Sepsis & Severe Infections: A Primer for Nurses

William Kelly, MSN, FNP-C

Updated June 2026 · Medically reviewed for nurses

16 min read

Sepsis is a potentially life-threatening condition that occurs when the body mounts a systemic response to an infection. It isn't caused by one specific organism — any infection (bacterial, viral, or fungal) can trigger it, though most hospital cases come from severe bacterial infections.

According to the CDC, sepsis is a leading cause of death in the United States — an estimated 1.7 million cases and about 270,000 deaths each year. The mortality rate can be as high as 50% in severe cases, and is highest in patients over 75 with multiple comorbidities. Recognizing and managing sepsis early is one of the most important things a nurse can do.

What Is Sepsis?

Sepsis is a common clinical syndrome representing the body's response to a severe infection. You'll care for septic patients in any department, but especially the ER and ICU. It is a severe condition with a poor prognosis.

Early sepsis — while not clearly defined — is the presence of infection and bacteremia (bacteria in the blood), which can and likely will progress to sepsis without intervention. Recognizing and intervening early significantly improves outcomes.

SIRS & the Sepsis-3 Criteria

Sepsis used to be identified using SIRS criteria (Systemic Inflammatory Response Syndrome). This is now outdated and no longer used to diagnose sepsis, but you'll still hear it referenced in the hospital. SIRS was defined as two or more of:

Temperature

Above 100.4°F (38°C) or below 96.8°F (36°C).

Heart Rate

Above 90 beats per minute.

Respiratory Rate

Above 20 breaths/min, or PaCO₂ below 32 mmHg.

WBC Count

Above 12,000/mm³, below 4,000/mm³, or more than 10% immature neutrophils (bands).

Over time it became clear the SIRS criteria were not sensitive or specific enough to accurately diagnose sepsis, so they were replaced by the Sepsis-3 criteria.

The Sepsis-3 framework requires a suspected/confirmed infection plus an elevated lactate, and at least one marker of organ hypoperfusion:

What Is Septic Shock?

Septic shock is a type of distributive shock. Under severe distress, the body releases a flood of mediators and toxins that cause vasodilation, drop the circulating blood volume, and tank the blood pressure. It is generally diagnosed when the patient has a MAP <65 mmHg and a lactate >2.0 mmol/L, often after the initial fluid bolus.

Common Causes of Sepsis

Any untreated or antibiotic-resistant infection can become systemic. Severe viral or fungal infections can cause sepsis, but bacterial sources are far more common:

Urinary Tract Infection

A common cause in the elderly. A bladder infection (cystitis) can travel up to the kidneys (pyelonephritis) and become sepsis — known as urosepsis.

Pneumonia

Bacterial infection of the lungs. Untreated, it commonly causes sepsis — severe sepsis occurs in nearly half of patients admitted with pneumonia.

Cellulitis

Infection of the skin and surrounding tissue. Patients often have risk factors — obesity, diabetes, and other comorbidities — that raise their odds of becoming septic.

Nursing Assessment of Sepsis

Because sepsis isn't caused by one thing, symptoms depend on the underlying infection — but several findings are common to nearly all septic patients.

Fever & Chills

A true fever is >100.4°F (38°C); sepsis often runs even higher (102–104°F). Chills and tremors are frequently significant.

Weakness & Fatigue

Fighting infection drains energy. Because sepsis is a systemic response, the toll is even greater.

Altered Mental Status

From decreased brain perfusion and the systemic reaction — drowsiness, lethargy, or confusion. More common in older, sicker, or dehydrated patients.

Other symptoms point to the source: pneumonia (productive cough, dyspnea), UTI (dysuria, frequency, flank or suprapubic pain), cellulitis (redness, swelling — often the legs), abdominal abscess (abdominal pain), or diverticulitis (abdominal pain, diarrhea, bloody stools).

The physical exam is essential — these patients are often very sick or on their way there. Not everyone with sepsis has the same findings, and some have none, so a thorough head-to-toe assessment matters.

Vital Signs

Fever >100.4°F (may be hypothermic in severe sepsis); BP often low (SBP <90 or MAP <65 is worrisome); HR tachycardic (90–140); RR often >20; SpO₂ may be low with respiratory sources.

Inspection

Neuro: AMS. HEENT: dry mucous membranes. Resp: fast breathing, distress. Skin: pale or flushed, possible rashes, redness, or swelling.

Auscultation

Heart often rapid and regular. Lungs may have crackles and/or rhonchi if a respiratory infection is present.

Palpation

Faint peripheral pulses, delayed cap refill. Suprapubic tenderness (UTI), CVA tenderness (pyelo/stone), abdominal tenderness (abscess), or midline spinal tenderness (spinal abscess).

Nursing Interventions for Sepsis

When you suspect sepsis, timing is everything — many departments have quality metrics and protocols to move fast. The sooner you act, the better the patient's chance of survival.

Workup & Labs

There's no single test that confirms sepsis — it's a clinical syndrome. But several labs and imaging studies are commonly ordered.

CBC

WBC usually >12,000/mm³, though severe sepsis can cause leukopenia <4,000/mm³. Bands >10% are consistent with sepsis (a "left shift").

CMP

Checks for organ damage and clues to the source: kidney function (Cr, BUN), liver function, acid-base (anion gap, CO₂), glucose, and electrolytes. A CO₂ <18 suggests acidosis, likely lactic.

Coags

PT/INR and PTT detect clotting abnormalities. Severe sepsis can activate the clotting cascade and lead to DIC.

Blood Cultures

Aerobic and anaerobic cultures from two different sites — used for gram stain, culture, and antibiotic sensitivities.

Procalcitonin

A non-specific inflammation marker. Helps gauge response to antibiotics (especially bacterial respiratory infections) and when to de-escalate.

Lactic Acid

A lactate >2 mmol/L indicates lactic acidosis and decreased tissue perfusion. Repeated every 4–6 hours until normal. Use a gray top and transport on ice.

Urinalysis

A must for anyone with sepsis — UTIs are a very common source. Leukocyte esterase, WBCs, nitrites, and bacteria support a UTI. See how to interpret a UA.

Other Collections

Wound swabs (aerobic/anaerobic), sputum culture for productive cough, or stool studies (culture, O&P, C. diff) as symptoms dictate.

Chest X-ray

Almost always ordered to look for pneumonia or other abnormalities.

CT Abdomen/Pelvis

With contrast if abdominal signs or elevated liver enzymes — contrast better visualizes abscesses, assuming kidney function allows.

CT Thorax

Sometimes recommended after CXR — a chest X-ray has only ~43% sensitivity for pneumonia, so CT picks up infection a CXR may miss.

Treatment of Sepsis

The first priority is to stabilize the vital signs and provide support; the second is to give antibiotics to kill the bacteria. Because mortality is high, both happen fast.

IV Fluidscrystalloid bolus

All septic patients get a bolus of crystalloid fluids (normal saline or LR). The recommended dose is 30 mL/kg bolus — a 70 kg patient gets ~2,100 mL. Run it wide open (pressure bags if hypotensive), finished within the first 3 hours of presentation.

Antipyreticsfor fever

Reducing fever cuts fluid losses and improves symptoms. Options: Tylenol 650 mg q4–6h (or 1000 mg q8h) and Ibuprofen 600–800 mg q4–6h or another NSAID.

Antibioticswithin the first hour

Broad-spectrum antibiotics should be given within the first hour of arrival to the ER. Choice depends on history, risk factors, and suspected source — typically MRSA coverage (Vanco) plus a broad-spectrum agent. Common regimens: Vanco + Zosyn, Vanco + Cefepime, or Vanco + Imipenem. Antifungals may be added if the patient is neutropenic or high-risk (often per Infectious Disease).

Norepinephrine (Levophed)first-line vasopressor

Mechanism: stimulates beta-1 and alpha-adrenergic receptors, increasing contractility, heart rate, and vasoconstriction to raise systemic BP and coronary flow.
Sepsis dosing: 0.05–0.15 mcg/kg/min, titrated to MAP ≥65 mmHg. Max: 1–3.3 mcg/kg/min. Always follow facility protocol and orders.
Side effects: hypertension, tachycardia, palpitations, headache, nausea/vomiting, peripheral vasoconstriction.
Pressors can be started peripherally in a pinch but eventually need a central line (extravasation risk). They must be closely titrated by a critical care nurse, with the goal tied to the MAP — not the systolic.

Glucocorticoidsrefractory cases only

Steroids like Solu-Medrol are generally not recommended in sepsis, but may be ordered by the critical care physician if the patient doesn't respond to fluids and vasopressors.

Monitoring & Complications

Once interventions are underway, close monitoring catches both improvement and deterioration:

Lactic Acid

Trend an elevated lactate every 4–6 hours until it falls below 2 mmol/L.

WBC & Bands

Trend at least daily until resolution; usually decrease with fluids and antibiotics.

Urine Output

A foley tracks kidney perfusion closely. Goal: ≥0.5 mL/kg/hr.

Cardiac Monitor

Septic patients are tachycardic and at increased risk for arrhythmias and MI. Monitor per protocol.

Cultures & Sensitivities

Gram stain ~24h; growth in ~48–72h. Antibiotics may be narrowed based on sensitivities.

Hemodynamics

Watch BP and MAP for hypotension and response to fluids/pressors. Goal MAP ≥65 mmHg.

Worsening Perfusion

Assess per protocol for pallor and sweating, confusion, and worsening vital signs.

IV & Extremities

Pressors cause vasoconstriction — watch sites and digits for delayed cap refill, distal pallor/cyanosis, and fingertip necrosis.

Fluid Overload

Heavy fluids plus systemic stress strain the heart — watch for increased SOB, JVD, and crackles/rales, especially with cardiac history.

Related Guides

Emergency

Six Steps for Sepsis Management

Critical Care

Types of IV Fluids

Labs

ABGs: Blood Gas Interpretation

Critical Care

RSI & Intubation