Sepsis and Septic Shock Nursing Care Plan

Nursing Diagnosis 1: Ineffective Tissue Perfusion

Tissue Perfusion Alteration related to Sepsis (Sepsis-3 definition: life-threatening organ dysfunction from a dysregulated host response to infection); septic shock if persistent hypotension requiring vasopressors to maintain MAP ≥ 65 with lactate > 2 mmol/L as evidenced by MAP < 65 mmHg despite ordered crystalloid resuscitation; Serum lactate > 2 mmol/L (initial 4.2 mmol/L); Mottled, cool extremities with capillary refill > 3 sec; Urine output < 0.5 mL/kg/hr × 2 consecutive hours; Altered level of consciousness, new confusion.

Interventions

• Monitor MAP continuously via arterial line per facility protocol; document at intervals matched to titration activity.
• Draw serum lactate on recognition and repeat at 2–4 hours per provider order; trend until within ordered parameters.
• Measure urine output hourly via indwelling catheter; notify the provider for UOP < 0.5 mL/kg/hr for 2 consecutive hours. Sustained UOP < 0.5 mL/kg/hr for ≥ 6 h can meet KDIGO Stage 1 AKI by urine-output criterion.
• Assess capillary refill, skin mottling (mottling score 0–5), and peripheral temperature at intervals matched to clinical acuity.
• Assess level of consciousness, orientation, and behavior every 1–2 hours using GCS or A&O × 4 per facility protocol.
• Monitor central venous pressure (CVP) and dynamic measures (PPV, SVV, passive leg raise) when available to support fluid-responsiveness assessment.
• Administer ordered crystalloid (commonly an initial 30 mL/kg of balanced solution within 3 hours per SSC 2021) per provider direction and facility protocol; monitor MAP, lactate, lung exam, and urine output after each bolus.
• Administer norepinephrine as ordered through central access when available; per SSC 2021, vasopressor initiation should not be delayed while central access is being obtained. Short-term peripheral administration through an appropriate large-bore IV in a proximal upper-extremity vein is acceptable per facility policy with active monitoring for extravasation.
• Administer vasopressin as ordered when added to a norepinephrine regimen (a common trigger range is norepinephrine approximately 0.1–0.5 mcg/kg/min, institution-specific) as a fixed (non-titrated) infusion.
• Monitor vasopressor infusion sites continuously for blanching, pain, or coolness; escalate per facility protocol and administer phentolamine as ordered for extravasation.
• Maintain head of bed at 30° unless contraindicated and reposition per facility protocol.
• Orient the patient and family to the ICU environment, monitors, and vasopressor lines; explain in plain language what common alarms mean.
• Educate the family on the goal of MAP within ordered parameters, the role of vasopressor support, and what ‘weaning the pressor’ means.
• Teach the patient (when awake) to report dizziness, chest pain, palpitations, or new visual changes promptly.
• Findings such as MAP below ordered parameters despite multiple vasopressors, lactate failing to clear, or new vasopressor-refractory shock should prompt urgent provider notification. Refractory shock may support consideration of hydrocortisone per SSC 2021.
• Coordinate with the provider team for source control (drainage, debridement, line removal) as soon as medically and logistically feasible.
• Notify the provider for sustained lactate > 4 mmol/L, anuria, or new altered mental status. Coordinate transfer to a higher level of monitoring or care per facility protocol when indicated.

Outcome: MAP is monitored and reported within ordered parameters on titrated vasopressor support; Lactate trend is documented and reported to the provider team; Urine output is monitored and reported per facility protocol.

Nursing Diagnosis 2: Impaired Breathing

Hyperthermia related to Sepsis (Sepsis-3 definition: life-threatening organ dysfunction from a dysregulated host response to infection); septic shock if persistent hypotension requiring vasopressors to maintain MAP ≥ 65 with lactate > 2 mmol/L as evidenced by Temperature > 38.3 °C (101 °F) or < 36 °C (96.8 °F); Rigors, diaphoresis, or shivering; Skin warm and flushed (hyperthermic phase) or cool and clammy (hypothermic phase); Tachycardia disproportionate to temperature; Patient-reported chills, malaise, or ‘feeling cold to the bone’.

Interventions

• Measure core temperature (bladder, esophageal, or rectal) at intervals matched to clinical acuity and facility protocol during active resuscitation.
• Identify and document the suspected infectious source on admission (lungs, urine, abdomen, skin/soft tissue, BSI, CNS, line).
• Assess for rigors, shivering, diaphoresis, and patient-reported chills.
• Monitor HR, RR, and SpO₂ in relation to temperature.
• Recognize hypothermic (cold) sepsis as a higher-mortality phenotype and escalate per facility protocol.
• Coordinate ≥ 2 sets of blood cultures from 2 separate sites (peripheral plus line, or 2 peripheral) before antibiotics when no significant delay is expected, per SSC 2021 and facility protocol.
• Administer broad-spectrum empirical antibiotics as ordered within the provider-directed window (commonly within 1 hour of recognition for septic shock or probable sepsis per the hour-1 bundle; within 3 hours for possible sepsis without shock if work-up is pending) per facility protocol.
• Apply tepid sponging, cooling blankets, or targeted temperature management as ordered for T > 39.5 °C; warmed blankets or a forced-air warmer as ordered for T < 36 °C.
• Administer scheduled acetaminophen as ordered for febrile comfort; clarify with the provider when NSAIDs are considered in the setting of AKI or GI bleed risk.
• Replace fluids as ordered during defervescence sweats; document insensible losses.
• Explain the rationale for drawing cultures before antibiotics and the importance of completing the ordered antibiotic course.
• Educate the family on the difference between fever as a defensive response and dangerously high temperature; reassure that fever alone does not equal worsening.
• Teach the patient (when awake) to report new chills, rigors, or feeling colder despite warming blankets promptly.
• Notify the provider for failure to defervesce by 48–72 h on appropriate antibiotics or for a new cold-sepsis presentation.
• Coordinate with infectious disease and pharmacy for antibiotic de-escalation at 48–72 h based on culture results and PCT trend per facility protocol.

Outcome: Core temperature is monitored and reported within ordered parameters; Rigors, shivering, and new diaphoresis are assessed and reported; HR is monitored as temperature trends; changes are reported per facility protocol.

Nursing Diagnosis 3: Fluid Volume Deficit

Fluid Volume Deficit related to Sepsis (Sepsis-3 definition: life-threatening organ dysfunction from a dysregulated host response to infection); septic shock if persistent hypotension requiring vasopressors to maintain MAP ≥ 65 with lactate > 2 mmol/L as evidenced by MAP < 65 mmHg before resuscitation; HR > 110 bpm with narrow pulse pressure; Capillary leak with bilateral peripheral and pulmonary edema (paradoxical); Third-spacing: anasarca, ascites, dependent edema; Dry mucous membranes, decreased skin turgor (early).

Interventions

• Maintain strict hourly intake and output; calculate cumulative balance per shift and over 24/48/72 hours per facility protocol.
• Report dynamic measures of fluid responsiveness (passive leg raise, pulse pressure variation, stroke volume variation) before each additional fluid bolus when available.
• Monitor for capillary leak: rapidly developing peripheral edema, anasarca, conjunctival edema, scrotal or labial edema.
• Auscultate lung sounds at intervals matched to clinical acuity during resuscitation; report new crackles or worsening oxygen requirement.
• Trend BUN, creatinine, sodium, chloride, and bicarbonate per provider order during active resuscitation.
• Administer ordered crystalloid (commonly an initial 30 mL/kg of balanced solution within 3 hours per SSC 2021) per provider direction and facility protocol.
• After the initial bolus, administer further fluid as ordered when dynamic assessment supports fluid responsiveness.
• Coordinate with the provider team when MAP is not responding to fluid alone; vasopressor initiation may be considered rather than continuing repeated boluses.
• Ensure adequate IV access (commonly two large-bore peripheral lines or central access for vasopressors) per facility protocol.
• Administer albumin 5% as ordered for patients receiving large-volume crystalloid (commonly > 4–6 L) per SSC 2021 weak recommendation and provider direction.
• Educate the patient and family on the dual goals of restoring perfusion and avoiding fluid overload; explain why edema does not always mean ‘too much fluid.’
• Teach the patient (when awake) to report new shortness of breath, chest tightness, or a feeling of drowning.
• Explain the role of daily weights and I&O once stable, particularly during the de-resuscitation phase.
• Notify the provider for net positive balance > 10% of body weight, new pulmonary edema, or worsening oxygenation despite ongoing hypotension.
• Coordinate de-resuscitation (diuresis or ultrafiltration) per provider order once perfusion is restored and source is controlled.

Outcome: MAP is monitored and reported within ordered parameters after ordered crystalloid resuscitation; HR is monitored as trends improve; pulse pressure is assessed and reported; Urine output is monitored and reported per facility protocol.

Nursing Diagnosis 4: Impaired Gas Exchange

Gas Exchange Impairment related to Sepsis (Sepsis-3 definition: life-threatening organ dysfunction from a dysregulated host response to infection); septic shock if persistent hypotension requiring vasopressors to maintain MAP ≥ 65 with lactate > 2 mmol/L as evidenced by Tachypnea > 22/min (qSOFA criterion); Increasing oxygen requirement (for example, NC → HFNC); PaO₂/FiO₂ ratio < 300 (mild ARDS < 300, moderate < 200, severe < 100); Bilateral infiltrates on CXR not explained by cardiac failure; Use of accessory muscles, intercostal retractions.

Interventions

• Monitor SpO₂ continuously and document RR, depth, effort, and accessory-muscle use at intervals matched to clinical acuity and facility protocol.
• Calculate and trend PaO₂/FiO₂ ratio with each ABG; report worsening trend to the provider team.
• Auscultate lung sounds at intervals matched to clinical acuity; document distribution of crackles, wheezes, or absent sounds.
• Review serial chest imaging for bilateral infiltrates not explained by cardiac failure when available.
• Monitor ABG per provider order during active respiratory failure; report pH, PaO₂, PaCO₂, and base deficit.
• Administer supplemental oxygen as ordered and titrate within provider parameters to support SpO₂ in the ordered range (commonly 92–96% to avoid liberal hyperoxia).
• Escalate stepwise (NC → high-flow nasal cannula → NIV → intubation) as ordered, based on response and work of breathing per facility protocol.
• Position the patient in high-Fowler’s when tolerated; prepare for and assist with prone positioning per facility protocol when ordered for moderate-to-severe ARDS (commonly considered at P/F < 150 once intubated).
• Coordinate with respiratory therapy and the provider team to support lung-protective ventilation per ARDSnet protocol and provider orders (commonly V_T 4–8 mL/kg predicted body weight, P_plat < 30, driving pressure < 15).
• Maintain HOB at 30° when supine, provide oral care with chlorhexidine per facility VAP-prevention protocol, support daily SAT/SBT per provider order, and ensure DVT and stress-ulcer prophylaxis are administered as ordered.
• Teach the patient and family the meaning of escalating oxygen devices and the goals of each step.
• Educate the patient (when awake) on pursed-lip and diaphragmatic breathing as a self-management tool while on NC or HFNC.
• Educate the family on what intubation involves, the expected ICU course, and signs of recovery to anticipate.
• Notify the provider for SpO₂ below ordered parameters on > 6 L NC, RR > 30 with retractions, or P/F dropping below 200.
• Coordinate with respiratory therapy and the intensivist for prone positioning, neuromuscular blockade per facility protocol in severe ARDS, or ECMO consultation when refractory hypoxemia is the dominant problem.

Outcome: SpO₂ is monitored and reported within ordered parameters on the lowest support that meets the goal; PaO₂/FiO₂ ratio is monitored and trend is reported per facility protocol; Respiratory rate is monitored and accessory-muscle use is reported.

Nursing Diagnosis 5: Impaired Kidney Function

Renal Alteration related to Sepsis (Sepsis-3 definition: life-threatening organ dysfunction from a dysregulated host response to infection); septic shock if persistent hypotension requiring vasopressors to maintain MAP ≥ 65 with lactate > 2 mmol/L as evidenced by Pre-resuscitation hypotension with MAP < 65; Lactate > 4 mmol/L on presentation; Rising creatinine ≥ 0.3 mg/dL within 48 h or 1.5× baseline; Urine output < 0.5 mL/kg/hr for ≥ 6 h; Nephrotoxic exposures: aminoglycosides, vancomycin trough, IV contrast.

Interventions

• Measure urine output hourly; calculate per kilogram per facility protocol.
• Trend serum creatinine and BUN at least daily; compare to baseline when available (commonly look back 7–365 days).
• Monitor potassium, phosphate, bicarbonate, calcium, and magnesium per provider order in evolving AKI.
• Review the medication list daily with the provider team or pharmacy for nephrotoxic agents and renal dosing.
• Evaluate for AEIOU indications for RRT: Acidosis, Electrolyte derangement, Ingestion (toxic), Overload (fluid), Uremia.
• Support MAP within ordered parameters with ordered fluid resuscitation and vasopressor administration per facility protocol.
• Administer ordered balanced crystalloid (LR or Plasma-Lyte) per provider direction when large-volume resuscitation is needed.
• Coordinate with pharmacy for renal dose adjustment of antibiotics per facility protocol; alert the provider when nephrotoxic alternatives exist.
• Hold ACE-I, ARB, and NSAIDs per provider order during acute illness.
• Prepare the patient and family for possible RRT (CRRT in ICU; IHD on the floor) when AKI progresses, per provider direction.
• Educate the patient and family on the role of the kidneys in sepsis and what AKI may mean for hospital course and recovery.
• Teach the patient and family the importance of avoiding NSAIDs and contrast after discharge until renal recovery is confirmed by the provider.
• Educate on long-term implications: outpatient nephrology follow-up, repeat creatinine, blood pressure control per facility discharge protocol.
• Notify the provider for UOP < 0.5 mL/kg/hr for 6 h, rising creatinine, hyperkalemia > 5.5, or worsening acidosis.
• Coordinate nephrology consultation for KDIGO Stage 2 or above per provider order and prepare for possible CRRT initiation per facility protocol.

Outcome: Urine output is monitored and reported per facility protocol; Creatinine and BUN trend is monitored and communicated to the provider team; Electrolytes (K⁺, HCO₃^–, phosphate) are monitored and changes are reported.

Sepsis is defined by Sepsis-3 (2016) as life-threatening organ dysfunction caused by a dysregulated host response to infection, operationalized as an acute increase of ≥ 2 SOFA points. The older SIRS-based definition is obsolete; qSOFA (RR ≥ 22, altered mentation, SBP ≤ 100) is a bedside prompt for further assessment and is not a screening tool on its own. Pathophysiology begins when pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) activate pattern-recognition receptors, triggering a massive cytokine release (TNF-α, IL-1, IL-6). This cytokine storm produces widespread endothelial dysfunction, glycocalyx degradation, and increased capillary permeability. The result is profound systemic vasodilation, third-spacing of intravascular fluid, microvascular thrombosis from coagulation-fibrinolysis imbalance, and impaired oxygen extraction at the tissue level. Tissue hypoperfusion drives anaerobic metabolism, lactate accumulation, and progressive multi-organ dysfunction (AKI, ARDS, hepatic dysfunction, DIC, sepsis-induced cardiomyopathy, encephalopathy). Septic shock is the subset with persistent vasopressor-dependent hypotension (MAP < 65) and lactate > 2 mmol/L despite adequate fluid resuscitation, carrying in-hospital mortality of > 40% per the Surviving Sepsis Campaign 2021 guidelines.

• MAP target: ≥ 65 mmHg
• Lactate target: < 2 mmol/L & trending down
• Antibiotic door-to-drug: ≤ 1 hr (septic shock) per facility protocol
• Crystalloid bolus: 30 mL/kg within 3 hr per SSC 2021
• Hour-1 Bundle: All 5 elements per facility protocol

• Makic, M. B. F., & Martinez-Kratz, M. R. (Eds.). (2023). Ackley and Ladwig’s Nursing Diagnosis Handbook: An Evidence-Based Guide to Planning Care (13th ed.). Elsevier.
• Evans, L., Rhodes, A., Alhazzani, W., et al. (2021). Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Critical Care Medicine, 49(11), e1063–e1143.
• Singer, M., Deutschman, C. S., Seymour, C. W., et al. (2016). The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA, 315(8), 801–810.
• Centers for Disease Control and Prevention. (2024). Get Ahead of Sepsis. U.S. Department of Health & Human Services. https://www.cdc.gov/sepsis/