tract infection → relief of obstruction (stent, nephrostomy)
  • Perforated viscus → surgical repair

Coordinate with the surgical / interventional / specialist team early. Do not wait for full clinical stabilization — source control is often what enables stabilization.

Fluid resuscitation

Per SSC 2026:

  • At least 30 mL/kg IV balanced crystalloid within the first 3 hours for sepsis-induced hypoperfusion or septic shock — consider individual patient characteristics, clinical context, and fluid responsiveness
  • Weight basis — actual body weight by default; adjusted or ideal body weight considered when BMI > 30, per provider order and facility practice
  • Reassess frequently rather than automatically continuing fluids after initial resuscitation — lung exam, oxygen needs, urine output, lactate trend, capillary refill, passive leg raise response, bedside ultrasound, cardiac history, renal function, and provider-specified targets
  • Avoid blind continued fluid administration beyond what improves perfusion — sepsis patients are at high risk of volume overload and pulmonary edema
  • Balanced crystalloids (lactated Ringer’s, Plasma-Lyte) are generally preferred over 0.9% saline in adult sepsis resuscitation based on recent evidence (SMART, BaSICS, PLUS trials), although 0.9% saline may be preferred in specific contexts such as traumatic brain injury
  • Albumin is not routine first-line resuscitation, but may be considered in selected patients who require large crystalloid volumes or who have cirrhosis, per provider order and institutional practice
  • Avoid starches (hydroxyethyl starches) — harm signal in sepsis

Vasopressors and steroids

Vasopressors

  • Norepinephrine is the first-line vasopressor for septic shock per SSC 2021/2026 — adrenergic vasoconstrictor (α₁ predominant, mild β₁ inotropy)
  • Vasopressin is commonly added when norepinephrine requirements are escalating — reduces norepinephrine requirement; specific dose thresholds and target ranges are protocol-dependent (per facility policy)
  • Epinephrine may be added if MAP remains inadequate despite norepinephrine and vasopressin, or as the inotropic option in septic cardiomyopathy
  • Phenylephrine for select cases (e.g., tachyarrhythmia limiting NE use)
  • Dopamine is no longer first-line for septic shock per SSC — higher arrhythmia risk without survival benefit
  • Peripheral vasopressor initiation may be appropriate short-term through a well-placed peripheral IV per facility policy; central access is preferred for ongoing therapy but should not delay treatment in shock

Steroids

  • IV hydrocortisone 200 mg/day (often 50 mg q6h or continuous infusion) per SSC 2021/2026 — for septic shock with persistent vasopressor requirement
  • Not for sepsis without shock
  • Not for shock that’s already resolving
  • Watch for hyperglycemia, hypernatremia, neuromuscular weakness

Nursing goals and outcomes

By the end of the shift / hospitalization, the patient will (choose what fits the individual patient):

  • Maintain MAP ≥ 65 mm Hg (or individualized provider target)
  • Maintain SpO₂ within an individualized target range
  • Demonstrate lactate clearance (or stable / trending-down lactate)
  • Maintain urine output ≥ 0.5 mL/kg/hr
  • Maintain mental status appropriate to baseline (no new confusion / agitation / delirium)
  • Receive empiric antibiotics within 1 hour of recognition for septic shock or probable / definite sepsis
  • Have source control achieved within the appropriate clinical window
  • Wean off vasopressors and supplemental oxygen
  • Pre-discharge, the patient and caregivers verbalize post-sepsis syndrome awareness and signs that warrant re-evaluation

Nursing interventions

Recognition and screening

  • Use the facility-approved sepsis screening tool at the bedside on every shift for at-risk patients
  • Recognize subtle changes — new confusion, decreased PO intake, falls in older adults — and escalate when present alongside known or suspected infection
  • Trend vital signs, mental status, urine output, and lactate

Hour-1 bundle execution

  • Coordinate the team — call provider, secure IV access (two large-bore preferred), draw labs (CBC, lactate, BMP, blood cultures × 2)
  • Administer antibiotics per provider order — within 1 hour for septic shock or probable/definite sepsis
  • Begin 30 mL/kg crystalloid for sepsis-induced hypoperfusion within 3 hours with reassessment
  • Prepare for vasopressor initiation — peripheral norepinephrine is acceptable short-term; central line preferred

Hemodynamic and respiratory support

  • Monitor MAP, HR, SpO₂, RR, mental status, urine output continuously per facility cadence
  • Apply supplemental oxygen to maintain SpO₂ within the individualized target (typically 94–98% per BTS for adults not at hypercapnic risk; 88–92% for hypercapnic-risk patients)
  • Position upright when tolerated to optimize V/Q matching
  • Coordinate ICU transfer for vasopressor-dependent or escalating respiratory failure

Medication considerations

  • Administer antimicrobials, fluids, vasopressors, and steroids per provider order
  • Review home medications (antihypertensives, diuretics, immunosuppressants) — notify provider and hold per provider order, facility protocol, or active standing order set
  • Monitor for adverse effects — vancomycin nephrotoxicity / ototoxicity, vasopressor extravasation, fluid overload

Source control and infection prevention

  • Identify and address the source — remove unnecessary lines and Foleys, coordinate drainage / surgery / IR consult
  • Apply WHO 5 Moments for Hand Hygiene
  • Use facility-appropriate isolation precautions
  • For deeper foundational reading on infection prevention bundles (CLABSI, CAUTI, SSI, VAP, C. difficile), see our infection care plan

Family and patient communication

  • Sepsis moves fast and is frightening. Keep families informed; explain the bundle as it’s happening.
  • Coordinate goals-of-care conversations early when prognosis is uncertain — palliative care can run alongside aggressive treatment

Education

Hospital Ward: Professional Black Head Nurse Wearing Face Mask Does Checkup of Patient's Vitals, Checking Heart Rate Computer, Intravenous or Iv Fluids Drip Bag. Caring Nurse Monitors Person Recovery

Nursing diagnosis for sepsis — 5 sample care plans

These five care plans cover the nursing diagnoses for sepsis you’ll see most often. Each uses NANDA-I–aligned educational language, current Sepsis-3 / SSC 2026 guidance, and the standard student template (diagnosis → defining characteristics / risk factors → goals → interventions with rationales → evaluation).

NANDA-I label verification. These examples use NANDA-I–aligned educational language. Verify exact diagnosis labels, definitions, defining characteristics, and related / risk factors in the licensed NANDA-I 2024–2026 text required by your school or facility before using these for graded paperwork or institutional documentation. Pay particular attention to Ineffective Tissue Perfusion (NANDA-I labels often specify a tissue bed – peripheral / cerebral / cardiac / renal – depending on edition), Risk for Shock risk factors, and the Acute Confusion related-factor list.

Clinical-use warning. These are educational examples for nursing care-plan development. They are not standing orders and should not be used to independently initiate antibiotics, vasopressors, fluids, corticosteroids, or ventilation changes outside provider orders and facility protocols.

Care Plan #1 — Ineffective Tissue Perfusion

The canonical high-priority nursing diagnosis for sepsis. The distributive-shock mechanism — vasodilation, capillary leak, microvascular dysfunction — is what makes sepsis a perfusion emergency.

Scenario. A 72-year-old patient admitted from the ED with urosepsis. Confusion (baseline alert), HR 118, BP 88/52 (MAP 64), RR 24, SpO₂ 92% on 3 L NC, T 38.6 °C, lactate 3.4. Two large-bore IVs in place. Crystalloid bolus started. Norepinephrine being prepared per provider order.

Diagnosis (NANDA-I–aligned)

Ineffective Tissue Perfusion related to sepsis-induced distributive shock with vasodilation, capillary leak, and microvascular dysfunction, as evidenced by MAP 64 mm Hg, lactate 3.4 mmol/L, new altered mental status, tachycardia, and decreased urine output.

Goals

  • Within 1 hour, the patient maintains MAP ≥ 65 mm Hg with fluid resuscitation and (if needed) initiation of norepinephrine per provider order.
  • Within 6 hours, lactate trends down and urine output reaches ≥ 0.5 mL/kg/hr.
  • The patient is upgraded to a higher level of care per facility criteria.

Interventions and rationales

InterventionRationale
Continuous hemodynamic monitoring (HR, BP, MAP, SpO₂); hourly urine output.Lactate clearance and urine output are key prognosticators.
Administer 30 mL/kg crystalloid within the first 3 hours per SSC 2026 with reassessment after each bolus.Restores intravascular volume; reassessment prevents overload.
Coordinate norepinephrine initiation per provider order if MAP < 65 despite adequate fluids; peripheral access is acceptable short-term but central line preferred.Norepinephrine is first-line vasopressor per SSC. Peripheral initiation should not delay therapy.
Trend lactate at recognition and re-measure if initial > 2 mmol/L.Lactate clearance is one of the most useful response markers.
Identify and address the source — for urosepsis, ensure the Foley is necessary and not obstructed; coordinate urology / IR for obstruction relief if present.Source control is essential to sepsis resolution.
Coordinate ICU evaluation per facility criteria.Vasopressor-dependent shock often requires ICU-level monitoring.
Educate the family — sepsis is frightening and moves fast; keep them informed in real time.Family-centered care during high-acuity intervention.

Evaluation

  • Did MAP reach ≥ 65 mm Hg?
  • Did lactate trend down and urine output improve?
  • Was source control addressed?

Care Plan #2 — Impaired Gas Exchange

Sepsis-induced acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are common — about a third of severe sepsis cases develop ARDS.

Scenario. A 58-year-old patient with septic shock from pneumonia, day 1 of ICU admission. Intubated, mechanically ventilated. PaO₂/FiO₂ 145 on FiO₂ 70%, PEEP 12. CXR shows bilateral infiltrates. No clinical evidence of cardiogenic pulmonary edema. Meets Berlin criteria for moderate ARDS.

Diagnosis (NANDA-I–aligned)

Impaired Gas Exchange related to sepsis-induced acute respiratory distress syndrome (ARDS) with alveolar inflammation, capillary leak, surfactant dysfunction, and ventilation–perfusion mismatch, as evidenced by PaO₂/FiO₂ 145, bilateral infiltrates on CXR, hypoxemia, and high FiO₂ / PEEP requirement.

Goals

  • Within 24 hours, PaO₂/FiO₂ improves with lung-protective ventilation (low tidal volume around 6 mL/kg of predicted body weight; plateau pressure goal ≤ 30 cm H₂O).
  • The patient maintains SpO₂ within the provider-specified target.
  • The patient does not develop ventilator-associated pneumonia (VAP) or other ICU complications.

Interventions and rationales

InterventionRationale
Coordinate lung-protective ventilation per provider order — typically low tidal volume around 6 mL/kg of predicted body weight, plateau pressure goal ≤ 30 cm H₂O, appropriate PEEP.ARDSnet protocol reduces ventilator-induced lung injury and mortality in sepsis-induced ARDS.
Coordinate prone positioning for moderate-to-severe ARDS (PaO₂/FiO₂ < 150) per provider order — generally for more than 12 hours daily when ordered and feasible.Prone positioning improves V/Q matching and reduces mortality in moderate-to-severe ARDS.
Apply the VAP bundle per SHEA/IDSA/APIC 2022 — minimize sedation, daily SATs/SBTs, early mobility when feasible, HOB elevation when tolerated, daily oral care with toothbrushing.Routine oral chlorhexidine is no longer recommended; the rest of the bundle reduces VAP risk.
Trend ABG, SpO₂, ventilator settings, and PaO₂/FiO₂.Tracks response to ventilation strategy.
Coordinate sedation management — light sedation when possible per provider order.Deep sedation prolongs ventilation and increases delirium risk.
Monitor for pneumothorax, ventilator-induced injury, and oxygen toxicity.Lung-protective ventilation reduces but does not eliminate these risks.

Evaluation

  • Is PaO₂/FiO₂ improving?
  • Is the patient free of VAP and other ventilator complications?
  • Has sedation been minimized to support extubation readiness?

Care Plan #3 — Risk for Shock

For patients with confirmed sepsis but not yet septic shock — the deterioration watch. Catching the transition to vasopressor-dependent shock is high-stakes.

Scenario. A 64-year-old patient admitted with cellulitis-related sepsis. Facility sepsis screen positive. HR 108, BP 102/64 (MAP 76), RR 22, lactate 2.6, T 38.4 °C. Antibiotics given within 1 hour. 30 mL/kg crystalloid completed within 2 hours. Now MAP 72 with HR still 104 and lactate trending 2.4 → 2.2.

Diagnosis (NANDA-I–aligned)

Risk for Shock related to active sepsis with hemodynamic warning signs (HR > 100, lactate elevation), capillary leak, and ongoing inflammatory response.

(Risk-for diagnoses use “related to” only — no “as evidenced by.”)

Goals

  • The patient maintains MAP ≥ 65 mm Hg without vasopressor initiation.
  • Lactate continues to trend down and reaches < 2 mmol/L.
  • HR trends down toward baseline; urine output remains ≥ 0.5 mL/kg/hr.
  • The patient does not progress to septic shock during the shift.

Interventions and rationales

InterventionRationale
Continuous monitoring of HR, BP, MAP, SpO₂, RR, mental status, urine output.Catches progression to shock early.
Trend lactate at 2–6 hours post-resuscitation; recognize lactate clearance as a positive response marker.Lactate trajectory predicts outcome better than a single value.
Use the facility sepsis screening tool every shift.Standardized screening catches deterioration earlier than gestalt.
Coordinate ongoing source control — for cellulitis, monitor erythema border, mark progression, escalate for necrotizing soft-tissue infection signs (pain out of proportion, bullae, crepitus, rapid spread).Source progression drives shock progression.
Maintain euvolemia — avoid blind continued fluid administration if hemodynamics are improving.Over-resuscitation increases pulmonary edema risk in sepsis.
Coordinate ICU-evaluation criteria with the provider — pre-define the threshold for transfer.Pre-defined criteria prevent delayed escalation.
Educate the patient and family on the recognition and response plan.Reduces anxiety; supports family advocacy if deterioration occurs.

Evaluation

  • Did the patient maintain MAP ≥ 65 mm Hg without vasopressors?
  • Is lactate trending toward normal?
  • Was deterioration caught early if it occurred?

Care Plan #4 — Hyperthermia

Fever is one of the most NCLEX-tested signs of sepsis, and it’s a real driver of metabolic demand. Hypothermia is the opposite-side sepsis red flag (especially in older adults).

Scenario. A 41-year-old patient admitted with pyelonephritis-related sepsis. T 39.5 °C, HR 116, BP 118/72, RR 22, rigors, severely flushed. Antibiotics in. Antipyretics given. Patient reports “feeling like I’m on fire.”

Diagnosis (NANDA-I–aligned)

Hyperthermia related to active sepsis with systemic inflammatory response, as evidenced by T 39.5 °C, tachycardia, rigors, flushed skin, and patient-reported sensation of overheating.

Goals

  • The patient reports improved comfort, avoids shivering, and maintains adequate hydration during the febrile period.
  • The patient shows no worsening hemodynamic, respiratory, or mental-status signs during the febrile period.
  • The patient and family verbalize that fever management in sepsis is primarily about comfort and safety — the goal is not necessarily to normalize temperature unless clinically indicated. SSC 2026 suggests against antipyretic therapy for the purpose of improving clinical outcomes in sepsis; antipyretics may still be used for pain, comfort, or other appropriate indications.

Interventions and rationales

InterventionRationale
Monitor temperature q4h (and PRN); track HR, BP, RR, SpO₂, mental status for sepsis progression.Fever-response tracking overlaps with sepsis screening.
Administer antipyretic (acetaminophen) per provider order for comfort, pain, or other appropriate indications — not to normalize temperature. Review total daily acetaminophen dose for hepatotoxicity risk.SSC 2026 suggests against routine antipyretic therapy to improve sepsis outcomes; dosing limits prevent harm.
Maintain adequate hydration per provider order — IV fluids or PO. Fever increases insensible fluid losses; hydration needs rise during febrile illness.Replaces fluid loss.
Use comfort measures (light bedding, cool environment) but avoid driving shivering — shivering increases metabolic demand and counteracts comfort goals.Reduces patient distress without thermogenic counter-response.
Recognize hypothermia (T < 36 °C) in older adults or critically ill patients as a sepsis red flag — escalate if present.Hypothermia in sepsis is associated with higher mortality than hyperthermia.
Escalate if fever is accompanied by shock signs, worsening pain, rising lactate, or mental-status change — don’t wait for the 72-hour rule.Deteriorating clinical signs override time-based thresholds.
Teach the family about fever as immune response and the comfort-focused antipyretic goal.Reduces unnecessary anxiety.

Evaluation

  • Did the patient report improved comfort and avoid shivering?
  • Did hydration remain adequate, and did hemodynamic, respiratory, and mental status remain stable?
  • Did the patient and family teach back the fever-comfort principle (not zero-fever)?

Care Plan #5 — Acute Confusion (Sepsis-Associated Encephalopathy)

Sepsis-associated encephalopathy (SAE) is a hallmark of severe sepsis. Cerebral microvascular dysfunction + cytokines + metabolic derangements produce delirium that is often the earliest sign of decompensation in older adults.

Scenario. A 78-year-old patient admitted with abdominal sepsis from cholangitis. Baseline alert and oriented. On day 2, the patient is suddenly agitated, attempting to climb out of bed, pulling at IV lines, oriented only to self. T 38.7 °C, HR 112, BP 96/58 (MAP 71), lactate 3.0. Family reports she’s never been like this before.

Diagnosis (NANDA-I–aligned)

Acute Confusion (Sepsis-Associated Encephalopathy) related to cerebral hypoperfusion, systemic inflammatory mediators, metabolic derangements, and sepsis progression, as evidenced by new altered mental status from baseline alert, agitation, disorientation, and behavioral change reported by family.

Goals

  • Within 8–24 hours of sepsis source control + supportive care, the patient’s mental status returns toward baseline.
  • The patient remains safe — no falls, no self-extubation, no line dislodgement.
  • The family is supported and informed throughout the delirium episode.

Interventions and rationales

InterventionRationale
Reorient frequently — visible clock, familiar voices, photos, glasses and hearing aids on.Non-pharmacologic delirium management is first-line.
Maintain a safe environment — low bed, bed alarm, padded rails, frequent rounding.Falls are the dominant safety risk in delirium.
Minimize sedating medications when clinically possible per provider order. Avoid benzodiazepines unless specifically indicated (alcohol withdrawal, status epilepticus).Benzodiazepines worsen delirium in older adults.
Address pain — under-treated pain worsens delirium.Multimodal pain management reduces delirium.
Promote day-night cycling — daytime activity, light, family visits; nighttime quiet, dim lights, clustered care.Sleep-wake cycle disruption drives ICU delirium.
Monitor for medical causes of new confusion — hypoglycemia, hypoxia, hypercapnia, electrolyte derangements, dehydration, urinary retention, fecal impaction, medication side effects.These are reversible delirium drivers.
Coordinate family presence — familiar voices reduce delirium duration.Family-centered care improves outcomes.
Document CAM-ICU or CAM delirium screen per facility protocol; trend score.Standardized delirium screening catches subtle subsyndromal delirium.

Evaluation

  • Is the patient’s mental status returning toward baseline?
  • Did the patient remain safe (no falls, no self-removal of lines)?
  • Were reversible delirium drivers identified and addressed?

Priority Nursing Diagnosis for Sepsis (Top 3 You Must Know)

If you remember nothing else for exams or clinicals—focus on these:

PriorityNursing DiagnosisRelated ToAs Evidenced By
1Ineffective Tissue PerfusionVasodilation, capillary leakHypotension, confusion, oliguria
2Impaired Gas ExchangeInflammatory response, ARDS riskHypoxia, tachypnea
3Deficient Fluid VolumeCapillary leak, feverTachycardia, low BP
4HyperthermiaInfectionFever, chills
5Risk for ShockSepsis progressionUnstable vitals
6Acute ConfusionReduced cerebral perfusionAltered LOC
7Risk for InfectionInvasive lines, immunosuppressionRisk factors present
8Deficient KnowledgeLack of understandingQuestions, nonadherence

Sepsis vs Septicemia vs Septic Shock

TermWhat it Means
SepticemiaPresence of bacteria in the bloodstream (older/non-specific term)
SepsisOrgan dysfunction due to dysregulated response to infection
Septic ShockSevere sepsis with persistent hypotension requiring vasopressors and lactate >2 mmol/L despite fluid resuscitation

Stages of shock

Shock progresses through four stages — useful for thinking about where your patient is on the trajectory:

StageHemodynamicsClinical picture
InitialDecreased perfusion at the cellular level; clinical signs subtleLactate may rise; subtle mental status change; warm skin (distributive shock)
CompensatoryBody activates baroreceptors and SNS — tachycardia, vasoconstriction, increased respiratory rate, ADH and aldosterone release“Warm shock” → “cool shock” transition; SBP may still be near-normal; lactate trending up; reduced urine output
ProgressiveCompensation fails — hypotension, severe hypoxia, organ dysfunction, profound lactic acidosisMAP < 65 despite fluids → vasopressor requirement; ARDS, AKI, delirium, coagulopathy
RefractoryIrreversible end-organ damage; multi-organ failurePersistent shock despite maximum therapy; mortality very high; supportive only

DIC in sepsis

Sepsis-associated disseminated intravascular coagulation (DIC) is a serious complication. Here’s what’s actually happening:

  1. Endothelial damage from sepsis exposes tissue factor, which activates the extrinsic coagulation cascade
  2. Microthrombi form throughout the microvasculature — they worsen organ ischemia and AKI
  3. Coagulation factors and platelets are consumed faster than the body can produce them
  4. Result: simultaneous microvascular thrombosis (worsening organ failure) and bleeding (low platelets, low fibrinogen, prolonged PT/aPTT, elevated D-dimer)

Use the ISTH DIC score to risk-stratify. Treatment is the underlying cause + supportive care: transfusion when bleeding or pre-procedurally; anticoagulation only in select thrombotic phenotypes per specialist.

Post-sepsis syndrome

Sepsis survivors face significant long-term consequences — a topic that’s been increasingly recognized over the past decade.

Common post-sepsis sequelae:

  • Cognitive impairment — memory problems, executive function decline
  • Anxiety, depression, PTSD-like symptoms
  • Functional decline — sometimes requiring rehabilitation
  • Increased risk of recurrent sepsis
  • Increased mortality risk for ~ 12 months post-discharge
  • Cardiovascular events
  • Post-ICU syndrome in ICU survivors (cognitive, physical, mental health)

Nursing role at discharge:

  • Connect with primary care for follow-up within 1–2 weeks
  • Refer to physical / occupational therapy when functional decline is present
  • Screen for depression and anxiety; refer to behavioral health
  • Provide written discharge instructions including “what is sepsis” educational materials for the patient and family
  • Connect with sepsis survivor support resources (Sepsis Alliance, ICU recovery clinics where available)

Escalation red flags

SignConcernAction
Positive facility sepsis screenSepsisActivate facility sepsis pathway (SSC 2026 — severity-based antimicrobial timing)
Lactate ≥ 2 (especially rising despite resuscitation)Tissue hypoperfusion / sepsisProvider notification; reassess source control, volume status
MAP < 65 unresponsive to fluidsSeptic shockVasopressors per provider; ICU evaluation
MAP < 65 with vasopressor requirement + lactate > 2 despite resuscitationSeptic shock (Sepsis-3 definition)ICU admission; consider hydrocortisone per SSC
Hypothermia (T < 36 °C) in critically ill patientSepsis red flag — higher mortality than hyperthermiaActive warming per facility; aggressive sepsis pathway
New altered mental status in known sepsis patientSepsis-associated encephalopathy / progressionProvider notification; rule out other causes (hypoglycemia, hypoxia, electrolytes)
Bilateral pulmonary infiltrates + PaO₂/FiO₂ ≤ 300Sepsis-induced ARDSLung-protective ventilation; ICU
Cellulitis with pain out of proportion, bullae, crepitus, rapid spreadNecrotizing soft-tissue infectionVascular surgery / general surgery emergency
Fever in neutropenic patient (T ≥ 38.3 °C, ANC < 500)Neutropenic sepsisBlood cultures + empiric broad-spectrum antibiotics within 1 hour
Platelets dropping with prolonged PT/aPTT and elevated D-dimerDICProvider notification; ISTH DIC score; supportive transfusion if bleeding
Patient with septic shock not responding to vasopressors after 6 hoursRefractory shock / advanced multi-organ failureICU optimization; consider mechanical circulatory support per specialist; goals-of-care conversation

Discharge and patient teaching

TopicWhat to teach
What is sepsisSepsis is a life-threatening organ dysfunction from infection. The patient survived a serious illness.
Return precautionsFever, new confusion, decreased PO intake, decreased urine output, increasing pain, new wound drainage, signs of recurrent infection. Call provider or return to ED.
Post-sepsis syndromeIt’s common to feel cognitive symptoms, fatigue, anxiety, depression for months after a sepsis admission. These are real and addressable.
AntibioticsFinish the prescribed course. Don’t share antibiotics. Watch for side effects (rash, diarrhea, kidney effects).
Wound or surgical site care (if applicable)Hand hygiene, dressing changes per discharge instructions, signs of recurrent infection.
Hand hygiene and infection preventionWHO 5 Moments framework simplified for the patient — wash before eating, after using the restroom, after wound care, before touching the face.
VaccinesInfluenza annually; pneumococcal, RSV, COVID-19 per ACIP.
Follow-upPrimary care within 1–2 weeks; specialty referrals as appropriate; consider sepsis-survivor / ICU recovery resources.
RehabPT / OT referral if functional decline is present.
Mental healthAnxiety, depression, PTSD-like symptoms are common after sepsis — connect with behavioral health when needed. Family support matters too.

Practice question

A nurse is caring for a 70-year-old patient with confirmed pneumonia, T 38.8 °C, HR 112, BP 90/58 (MAP 69), RR 26, lactate 3.4, and new confusion. The patient has received 30 mL/kg crystalloid over the past 90 minutes; MAP is now 64. Which nursing actions are appropriate? (Select all that apply.)

  • A. Activate the facility sepsis pathway and notify the provider
  • B. Repeat lactate measurement to assess for clearance
  • C. Withhold vasopressors until the patient transfers to ICU and gets a central line
  • D. Coordinate empiric broad-spectrum antibiotics if not yet administered
  • E. Prepare to initiate peripheral norepinephrine per provider order while ICU transfer is arranged

Answer: A, B, D, E.

  • A — Positive facility sepsis screen with persistent MAP < 65 despite fluid resuscitation; activate pathway.
  • B — SSC 2026 recommends re-measuring lactate when the initial is > 2 mmol/L to assess clearance.
  • D — Antibiotics within 1 hour are required for septic shock per SSC 2026.
  • E — Peripheral norepinephrine is acceptable short-term per recent evidence; central line is preferred but should not delay vasopressor initiation when shock is recognized.
  • C — Incorrect. Delaying vasopressors to wait for central access in a patient with septic shock is associated with worse outcomes. Peripheral norepinephrine can and should be initiated.

FAQs

What is the priority nursing diagnosis for sepsis?

Ineffective Tissue Perfusion is the canonical high-priority nursing diagnosis for sepsis. The distributive-shock mechanism (vasodilation, capillary leak, microvascular dysfunction) makes perfusion the central physiological problem. Other commonly used NANDA-I-aligned labels include Impaired Gas Exchange, Risk for Shock, Hyperthermia, and Acute Confusion (sepsis-associated encephalopathy). These are NANDA-I–aligned educational labels — verify exact wording against the licensed NANDA-I 2024–2026 text required by your school or facility.

What’s the difference between sepsis and septic shock?

Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection (Sepsis-3, 2016). Septic shock is sepsis plus persistent hypotension requiring vasopressors to maintain MAP ≥ 65 mm Hg and lactate > 2 mmol/L despite adequate fluid resuscitation. Septic shock has a mortality of about 40% compared to about 10% for sepsis without shock.

What is the MAP target in sepsis?

SSC 2026 generally uses an initial MAP target around 65 mm Hg, with 60–65 mm Hg sometimes appropriate for adults ≥ 65 with septic shock rather than higher MAP targets. Verify with provider for patients with chronic hypertension or other reasons to use a higher individualized target. Calculate MAP = (SBP + 2 × DBP) / 3 or MAP = DBP + ⅓ × (SBP − DBP).

How quickly should antibiotics be given in sepsis?

Per Surviving Sepsis Campaign 2026: administer antimicrobials immediately, ideally within 1 hour of recognition, for septic shock or high-likelihood sepsis without shock. For possible sepsis without shock, perform a rapid time-limited evaluation; if concern persists, give antimicrobials within 3 hours from when sepsis was first suspected (per provider order and facility policy). Don’t delay therapy for cultures in severely ill patients — collect rapidly and start empiric broad-spectrum coverage.

What’s the difference between qSOFA, SOFA, and SIRS?

SIRS (Systemic Inflammatory Response Syndrome) is the older framework — T > 38 or < 36, HR > 90, RR > 20 or PaCO₂ < 32, WBC abnormal. Sensitive but not specific. SOFA (Sequential Organ Failure Assessment) is the formal organ-dysfunction score used in the Sepsis-3 definition (≥ 2 increase from baseline). qSOFA is the bedside short version (RR ≥ 22, altered mental status, SBP ≤ 100) — useful for escalation cues but should not be used alone as the screening tool per SSC 2026. Use your facility-approved screening tool (NEWS2, MEWS, SIRS-based, or organizational pathway).

What is post-sepsis syndrome?

Post-sepsis syndrome refers to the long-term consequences sepsis survivors face — cognitive impairment, anxiety, depression, PTSD-like symptoms, functional decline, and increased mortality risk for about 12 months post-discharge. It’s increasingly recognized and addressable through primary care follow-up, behavioral health, rehabilitation, and survivor support resources.


References

  1. Herdman TH, Kamitsuru S, Lopes CT (eds). NANDA International Nursing Diagnoses: Definitions and Classification, 13th ed., 2024–2026. Thieme. https://nanda.org/
  2. Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016. https://jamanetwork.com/journals/jama/fullarticle/2492881
  3. Evans L, Rhodes A, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021 (with 2026 update). Critical Care Medicine. https://journals.lww.com/ccmjournal/Fulltext/2021/11000/Surviving_Sepsis_Campaign__International.21.aspx
  4. National Institute for Health and Care Excellence (NICE). Suspected sepsis: recognition, diagnosis and early management — by population. NG253 (adults 16+ not pregnant), NG254 (under 16s), NG255 (pregnant or recently pregnant). Published November 19, 2025. NG253 · NG254 · NG255
  5. Centers for Disease Control and Prevention. Sepsis. https://www.cdc.gov/sepsis/index.html
  6. Levy MM, Evans LE, Rhodes A. The Surviving Sepsis Campaign Bundle: 2018 Update. Critical Care Medicine. https://journals.lww.com/ccmjournal/Fulltext/2018/06000/The_Surviving_Sepsis_Campaign_Bundle__2018_Update.32.aspx
  7. ARDS Definition Task Force; Ranieri VM, Rubenfeld GD, Thompson BT, et al. Acute Respiratory Distress Syndrome: The Berlin Definition. JAMA. https://jamanetwork.com/journals/jama/fullarticle/1160659
  8. Klompas M, Branson R, Cawcutt K, et al. Strategies to Prevent Ventilator-Associated Pneumonia, Ventilator-Associated Events, and Nonventilator Hospital-Acquired Pneumonia in Acute-Care Hospitals: 2022 Update. SHEA/IDSA/APIC. https://www.cambridge.org/core/journals/infection-control-and-hospital-epidemiology/
  9. Russell JA. Vasopressor Therapy in Critically Ill Patients with Shock. Intensive Care Medicine. https://link.springer.com/article/10.1007/s00134-019-05801-z
  10. Annane D, Renault A, Brun-Buisson C, et al. Hydrocortisone plus Fludrocortisone for Adults with Septic Shock (APROCCHSS). New England Journal of Medicine. https://www.nejm.org/doi/full/10.1056/NEJMoa1705716
  11. Prescott HC, Angus DC. Enhancing Recovery from Sepsis: A Review. JAMA. https://jamanetwork.com/journals/jama/fullarticle/2670759
  12. National Library of Medicine (NCBI Bookshelf). Sepsis. https://www.ncbi.nlm.nih.gov/books/NBK547669/

Source notes. NANDA-I diagnoses, definitions, defining characteristics, and related / risk factors should be verified in the licensed NANDA-I 2024–2026 text before clinical documentation. The Surviving Sepsis Campaign, NICE NG253/NG254/NG255 (by population), SHEA/IDSA/APIC VAP/HAP guidance, and ACIP vaccine recommendations are updated periodically — cite the most current edition.

Mike Linares, MSN RN headshot
Written by:
Owner & Founder

Education: Associate Degree in Nursing, Cerritos Nursing School Master of Science in Nursing, Capella University | Specialization: Nursing Education

Mike Linares has over a decade of experience in the medical field, beginning with four years as an ambulance worker in Orange County followed by another four years as an EMT, during which he also taught EKG for paramedics.

Mackenzie Butler, DNP, MSN, RN-BC
Medically reviewed on June 10, 2026 by:
Head of Nursing

Education: Doctor of Nursing Practice, Indiana State University Master's of Science in Nursing Management & Leadership, Western Governors University

Mackenzie has spent over a decade leading high-impact nursing programs.

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