Surgical sepsis & source control — recognition, resuscitation and definitive management

A 68-year-old smoker arrives hypotensive on fluids with a Hinchey IIb diverticular abscess and free fluid on CT. A 74-year-old cirrhotic arrives with septic shock from a perforated ulcer. Both are "septic surgical patients", but one needs antibiotics plus drainage with a hair-trigger for theatre, while the other needs an immediate operation framed by a bundle that shows no survival signal in cirrhosis. This page is the framework that tells those two apart — with the numbers that govern each decision.^[23][7]

Definition — Sepsis-3, and what it retired

Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection.^[1] Three deliberate breaks from the 2001 definitions sit inside that sentence: the excessive focus on inflammation was abandoned, the misleading model of sepsis marching as a continuum through "severe sepsis" to shock was rejected, and the systemic inflammatory response syndrome (SIRS) criteria were judged to have inadequate specificity and sensitivity.^[1] The task force concluded the term "severe sepsis" was redundant — it is retired, not redefined.^[1]

Operationally, organ dysfunction is an increase in the Sequential Organ Failure Assessment (SOFA) score of 2 points or more, which is associated with an in-hospital mortality greater than 10%.^[1] Septic shock is the subset of sepsis in which particularly profound circulatory, cellular and metabolic abnormalities are associated with a greater risk of mortality than with sepsis alone.^[1]

The surgical corollary is the complicated versus uncomplicated intra-abdominal infection distinction: uncomplicated disease stays within one organ, while complicated infection extends beyond it into peritonitis — and only the complicated form poses the source-control decisions this page exists to govern. The global management standard for these infections is set by the WSES consensus process, whose GRADE-appraised executive summary covers all aspects of intra-abdominal infection management.^[28]

Epidemiology — the cohorts that anchor every timing argument

The Ferrer performance-improvement cohort is the scale against which all antibiotic-timing claims are measured: 28,150 patients with severe sepsis and septic shock evaluated from January 2005 through February 2010, with 17,990 receiving antibiotics after sepsis identification and entering the analysis — and an in-hospital mortality of 29.7% for the cohort as a whole.^[4] At the extreme end, severe complicated intra-abdominal sepsis carries mortality rates over 80% in some settings, with early antibiotics and operative source control named as the principles of treatment.^[20]

Nosocomial acquisition worsens the picture unevenly: the impact of nosocomial sepsis on outcome is more pronounced in medical admissions and tends to increase over time — though the estimates are sensitive to sepsis definitions, so quote the direction, not a fixed number.^[11] For the ICU patient with hospital-acquired bloodstream infection, the stakes of the first prescription are quantified: the population attributable fraction of 28-day mortality from inadequate therapy within 24 hours was 9.15%.^[10] Get the first antibiotics right, within the hour and within the day, because both windows carry measured mortality.

Pathophysiology — dysregulation, contamination, and the compartment

The dysregulated host response is the mechanism the definition names: infection triggers a response that escapes containment and produces life-threatening organ dysfunction, which is why inflammation alone is an inadequate model and why anti-inflammatory logic never became therapy.^[1] In secondary peritonitis the surgical form of that escape is contamination → bio-mediator generation → third-spacing and hypovolaemia → progressive multiorgan failure — a self-perpetuating loop that antibiotics slow but only source control breaks, since ongoing contamination re-feeds every downstream step.

The open-abdomen literature adds the resuscitation-driven second loop: damage-control resuscitation may lead to postoperative intra-abdominal hypertension or abdominal compartment syndrome, which may result in a vicious, self-perpetuating cycle leading to severe physiologic derangements and multiorgan failure unless interrupted by abdominal decompression.^[22] This is the physiological reason the abdomen is sometimes left open — not as routine, but as decompression and damage-control completion.

The COOL rationale proposes a third, still-unproven mechanism: open-abdomen management with active negative peritoneal pressure therapy to remove inflammatory ascites and ameliorate the systemic damage of severe complicated intra-abdominal sepsis.^[20] The honest viva framing is that although there is now a biologic rationale for such an intervention as well as non-standardized and erratic clinical utilization, this remains a novel therapy with potential side effects and clinical equipoise.^[20] There are definite risks of leaving the abdomen open whenever it might possibly be closed.^[21]

Clinical presentation and examination

Expect the spectrum from early sepsis — tachycardia, tachypnoea, fever or hypothermia, ileus, oliguria — through florid secondary peritonitis with guarding and rigidity, to vasopressor-dependent shock. The examination findings that mandate operative source control rather than further imaging are generalised peritonism with shock physiology: free uncontained contamination declares itself at the bedside, and the COOL eligibility phenotype names exactly this patient — free uncontained intra-peritoneal contamination with septic shock or equivalent physiological derangement.^[20]

Blunted presentations are the examiner's favourite trap: the elderly, the immunocompromised, the cirrhotic and the steroid-treated patient may never mount the textbook response, yet age and immunosuppression are formal components of the WSES severity score precisely because they mark risk the vital signs hide.^[3] Lower the threshold to act in these groups rather than waiting for physiology that may never declare itself.

For the open abdomen already under management, bedside assessment is fascial status, effluent character and volume, skin and viscera protection, and signs of fistula or compartment hypertension — with the governing rule that abdominal fascia-to-fascia closure should be done as soon as the patient can physiologically tolerate it.^[22] For the diverticular abscess under non-operative care, persistent sepsis physiology despite antibiotics with or without drainage — particularly Hinchey IIb disease in a smoker — is the bedside signal of failure demanding conversion.^[23]

Differential diagnosis — source, stage, and setting

Three axes sort the septic surgical patient. Source: complicated versus uncomplicated intra-abdominal infection — the distinction that drives whether source control enters the plan at all.^[28] Stage: diverticular abscess disease (Hinchey Ib–IIb patterns, WSES Ib–IIa equivalents) managed initially non-operatively, versus generalized faeculent peritonitis requiring operative source control.^[23] Setting: community versus healthcare-associated acquisition — origin and setting enter the WSES severity score because they change both likely microbiology and prognosis.^[3]

Two evidence notes sharpen counselling. After successful conservative care of diverticular disease, 79 patients in the Perrone cohort had new episodes (38.1%) and 23 had high-severity new episodes (11.1%), with 11 patients undergoing surgery (7.7%) — so recurrence is common but usually lower-severity, and non-operative treatment is described as an effective and safe option in selected patients with complicated diverticulitis.^[24] And where operation becomes necessary for diverticular disease, the choice of laparoscopic versus open resection has insufficient evidence to support or refute either approach for safety and effectiveness — state the equipoise rather than inventing a preference.^[26]

Non-surgical mimics and concurrent sources must be actively excluded: hospital-acquired bloodstream infection without an intra-abdominal source carries its own 9.15% attributable mortality from inadequate early therapy, so the septic surgical inpatient with no abdominal source is a line-and-urine-and-chest hunt, not a laparotomy.^[10]

Bedside assessment and triage — the first 15 minutes

Run resuscitation, antibiotics, lactate, cultures and the surgical source hunt simultaneously — no step waits for another. Blood cultures precede the first antibiotic dose but never delay it past the first hour, because adequacy within 24 hours carries a measured mortality fraction and the per-hour penalty starts at 60 minutes.^[10][4]

Use qSOFA outside the ICU and SOFA inside it, and know why. Among ICU encounters with suspected infection, the predictive validity for in-hospital mortality of SOFA was not significantly different from the more complex LODS but was statistically greater than SIRS and qSOFA — supporting SOFA in clinical criteria for sepsis.^[2] Among encounters with suspected infection outside the ICU, the predictive validity of qSOFA was statistically greater than SOFA and SIRS — supporting qSOFA as a prompt to consider possible sepsis on the ward and in the emergency department.^[2] qSOFA is the prompt; SOFA is the criterion. Neither is a screening test, and SIRS retains no definitional role.

The shock resuscitation target the definitions imply is a mean arterial pressure of at least 65 mm Hg on vasopressors once shock physiology declares itself — titrate norepinephrine against perfusion endpoints (mentation, urine output, lactate clearance, capillary refill) rather than chasing a higher number.^[1][12] Triage the diverticular abscess at first contact by CT Hinchey/WSES stage, sepsis physiology, and the smoking and abscess-gas risk flags into antibiotics-alone, antibiotics-plus-drainage, or operation.^[23] Trigger damage-control thinking at the index laparotomy for free uncontained contamination with shock physiology — a Predisposition-Infection-Response-Organ Dysfunction score of 3 or more, or a WSES Sepsis Severity Score of 8 or more marks the COOL-eligible phenotype.^[20]

Laboratory investigations

Order the physiology panel that maps to decisions: lactate for hypoperfusion, blood cultures before antibiotics, and the organ-function panel that populates SOFA domains (creatinine and urine output, bilirubin, platelets, PaO2/FiO2, Glasgow Coma Scale, blood pressure and vasopressor requirement).^[1][2] In the cirrhotic septic, add the stratification the evidence supports: clinicians could utilize CLIF-SOFA scores and lactate levels for mortality risk stratification and put more emphasis on the feasibility of source control to improve prognosis.^[7]

Biomarkers have a limited, defined role in this topic: the COOL bio-mediator panel is trial physiology, not bedside decision-making. Monitor adequacy of source control with lactate clearance and resolving organ dysfunction — non-resolution mandates re-look, not prolonged antibiotics.^[8] The stopping signal is physiological resolution: fixed-duration therapy of approximately 4 days after adequate source control matched a longer course extending until after the resolution of physiological abnormalities — so the labs that declared the emergency also declare its end.^[8]

Clinical scores and decision tools

Sepsis-3 thresholds. SOFA increase of 2 or more (≈ greater than 10% mortality) defines sepsis; shock adds vasopressor-dependent hypotension with profound circulatory, cellular and metabolic abnormality and greater mortality than sepsis alone.^[1] These are criteria, not screening instruments.

qSOFA versus SOFA by setting. In the ICU, SOFA ≈ LODS outperforms SIRS and qSOFA; outside the ICU, qSOFA outperforms SOFA and SIRS as the prompt to consider sepsis.^[2] Quote the Seymour predictive-validity basis when the examiner asks "why not SIRS everywhere" — because Sepsis-3 tested exactly that comparison.

WSES Sepsis Severity Score. Built from the clinical conditions at admission (severe sepsis/septic shock physiology), the origin of the complicated intra-abdominal infection, the delay in source control, the setting of acquisition, and risk factors such as age and immunosuppression.^[3] Validated in the WISS prospective multicentre study — 4,533 patients across 132 institutions worldwide over four months, mean age 51.2 years — where a score above 5.5 was the best predictor of mortality with sensitivity 89.2%, specificity 83.5% and positive likelihood ratio 5.4.^[3]

Supporting scores. In the open-abdomen versus primary-closure cohort, only the Mannheim Peritonitis Index resulted an independent factor of mortality (odds ratio 1.080) — quote MPI when asked what actually predicted death once the abdomen was open.^[19] PIRO of 3 or more and WSES-SSS of 8 or more mark COOL eligibility and hence damage-control candidacy.^[20] CLIF-SOFA plus lactate stratifies the cirrhotic septic.^[7]

Apply the scores to disposition: SOFA-defined sepsis with a high WSES-SSS goes to ICU and usually to theatre within the 6-hour clock; qSOFA-positive ward patients get the bundle and a surgical review now; the stable contained abscess with a low score is managed on the ward with drainage and observation.^[1][3][23]

^{[1] [3] [19] [20]}

Imaging — strategy and test performance

The default in suspected complicated intra-abdominal infection is contrast CT to confirm the source, stage Hinchey/WSES, and plan drainage versus operation — and it is skipped only when generalised peritonitis with shock makes the decision without it.^[23][28] CT staging directs the diverticular-abscess pathway: first-episode Hinchey Ib–IIb-pattern abscesses start non-operative with antibiotics with or without percutaneous drainage, while free perforation with faeculent peritonitis is operative.^[23]

The ACP diverticulitis guideline positions CT precisely: clinicians should use abdominal CT imaging when there is diagnostic uncertainty in suspected acute left-sided colonic diverticulitis — a conditional recommendation on low-certainty evidence, developed from a systematic review covering CT diagnosis alongside hospitalization, antibiotics and percutaneous drainage.^[27] That conditional position governs the uncertain case; it does not apply to the frankly peritonitic patient, who needs theatre rather than confirmation.

CT features flag likely non-operative failure before it happens: Hinchey IIb pattern (adjusted odds ratio 2.54), tobacco smoking (adjusted odds ratio 2.01) and intracavitary air bubbles (adjusted odds ratio 1.59) independently predict failure of conservative treatment — so consent the IIb smoker with abscess gas for probable conversion and monitor with escalation intensity to match.^[23] For the open abdomen and the undrained collection, CT identifies residual or localized sepsis mandating re-intervention between bedside assessments of closure and effluent.^[22]

Resuscitation and antibiotics — the hour-1 bundle from the evidence

Deliver the bundle as the trials describe it: broad-spectrum antibiotics inside the first hour, cultures first without delaying, fluids, lactate measurement, and the simultaneous surgical source hunt. Hospital mortality adjusted for severity, ICU admission source and geographic region increased steadily after 1 hour of time to antibiotic administration — and there was a linear increase in mortality risk for each hour of delay.^[4] That linear per-hour penalty in 17,990 analysed patients is the sentence that defends the whole bundle.

Then handle the sceptic's paper honestly. In a 593-patient emergency-department cohort (55.9% complete-bundle), 28-day mortality was 3.9% overall with no significant difference between complete and incomplete bundle groups (3.6% versus 4.2%) — and the authors concluded complete Hour-1 bundle treatment in the emergency department was not significantly associated with 28-day mortality.^[5] The fellowship answer reconciles rather than dismisses: a small, low-mortality, single-centre ED cohort cannot refute a 28,150-patient mortality gradient — but it proves a complete bundle without source control changes nothing, which is exactly why the surgical source hunt runs inside the hour rather than after it.^[4][5] The bundle literature itself frames this correctly: initial interventions in sepsis are a cornerstone for prognosis, and even though the evidence supporting the hour-1 bundle is perfectible, real-life application of thoughtful and organized sepsis care has improved survival and quality of care in settings promoting compliance to evidence-based treatments.^[6]

The cirrhotic septic is the special resuscitation case: application of the hour-1 bundle did not reveal a significant survival benefit to cirrhotic patients with septic shock — so stratify with CLIF-SOFA and lactate and weight the feasibility of source control above bundle-completion box-ticking.^[7]

Give the STOP-IT rule precisely: in patients with intra-abdominal infection who had undergone an adequate source-control procedure, outcomes after fixed-duration therapy of approximately 4 days were similar to those after a longer course of approximately 8 days extending until after resolution of physiological abnormalities.^[8] The planned re-laparotomy extension holds the same line: short-course therapy showed no increase in intra-abdominal infection recurrence compared with longer courses, with no differences in secondary outcomes.^[9] Four days after adequate control; longer only when control was inadequate — which is a re-look problem, not an antibiotic problem.

Broaden, narrow or stop by setting and adequacy: hospital-acquired sources demand cover for resistant organisms from the first dose (inadequate therapy within 24 hours carries a 9.15% attributable mortality fraction in ICU bloodstream infection), then de-escalate on cultures and resolving physiology toward the 4-day stop.^[10][8]

Vasopressors and the EGDT context

State the ladder with numbers. Compared with dopamine, norepinephrine was associated with decreased all-cause mortality (relative risk 0.89, absolute risk reduction 11%, number needed to treat 9) and with lower risk of major adverse events and cardiac arrhythmias — the evidence base for regarding norepinephrine as the first-line vasopressor in septic shock.^[12] The dopamine side of the ledger is explicit: in randomized trials dopamine was associated with increased mortality (relative risk 1.12) and, where reported, arrhythmias more than twice as frequent as with norepinephrine (relative risk 2.34).^[13] A second meta-analysis confirms the pattern across 11 randomized trials and 4,803 patients: no mortality or blood-pressure-achievement difference against other pressors, but arrhythmia risk favouring norepinephrine (relative risk 0.64).^[14] The bedside translation most experts endorse is norepinephrine as the first-line agent in septic shock.^[14]

Start norepinephrine early to a mean arterial pressure of at least 65 mm Hg with perfusion endpoints, and add a second agent when the pressure target costs excessive dose or perfusion fails to follow — the definition of shock already tells you pressure alone never sufficed.^[1][12]

What ProCESS, ARISE and ProMISe killed was protocolized early goal-directed therapy, not resuscitation. All three trials confirmed no survival benefit of EGDT compared with usual resuscitation.^[17] The ARISE/ProCESS/ProMISe systematic review found EGDT not superior to usual care for emergency-department septic shock but associated with increased ICU resource utilisation.^[16] And the individual-patient PRISM meta-analysis closed the debate: EGDT did not result in better outcomes than usual care and was associated with higher hospitalization costs across a broad range of patient and hospital characteristics.^[15]

How to answer the viva trap — "EGDT is dead so resuscitation does not matter": protocolized catheter-and-target EGDT is dead; time-critical resuscitation — antibiotics inside the hour, fluids, norepinephrine first, source control inside 6 hours — is very much alive, because every surviving element carries its own mortality gradient.^[15][4][18]

Source control — timing and modality

State the 6-hour rule with its numbers. In 111 open-abdomen-managed severe intra-abdominal infections (in-hospital mortality 21.6%, primary fascial closure 90.9%), time to source control of 6 hours or more was significantly associated with poor prognosis and lower fascial-closure rate — mortality 27.0 versus 9.0%, closure 86 versus 100% — with a direct increase in mortality and reduction in closure rate for each further 6-hour delay.^[18] Time to source control plays a determinant prognostic role in severe intra-abdominal infections: that is the quoted conclusion, not an extrapolation.^[18]

Define adequate source control as elimination of the ongoing contamination source with restoration of anatomy or controlled drainage — in ascending invasiveness: antibiotics plus percutaneous drainage for the contained abscess; operative resection, repair or washout for free perforation or uncontrolled sepsis; planned re-look where contamination cannot be cleared in one visit.^[23][22]

Defend percutaneous-drainage-first for diverticular abscess with the DivAbsc2023 numbers: first-episode CT-diagnosed abscesses managed initially non-operatively with antibiotics alone or with percutaneous drainage failed in 27.04% — roughly one in four converting to emergency surgery.^[23] Drain by strategy, not by centimetre: in abscesses above 5 cm, percutaneous drainage was not associated with the risk of failure or success of non-operative treatment — so size alone neither mandates nor forbids the drain.^[23] Note how rarely the drain is actually used in conservative cohorts (12 drainages in 211 patients, 5.7%) alongside near-universal bowel rest and antibiotics (98.5%) — drainage-first is a strategy for the abscess that needs it, not a reflex for every collection.^[24]

When drainage-first fails, it fails predictably: Hinchey IIb pattern, smoking and abscess gas flag conversion, and the wider literature warns that complicated diverticulitis with abscess formation carries a high probability of eventual resective surgery, with conservative management risking chronic or recurrent symptoms.^[25] Consent accordingly: about one in four fail non-operative care; young smokers with IIb disease need vigilant monitoring for septic progression; recurrence after success runs at 38.1% but usually at lower severity, with 7.7% eventually operated.^[23][24]

Open abdomen, damage control and re-laparotomy

Give the WSES indications in concept: the abdomen cannot be closed due to visceral oedema, the inability to control the compelling source of infection, the necessity to re-explore as a planned second-look laparotomy, completion of previously initiated damage-control procedures, abdominal wall disruption, or intra-abdominal hypertension and compartment syndrome requiring decompression.^[22] Two governing rules bound every decision: use the open abdomen only in patients who would most benefit from it, and perform fascia-to-fascia closure as soon as the patient can physiologically tolerate it.^[22]

Present the open-versus-primary-closure evidence honestly. In 176 severe peritonitis patients with WSES-SSS of 7 or more (128 primary closure, 48 open abdomen), there were no statistical differences in mortality between the two groups — but complications were higher in the open-abdomen group, with higher short-term complications and incisional hernias, and only MPI independently predicted mortality.^[19] The conclusion is quotable: open abdomen in severe secondary peritonitis does not improve mortality and is associated with higher short-term complications and incisional hernias.^[19] Selective, not routine — the numbers forbid any stronger claim.

Describe the COOL phenotype and design for the examiner: free uncontained intra-peritoneal contamination with septic shock, or PIRO of 3 or more, or WSES-SSS of 8 or more; fascia closure versus open abdomen with active negative peritoneal pressure therapy; primary outcome 90-day survival.^[20] It remains the trial that will answer whether inflammatory-ascites removal helps — equipoise until it reports.

Manage the open abdomen day-to-day with active negative-pressure dressings, effluent and fluid accounting, nutrition, fascial traction, early closure planning, and fistula and frozen-abdomen precautions — always under the close-as-soon-as-tolerated rule.^[22][21] For planned re-laparotomy versus on-demand re-look: decide by whether contamination could be cleared at the index operation, and let the short-antibiotic rule simplify the pathway — no excess recurrence with short courses even in planned re-laparotomy patients.^[9]

Special populations

• Elderly and frail: age is a formal WSES-SSS component because blunted physiology hides risk — the 6-hour clock ticks louder here, with goals-of-care and operative risk modifying the pathway (laparoscopy versus laparotomy, ICU ceilings) without abandoning timely source control.^[3][18]
• Cirrhotic: no demonstrated hour-1 bundle survival benefit; stratify with CLIF-SOFA plus lactate and let source-control feasibility dominate prognosis and counselling.^[7]
• Immunocompromised, steroid-treated and diabetic: immunosuppression is a scored risk factor at admission — lower the imaging threshold, broaden empiric cover for healthcare-associated organisms, and escalate earlier to drainage or operation since signs under-call severity.^[3][10]
• Exam-strategy note (not a literature claim): when the viva adds pregnancy or a low-resource setting to this stem, the scoring move is to restate which principles transfer unchanged (Sepsis-3 definitions, first-hour antibiotics, norepinephrine-first, the 6-hour source-control clock) and which step adapts to context (imaging modality, operative access, critical-care availability) — then ask the examiner which constraint they want tested.

Evidence, guidelines and controversies — the regional picture

• International (WSES, surgeon-led): the 2016 consensus executive summary is the GRADE-appraised framework for all intra-abdominal infection management, and the WSES open-abdomen guidelines set the selective-use and early-closure rules.^[28][22] The WISS validation cohort behind the severity score spanned 132 institutions worldwide.^[3]
• US (Surviving Sepsis Campaign / ACP physician tradition): the Hour-1 Bundle was published in 2018 as the time-critical framework; the quotable bundle numbers come from secondary bundle cohorts rather than the campaign documents themselves.^[5][6] The ACP diverticulitis guideline (conditional, low-certainty) positions CT for diagnostic uncertainty and systematizes the hospitalization–antibiotics–drainage pathway.^[27]
• Sepsis-3 (SCCM/ESICM task force): replaces the 2001 definitions with 31-society endorsement behind the dysregulated-response model; "severe sepsis" retired, SOFA operationalized, SIRS demoted.^[1]
• Live controversies: the ED hour-1 null cohort versus the Ferrer gradient (small low-mortality sample versus 28,150-patient dose-response); routine versus selective open abdomen (no mortality difference, more complications — COOL-testing); drainage by centimetre versus by strategy (the greater-than-5-cm subgroup shows no signal); and laparoscopic versus open resection for diverticular disease (Cochrane: insufficient evidence either way).^{[5][4][19][23][26]}

Revision summary

Define sepsis by Sepsis-3 — dysregulated response with organ dysfunction, SOFA +2 ≈ greater than 10% mortality, shock as the profound subset; severe sepsis retired, SIRS inadequate.^[1] Stratify with SOFA in ICU and qSOFA outside it, and score the surgical abdomen with WSES-SSS (above 5.5: sensitivity 89.2%, specificity 83.5%).^[2][3] Give antibiotics inside the first hour — mortality rises steadily after 1 hour with a linear per-hour penalty across 17,990 patients.^[4] Start norepinephrine first (relative risk 0.89, NNT 9 over dopamine; dopamine arrhythmia relative risk 2.34); accept the small ED null cohort as proof that bundles without source control change nothing.^[12][13][5] Stop antibiotics at 4 days after adequate source control — equal to 8 days, including planned re-laparotomy.^[8][9] Control the source within 6 hours (27.0 versus 9.0% mortality; closure 86 versus 100%; worse every further 6 hours).^[18] Drain contained abscesses percutaneously first, converting for IIb disease, smoking or abscess gas (failure predictors 2.54 / 2.01 / 1.59); consent to ~1-in-4 failure and 38% recurrence at usually lower severity.^[23][24] Open the abdomen selectively (no mortality gain, more complications; MPI the predictor), close fascia-to-fascia as soon as tolerated, and cite COOL equipoise when asked what comes next.^[19][22][20]

^{[4] [12] [8] [18] [3] [23]}

The planned re-laparotomy extension found short versus long courses at 41.2 versus 44.4% composite (p 0.781) with no excess recurrence.^[7]

References28ShowHide

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