Peritonitis nursing care: assessment, interventions, and NCLEX tips

Peritonitis — inflammation of the peritoneum — is one of the highest-stakes conditions nursing students encounter in clinical practice and on the NCLEX. It can develop as a complication of appendicitis, diverticulitis, bowel perforation, or abdominal surgery, and it escalates to sepsis, septic shock, and multi-organ failure with striking speed. Recognizing it early and responding with the right interventions can be the difference between a patient who recovers and one who doesn’t.

This reference covers the full clinical picture: pathophysiology, causes and classification (including the often-skipped tertiary type), nursing assessment from first complaint through deterioration, diagnostic workup, medical and surgical management, priority nursing interventions, complications to monitor, and high-yield NCLEX points.

Pathophysiology

The peritoneum is a thin serous membrane composed of two layers: the parietal peritoneum lining the abdominal and pelvic walls, and the visceral peritoneum covering the abdominal organs. Between them is the peritoneal cavity, which normally contains only a small amount of sterile serous fluid that lubricates the organs.

When bacteria, bile, gastric acid, bowel contents, or blood enter the peritoneal cavity, the peritoneum mounts a rapid inflammatory response. Inflammatory mediators — prostaglandins, leukotrienes, histamine — are released, triggering vasodilation, increased capillary permeability, and massive fluid shifts into the peritoneal space. This is the third-spacing phenomenon: large volumes of fluid move from the intravascular compartment into the peritoneal cavity and bowel wall, reducing effective circulating volume. A patient with peritonitis can sequester several liters of fluid within hours — which is why early, aggressive IV fluid resuscitation is a nursing priority.

Gut motility ceases as the inflammatory process spreads, producing paralytic ileus. Bowel distension worsens as gas and fluid accumulate. Simultaneously, bacteria and their endotoxins are absorbed through the inflamed peritoneum into the bloodstream, triggering the systemic inflammatory response syndrome (SIRS). Without source control and antibiotics, this cascade progresses to sepsis, septic shock, and multi-organ failure.

The parietal peritoneum is innervated by somatic sensory nerves — it can precisely localize pain. This explains why peritonitis causes exquisitely tender, well-localized abdominal pain that worsens dramatically with any movement or palpation.

Causes and classification

Primary peritonitis

Also called spontaneous peritonitis, primary peritonitis occurs without a clear identifiable intra-abdominal source. The most clinically important form is spontaneous bacterial peritonitis (SBP), which develops in patients with cirrhosis and ascites.

In SBP, the pathophysiology differs from secondary peritonitis. Patients with cirrhosis have impaired immune defenses: reduced opsonic activity of ascitic fluid (low complement and immunoglobulin levels), defective neutrophil function, and bacterial translocation from the gut. Intestinal bacteria — most often gram-negative organisms such as Escherichia coli and Klebsiella pneumoniae, and gram-positive organisms such as Streptococcus pneumoniae — translocate across the gut wall and seed the ascitic fluid via the bloodstream or lymphatics. SBP is diagnosed when ascitic fluid polymorphonuclear (PMN) cell count exceeds 250 cells/mm³. It carries a high mortality (10–30%) and frequently precipitates hepatorenal syndrome. Albumin infusion alongside antibiotics has been shown to reduce renal impairment and in-hospital mortality.

Secondary peritonitis

The most common type. Results from perforation or rupture of an abdominal organ releasing its contents into the peritoneal cavity. Common causes include:

• Perforated appendix — the most frequent cause in young adults; untreated appendicitis progresses to rupture within 24–72 hours
• Diverticular perforation — a common cause in older adults; a perforated diverticulum spills fecal material into the peritoneum
• Perforated peptic ulcer — gastric acid spills into the peritoneum; patients often describe sudden “tearing” epigastric pain
• Bowel perforation — from trauma, ischemic bowel, Crohn’s disease, or colorectal cancer
• Post-surgical — anastomotic leak, inadvertent enterotomy, or intra-abdominal abscess after abdominal surgery

Tertiary peritonitis

The least discussed type, but clinically important. Tertiary peritonitis is persistent or recurrent intra-abdominal infection that fails to resolve after adequate treatment of primary or secondary peritonitis. It typically occurs in critically ill, immunocompromised patients in the ICU. The organisms responsible are often resistant nosocomial pathogens — Candida species, Enterococcus, coagulase-negative staphylococci — which are poorly responsive to standard antibiotic regimens. Tertiary peritonitis carries very high mortality and represents a failure of host defenses rather than inadequate source control.

Nursing assessment

Subjective findings

The patient with peritonitis typically presents in obvious distress. Obtain a focused history:

• Pain: onset (sudden vs. gradual), character (sharp, stabbing, constant), location (diffuse vs. localized), radiation, aggravating factors (movement worsens pain significantly — patients often lie still and resist any touch)
• GI symptoms: nausea, vomiting, anorexia, last bowel movement, passage of gas
• Prior abdominal history: known appendicitis, diverticulitis, peptic ulcer disease, recent abdominal surgery, cirrhosis with ascites
• Fever or chills
• Timeline: how quickly symptoms developed (rapid onset suggests perforation; gradual onset may suggest SBP or localized infection)

Objective findings

Vital signs:

• Fever (>38.5°C / 101.3°F) — may be absent in immunocompromised patients or those on corticosteroids
• Tachycardia — early compensatory response to reduced circulating volume and pain
• Tachypnea — splinting (shallow breathing to minimize diaphragmatic movement) plus early sepsis
• Hypotension — a late and ominous sign indicating hypovolemia and/or distributive shock from sepsis; do not wait for hypotension to act

Abdominal examination — four hallmark findings:

1. Board-like rigidity: The abdominal wall muscles contract involuntarily in response to peritoneal irritation, producing a hardened, wooden abdomen on palpation. This is involuntary guarding — it persists even when the patient tries to relax.

2. Voluntary guarding: The patient consciously tenses the abdomen when the examiner’s hand approaches. Distinguish this from involuntary rigidity — both are significant, but rigidity is the more alarming finding.

3. Rebound tenderness (Blumberg’s sign): Apply slow, steady pressure to the abdomen, then release quickly. A sharp increase in pain on release — rebound tenderness — indicates parietal peritoneal irritation. The mechanism: rapid displacement of the inflamed parietal peritoneum on release triggers a burst of somatic pain signals. Blumberg’s sign is positive when pain is worse on release than on pressure. Report a positive Blumberg’s sign immediately.

4. Absent bowel sounds: Paralytic ileus develops as the inflammatory process inhibits peristalsis. Auscultate all four quadrants for at least one minute before documenting absent bowel sounds.

Additional findings:

• Abdominal distension — from ileus, fluid accumulation, and gas
• Tenderness on percussion — even light percussion causes significant pain
• Shifting dullness — if ascites is present (particularly relevant in SBP)
• Referred shoulder pain — diaphragmatic irritation from free peritoneal air or fluid can cause ipsilateral shoulder tip pain (Kehr’s sign)

Signs of sepsis progression:

• Altered mental status (confusion, agitation) — early sign of cerebral hypoperfusion
• Mottling, cool/clammy extremities — peripheral vasoconstriction in shock
• Decreased urine output (<0.5 mL/kg/hr) — renal hypoperfusion
• Rising lactate on serial measurements — tissue hypoxia; lactate ≥2 mmol/L triggers sepsis protocol

Diagnostic workup

Laboratory

Imaging

• Upright chest X-ray: Free air under the diaphragm (pneumoperitoneum) is diagnostic of bowel perforation; present in approximately 75% of perforated viscus cases. Upright position is essential — free air rises.
• CT abdomen/pelvis with contrast: Gold standard; identifies the source of perforation, extent of contamination, abscess formation, and bowel ischemia.
• Abdominal ultrasound: Useful in bedside assessment for free fluid; preferred in pregnant patients; less sensitive than CT for source identification.

Medical and surgical management

Antibiotic therapy

Empiric broad-spectrum IV antibiotics are started immediately after blood cultures are drawn — do not delay antibiotics waiting for imaging results. Standard coverage targets the gram-negative aerobes and anaerobes of the GI tract:

• Piperacillin-tazobactam (Zosyn) — first-line in many institutions; covers gram-negative rods, gram-positive organisms, and anaerobes
• Cefoxitin or cefotetan — second-generation cephalosporins with anaerobic coverage for community-acquired peritonitis
• Metronidazole (Flagyl) + ceftriaxone — common combination regimen
• Carbapenems (meropenem, imipenem) — reserved for health care-associated or tertiary peritonitis, known resistant organisms, or patients with recent antibiotic exposure
• Fluconazole or micafungin — added when Candida is isolated (tertiary peritonitis, immunocompromised patients)

For SBP: cefotaxime 2g IV every 8 hours for 5 days is the standard of care; albumin 1.5 g/kg IV on day 1 and 1 g/kg on day 3 reduces risk of hepatorenal syndrome.

Surgical intervention

Source control is the definitive treatment for secondary peritonitis. Options depend on the cause and patient stability:

• Exploratory laparotomy: open approach, allows thorough peritoneal washout, repair or resection of the perforated source
• Laparoscopic washout: minimally invasive; appropriate in select stable patients
• Damage control surgery: abbreviated initial surgery in hemodynamically unstable patients; definitive repair deferred to a second look operation
• Percutaneous drainage: CT-guided drainage of loculated abscesses when surgery is too high risk

NPO status is maintained from the time of diagnosis — the bowel must rest, and the patient is likely going to the operating room.

Nasogastric tube decompression

An NG tube to low intermittent suction decompresses the stomach and reduces the risk of aspiration in the ileus patient. It also reduces nausea and abdominal distension.

Nursing interventions

Priority nursing actions

1. Fluid resuscitation Third-spacing and NPO status rapidly deplete intravascular volume. Initiate IV access (two large-bore peripheral IVs, 18-gauge or larger) and administer IV crystalloids as ordered — typically isotonic saline (0.9% NaCl) or lactated Ringer’s. Monitor closely: large fluid volumes are often required in the first hours, but over-resuscitation worsens abdominal compartment syndrome and pulmonary edema. Target: urine output ≥0.5 mL/kg/hr.

2. Intake and output monitoring Insert a urinary catheter for accurate hourly urine measurements. Strict I&O is essential — output is the most reliable real-time indicator of fluid resuscitation adequacy. Document all sources of output: urine, NG drainage, emesis, wound drainage.

3. Pain management Pain control is both humane and diagnostically important. IV opioid analgesia (morphine, hydromorphone, fentanyl) is standard. Use a validated pain scale (0–10 NRS or CPOT in non-verbal patients) to reassess pain after each intervention and before and after procedures. Communicate changes in pain character or sudden worsening immediately — a sudden relief of pain followed by diffuse worsening can indicate perforation. Use SBAR when communicating pain changes to the provider:

• Situation: Patient reports sudden increase in pain severity (0→9/10) with diffuse spread
• Background: Admitted for localized peritonitis secondary to diverticular perforation 4 hours ago
• Assessment: Board-like rigidity now palpable in all four quadrants; HR 118, BP 94/60
• Recommendation: Requesting urgent provider evaluation for perforation/hemodynamic compromise

4. Positioning Place the patient in semi-Fowler’s position (head of bed 30–45 degrees). Rationale: gravity pools peritoneal exudate and free fluid in the pelvic cul-de-sac, the most dependent and best-drained area of the peritoneal cavity, limiting spread to the diaphragm and mediastinum. Semi-Fowler’s also reduces diaphragmatic compression from abdominal distension, easing breathing.

5. NPO status and NG tube care Maintain strict NPO. Provide oral hygiene every 2 hours (NPO patients are at high risk for oral dryness, cracking, and aspiration risk from dry secretions). For patients with an NG tube: confirm placement by aspirating gastric contents and checking pH (<5.5 confirms gastric placement); secure the tube to prevent pressure injury on the naris; document the character and volume of NG output; irrigate with 30 mL normal saline as ordered to maintain patency.

6. Vital signs and early sepsis recognition Monitor vital signs every 15–30 minutes in the acute phase. Apply SIRS criteria as a bedside screening tool:

• Temperature >38°C or <36°C
• Heart rate >90 bpm
• Respiratory rate >20 breaths/min
• WBC >12,000 or <4,000/mm³

Two or more SIRS criteria with a suspected infection = sepsis. Three or more = severe sepsis. Escalate immediately if sepsis criteria are met — activate your institution’s sepsis bundle (blood cultures, lactate, broad-spectrum antibiotics, fluid bolus, vasopressors if needed for refractory hypotension).

7. Post-surgical wound care After laparotomy, assess the wound at every care interaction. Watch for dehiscence (separation of wound edges — more common with distension and malnutrition), evisceration (protrusion of bowel through wound — cover immediately with sterile saline-moistened gauze), and infection (erythema, induration, purulent drainage, fever). Document drain output (character, volume, odor); notify the provider of any change in drain output character.

Nursing interventions table

Complications to monitor

Sepsis and septic shock: The most immediately life-threatening complication. Bacterial translocation from the inflamed peritoneum into the bloodstream triggers SIRS and sepsis. Watch for rising lactate, altered mental status, worsening hypotension unresponsive to fluids (septic shock), and oliguria.

Paralytic ileus: Inhibition of peristalsis by the inflammatory process. Manifests as absent bowel sounds, abdominal distension, inability to tolerate oral intake, and nausea/vomiting. Usually resolves as the underlying infection is treated; prolonged ileus requires prolonged NG decompression and parenteral nutrition.

Intra-abdominal abscess: Loculated pockets of infection may persist or develop after initial treatment, particularly after bowel perforation. Signs include persistent or new fever after apparent clinical improvement, localized abdominal pain, and elevated WBC on follow-up labs. CT-guided drainage or reoperation may be required.

Adhesion formation: Fibrosis of the peritoneal surfaces during healing creates adhesions — fibrous bands between visceral and parietal peritoneal surfaces. Adhesions are the most common cause of small bowel obstruction in adults (responsible for approximately 60–70% of cases) and may present months to years after the initial peritonitis episode.

Hepatorenal syndrome (in SBP): In patients with cirrhosis and SBP, the systemic inflammatory response and reduced effective arterial volume can trigger vasoconstriction of the renal vasculature, precipitating acute kidney injury. Early albumin infusion alongside antibiotics significantly reduces this risk.

Multi-organ failure: The end stage of uncontrolled sepsis. Renal failure (rising creatinine, oliguria), acute respiratory distress syndrome (ARDS), hepatic failure, coagulopathy (DIC), and cardiovascular collapse can develop in sequence or simultaneously. ICU-level care and organ support are required.

NCLEX tips

• Priority sign of peritonitis: Board-like abdominal rigidity (involuntary guarding) is the most critical physical finding — report it immediately and anticipate surgical intervention.
• Blumberg’s sign = rebound tenderness. Pain is worse on quick release of pressure than on application — this indicates parietal peritoneal irritation.
• Semi-Fowler’s position is the correct positioning for peritonitis — gravity drains peritoneal contents to the pelvis and limits upward spread.
• Absent bowel sounds in a peritonitis patient = paralytic ileus. Do not administer oral medications or fluids.
• Third-spacing removes large fluid volumes from circulation — anticipate the need for aggressive IV fluid resuscitation and monitor urine output hourly.
• Draw blood cultures before giving antibiotics — this is a consistent NCLEX priority. Starting antibiotics before cultures destroys the diagnostic value of cultures.
• Hypotension is a late sign in peritonitis. Tachycardia precedes hypotension — do not wait for hypotension to escalate concern.
• SBP in cirrhosis is diagnosed by paracentesis: PMN count >250 cells/mm³ in ascitic fluid. The patient may not have classic peritonitis signs — presentation is often subtle (mild abdominal discomfort, low-grade fever, worsening encephalopathy).
• NG tube placement: Confirm by aspirating and checking pH (<5.5 = gastric). Never use the auscultation/air injection method — it is no longer considered reliable.
• Tertiary peritonitis = persistent infection in ICU patients despite adequate treatment; associated with resistant organisms and high mortality. If NCLEX presents this scenario, think immunocompromised patient with Candida or resistant gram-positives.

Related conditions

Peritonitis most commonly develops as a complication of other abdominal conditions. The appendicitis nursing reference covers pre- and post-perforation assessment and the Alvarado scoring system. The diverticulitis nursing reference addresses the diverticular perforation pathway in detail. The bowel obstruction nursing reference covers ileus and obstruction, which often complicate peritonitis recovery. Once peritonitis escalates to systemic infection, the sepsis nursing reference applies directly — the assessment and bundle interventions overlap significantly.