Day-two post-laparotomy, saturations 89 percent on 4 litres, respiratory rate 28, basal crackles, a nasogastric tube draining a litre, two units transfused overnight, and a wound epidural running. Is this atelectasis, aspiration, TRALI, fluid overload, or early ARDS — and do you recruit the lung, diurese, transfuse differently, reverse the block, fix the analgesia, or reach for NIV? The examiner will watch you split the five forks by trial, quote ARISCAT risk, defend your intraoperative PEEP, choose the reversal agent by SNaPP, and time NIV by Jaber rather than by hope. This page teaches every move with each number taken from the paper named beside it.^[2]^[17]^[29]

Overview & Definition — the five failures behind one desaturation

A postoperative pulmonary complication is a composite, not a single disease: the ARISCAT derivation counted respiratory infection, respiratory failure, bronchospasm, atelectasis, pleural effusion, pneumothorax, or aspiration pneumonitis as one outcome family.^[2] Name the composite aloud before you act, because each member has its own trial set — atelectasis answers to reversal and mobilisation, aspiration to fasting and extubation planning, TRALI to donor strategy, ARDS to low stretch, and hypoxaemia to NIV — and the viva punishes crossed wires.^[17]^[36]^[34]^[1]^[29]

The strategic arc of the whole topic fits one sentence: randomised trials show routine high PEEP with recruitment does not protect, routine postoperative CPAP and HFNC do not prevent failure, and incentive spirometry alone does not cut complications — while pharmacological reversal, epidural analgesia, and curative NIV for established failure each moved their endpoint — so prevent with reversal, ventilation discipline and analgesia, and treat failure with NIV rather than prophylaxis.^[5]^[26]^[27]^[33]^[17]^[23]^[29]

Classification — five forks from one desaturation

Atelectasis and splinting: the common post-laparotomy failure — basal collapse from diaphragmatic dysfunction, pain-limited breathing and residual paralysis — answers to reversal, analgesia and mobilisation, and dominates the SNaPP endpoint (atelectasis drove the composite).^[17]
Aspiration pneumonitis and pneumonia: witnessed or silent soiling around induction, positioning or extubation — rare (single digits per 10,000) but examined through fasting policy and extubation planning rather than through ventilation settings.^[36]^[37]
Transfusion-related lung injury: permeability oedema within hours of plasma-containing products — answers to donor strategy and the TRALI-versus-overload fork, not to ventilator dials.^[34]^[35]
ARDS in the surgical patient: low-stretch physiology borrowed from ARMA — quote the anchor here, and send proning, rescue and extracorporeal logic to the ARDS topic where it lives.^[1]
Simple postoperative hypoxaemia: desaturation without a named disease — the HFNC-responsive layer that must never delay NIV or a definitive airway when failure declares itself.^[31]

Each fork has its own numbers, and the rest of this page keeps them separated.^[2]

Epidemiology & Risk Factors — the denominators that frame every decision

ARISCAT studied 2464 patients across 59 hospitals and found 252 events in 123 patients (5 percent), with 30-day death at 19.5 percent when a PPC occurred versus 0.5 percent without — the mortality gap that makes this topic examinable.^[2] The emergency-laparotomy contrast is far grimmer: 1080 major emergency abdominal cases with 39.9 percent developing at least one PPC and 13.9 percent a severe PPC, carrying 30-day death of 21.0 percent and 46.3 percent respectively.^[3] After esophagectomy, 194 of 454 patients (42.7 percent) developed PPCs.^[12] SNaPP randomised 3498 abdominal or thoracic patients across 44 hospitals with PPC-or-death at 19.0 versus 21.5 percent.^[17] PRISM analysed 4793 patients across 70 hospitals in six countries with its composite at 8.1 versus 8.2 percent.^[26] PROXI randomised 1400 acute or elective laparotomies across 14 Danish hospitals.^[13] PROVHILO recruited 900 at-risk open-abdominal patients across 30 centres on three continents.^[5] PROBESE randomised 2013 obese adults across 77 sites in 23 countries.^[6] iPROVE analysed 967 patients across 21 Spanish hospitals.^[7] The 2026 driving-pressure trial completed 1435 patients across 29 sites in 5 countries.^[10]

Risk concentrates where the surgeon already worries: the seven ARISCAT factors are low preoperative saturation, respiratory infection in the prior month, age, preoperative anaemia, upper abdominal or intrathoracic surgery, duration of at least 2 hours, and emergency surgery.^[2] The emergency-laparotomy multivariable set adds pulmonary history, hypertension, cerebral disease, frailty, preoperative ICU admission, contaminated wounds, perforated ulcer findings, reoperation and protracted ileus — on top of a rising ARISCAT score.^[3] Head-and-neck surgery adds ischaemic heart disease, anaemia, nicotine dependence and advanced age as independent respiratory-failure risks.^[19]

Pathophysiology — driving pressure, mechanical power and the diaphragm

Driving pressure is the mechanism anchor: across 17 randomised trials with 2250 patients, each 1-unit rise in driving pressure raised PPC odds (OR 1.16) with no tidal-volume association, and driving pressure was the only significant mediator of protective-ventilation benefit.^[8] The PEEP paradox follows directly: raising PEEP so that driving pressure rises raised PPC odds more than three-fold (OR 3.11) — PEEP helps only when it lowers driving pressure, which is why routine high PEEP failed in every trial that tested it.^[8]^[5]^[6]

Mechanical power summarises the same injury as energy: across 2860 orthopaedic operations, each 0.1 J/min/kg increment worsened PACU oxygenation and raised PPC odds by 55 percent (OR 1.55), with driving pressure carrying comparable signal.^[11] The esophagectomy cohort confirms the pressures at the bedside: plateau and driving pressures tracked PPCs in both one-lung and two-lung phases, with tidal volume and mechanical power joining during one-lung ventilation.^[12]

The diaphragm is the second mechanism every surgeon must narrate: sugammadex preserved deep-breathing diaphragmatic excursion far better than neostigmine (deterioration 0.05 versus 0.28 cm) with a higher oxygenation index — the muscle measurement behind the SNaPP atelectasis signal.^[22]^[17] Spontaneous recovery of block, left to wear off unaided, stands as an independent PPC risk factor — so the diaphragm story ends with a prescription, not a metaphor.^[21]

Clinical Presentation — the surgical patient facing respiratory failure

The atelectasis candidate declares through splinting: day 1 to 2 post-laparotomy, basal collapse, pain-limited inspiration, low saturation that corrects with sitting and coughing — the SNaPP phenotype, where reversal choice already wrote half the outcome intraoperatively.^[17]^[21] The aspiration candidate declares through soiling: witnessed regurgitation, new infiltrate after induction or extubation, difficult airway or liberal-fluid fasting context — investigate the airway story, not the ventilator.^[36]^[37] The TRALI candidate declares through transfusion timing: distress with a P/F below 300 within 6 hours of plasma, with antibody-positive product in the history — split permeability from circulatory overload before treating.^[35]^[34] The Jaber candidate declares through established failure: post-abdominal hypoxaemia with tachypnoea and work of breathing within 7 days — the NIV-responsive patient, distinct from the PRISM prophylaxis population who were not yet failing.^[29]^[26] The obese candidate declares through habitus: BMI above 30 with extubation looming — where prophylactic NIV cut treatment failure and the BMI-40 subgroup gained most.^[30]

Practical assessment at the bedside: combine timing (hours post-transfusion, days post-operation), work of breathing, saturation trajectory, pain and block status, fluid balance, and the chest examination — then name the fork before ordering anything.^[2]

Differential Diagnosis — the five forks worked aloud

Split atelectasis (basal, splinted, reversal-responsive — the SNaPP atelectasis excess of 18.4 per cent versus 21.1 per cent) from aspiration (infiltrate after soiling — the 3.7-per-10,000 fasting-policy event) from TRALI (post-transfusion permeability — the donor-strategy-preventable event) from overload (congestive pattern among the 19 distressed FFP recipients) from ARDS (low-stretch physiology — the ARMA anchor).^[17]^[36]^[34]^[35]^[1] Split established hypoxaemic failure (Jaber NIV territory — reintubation 33.1 versus 45.5 percent) from the merely at-risk postoperative patient (PRISM territory — routine CPAP changed nothing at 8.1 versus 8.2 percent).^[29]^[26] Split the obese extubation (EXTUBOBESE NIV territory — failure 13.4 versus 23.9 percent) from the routine extubation (standard oxygen suffices — OPERA territory).^[30]^[27]

Name the category aloud before acting — the viva rewards the candidate who separates what NIV fixes from what only reversal, analgesia, diuresis or reintubation fixes.^[29]^[17]

Clinical & Bedside Assessment — ARISCAT honestly, scores humbly

Use ARISCAT to stratify, never to dictate: its derivation discriminated excellently (AUC 90 percent development, 88 percent validation), but a Catalonia validation managed only AUC 0.567 with insignificant regression, and an ICU comparison found every score below AUC 0.70 with ARISCAT at 0.60 — so quote the seven factors, state the external humility, and assess the patient in front of you.^[2]^[4] At the bedside, score the ARISCAT seven, add the emergency-laparotomy extras (frailty, ICU admission, contamination, ileus), and set the monitoring level — the score describes vulnerability without prescribing any ventilator number.^[3]^[8]

Investigations — gases, images and the honest threshold gap

Draw gases to stage failure (the Jaber entry phenotype was hypoxaemia with tachypnoea or visible work of breathing; the FFP study staged distress at P/F below 300), image to split atelectasis from infiltrate from effusion from overload, and review the transfusion record whenever distress follows plasma within hours.^[29]^[35] State the threshold honesty the examiner probes: no verified adult extubation-readiness, residual-block, or TRALI-versus-TACO numeric cutoff sits in this pack — the trials report strategies and events, so quote events and name the gap rather than inventing a number.^[21]^[34]

Management — Risk stratification: who gets watched, and how closely

Every post-laparotomy patient gets an ARISCAT-style risk pass: low saturation, recent chest infection, age, anaemia, upper abdominal or thoracic incision, long operation, emergency listing — seven bedside facts that predict the 5-percent event rate and its forty-fold mortality gradient.^[2] The emergency laparotomy, the esophagectomy and the head-and-neck flap reconstruction start in the high-risk lane by definition — 39.9 percent, 42.7 percent, and HR-graded respiratory failure respectively — so they earn senior review, planned analgesia, and a declared rescue plan before failure.^[3]^[12]^[19]

Management — Intraoperative ventilation: low stretch, low PEEP, and the negative triad

Ventilate the operation at low tidal volumes with low PEEP and no routine recruitment — because PROVHILO tested high PEEP 12 with recruitment against low PEEP ≤2 without, all at 8 mL/kg, and found PPC at 40 versus 39 percent (RR 1.01) with more hypotension and vasoactive use on high PEEP.^[5] In the obese patient the same answer holds: PROBESE tested high PEEP 12 with recruitment against low PEEP 4 in BMI ≥35 and found PPC at 21.3 versus 23.6 percent (RR 0.93, P 0.23) — better intraoperative oxygenation (hypoxaemia 5.0 versus 13.6 percent) that bought no clinical outcome.^[6] Individualising the open-lung approach changed nothing either: iPROVE's four arms landed between 46 and 51 percent complications with no significant difference.^[7] The 2026 close repeats the lesson with driving-pressure guidance: 1435 at-risk open-abdominal patients, PPC 19.8 versus 17.4 percent (P 0.23), more hypotension and vasoactive use with guided high PEEP, more desaturation with low PEEP.^[10] Even in bariatric surgery, driving-pressure-titrated PEEP improved mechanics without cutting PPCs (70.7 versus 75.9 percent, P 0.68).^[9]

State the viva sentence: PEEP is a driving-pressure instrument, not a doctrine — use the lowest pressure that keeps driving pressure down, and never recruit by routine.^[8]^[5]

Management — Oxygen: PROXI negativity and the low-FiO2 tension

Do not prescribe 80 percent perioperative oxygen to prevent infection or lung injury after laparotomy: PROXI randomised 1400 laparotomies to 80 versus 30 percent oxygen during and 2 hours after surgery and found SSI at 19.1 versus 20.1 percent with atelectasis, pneumonia, respiratory failure and 30-day death all indistinguishable.^[13] Set the examined tension honestly: a 255-trial review of 55,260 abdominal-surgery participants claims high-certainty benefit for LOW FiO2 (RR 0.81) with moderate-certainty benefit for lung-protective ventilation, physiotherapy, analgesia and nutrition — quote it as that review's finding, reconcile it against PROXI's null, and never present either as settled doctrine.^[14]^[13] Where HFNC earns mention intraoperatively, it is narrow: 64 bariatric patients with early HFNC had less hypoxaemia (28.6 versus 80.0 percent, RR 0.35) and less atelectasis (31 versus 77 percent) — a small, specific, cited win, not a general oxygen policy.^[15]

Management — Reversal: sugammadex by SNaPP, and never by waiting

Reverse every block pharmacologically with sugammadex rather than neostigmine in abdominal and thoracic surgery: SNaPP's 3498 patients showed PPC-or-death at 19.0 versus 21.5 percent (RR 0.88, P 0.049), driven by atelectasis (18.4 per cent versus 21.1 per cent) with pneumonia, aspiration and ARDS unchanged.^[17] The cohorts close the argument across contexts: 15,730 matched UGI-endoscopy patients had extubation failure at 3.88 versus 5.79 percent (NNT 52) with less atelectasis and fewer unplanned ICU admissions.^[18] In 2576 matched head-and-neck flap patients, sugammadex cut 30-day respiratory failure (HR 0.67) with benefit persisting at 90 days.^[19] In 68,062 matched COPD patients, sugammadex cut 30-day pneumonia (1.8 versus 2.1 percent, HR 0.84) — but raised ICU admissions (HR 1.22) with no mortality or exacerbation difference, benefit concentrating in the elderly and academic centres.^[20] And the reversal-versus-waiting question is settled: pharmacological reversal protected (OR 0.62), so spontaneous recovery is the risk factor, never the plan.^[21]

Management — Analgesia: epidurals for the lung, blocks by evidence

Place thoracic epidural analgesia for major open abdominal surgery expecting a respiratory-failure dividend, not a mortality one: MASTER's 888 high-risk patients showed any-morbidity-or-death at 57.1 versus 60.7 percent (P 0.29) with equal 30-day death — and respiratory failure, alone among eight system endpoints, fell from 30 to 23 percent (P 0.02) with better pain scores and no major catheter harm.^[23] After esophagectomy the meta-analysis agrees: 16,146 patients, less pain, 2.3 fewer hospital days and fewer pulmonary complications (RD −0.10) — at the price of catheter complications and more vasoactive use, with no mortality, reintubation or ICU-stay difference.^[25] After thoracoscopic lung resection, update the default: single-shot intercostal block proved noninferior to TEA for pain while paravertebral block did not — both with less opioid and better mobility.^[24] The mechanism sentence the viva wants: analgesia prevents failure by defeating splinting — which is why a 255-trial review credits analgesia at moderate certainty (RR 0.73).^[14]

Management — Prophylactic support: PRISM and OPERA say no

Do not order routine postoperative CPAP to prevent failure after major open abdominal surgery: PRISM's 4793 patients showed pneumonia, reintubation or death at 8.1 versus 8.2 percent (OR 1.01, P 0.95) — routine prophylactic CPAP is not recommended, while CPAP keeps its treatment role once failure exists.^[26] Do not order early preventive HFNC after extubation expecting fewer pulmonary complications: OPERA's 220 major-abdominal patients showed hypoxaemia ARR 4 percent (P 0.57) and PPC-free ARR 7 percent (P 0.40) — no pulmonary-outcome gain over standard oxygen.^[27] In recovery, HFNC trims atelectasis (OR 0.33) and hypoxaemia (OR 0.42) across 25 trials with 4260 patients without cutting reintubation (OR 0.93) — so use it for comfort and oxygenation, and never let it delay NIV or a definitive airway.^[31]

Management — Curative rescue: NIV for established failure, early

Start NIV promptly when hypoxaemic failure declares after abdominal surgery: Jaber's 293 patients across 20 ICUs showed reintubation at 33.1 versus 45.5 percent (ARR −12.4, P 0.03) with more ventilator-free days and fewer healthcare-associated infections (31.4 versus 49.2 percent), 90-day death trending favourably but nonsignificant.^[29] After cardiothoracic surgery, HFNC and BiPAP are equivalent rescue choices: BiPOP's 830 patients showed treatment failure at 21.0 versus 21.9 percent (noninferior) with equal ICU death — choose by tolerance and skin (breakdown 10 versus 3 percent on BiPAP), not by superiority.^[28] In the obese postoperative patient, lean toward NIV at extubation: EXTUBOBESE's 585 patients showed treatment failure at 13.4 versus 23.9 percent (ARD −10.5) with equal reintubation, benefit concentrating at BMI ≥40.^[30]

Management — Physiotherapy: prescribe the bundle, retire the talisman

Keep mobilisation and physiotherapy as care, and stop prescribing incentive spirometry alone as prophylaxis: 224 bariatric patients showed identical hypoxaemia with or without the device at 6, 12 and 24 hours.^[32] After lung resection, 387 patients showed 30-day PPC at 12.3 versus 13.0 percent for physiotherapy-plus-device versus physiotherapy alone, with pneumonia, ventilation, stay and readmission all identical.^[33] The 117-trial synthesis found no high-quality evidence for any single intervention class — while the newer 255-trial review credits physiotherapy at moderate certainty (RR 0.55) — so the examined position is a bundle (mobilisation, deep breathing, cough support, analgesia enabling all three), never a plastic device alone.^[38]^[14]

Management — Transfusion lung injury: donor strategy and the overload fork

Prevent TRALI through the blood bank, not the ventilator: low-risk donor strategies for plasma cut TRALI onset (OR 0.61 overall, 0.51 in TRALI-prone populations).^[34] The surgical bedside data agree: among 82 FFP recipients, 19 developed distress within 6 hours — male-only FFP protected (OR 0.219) while bypass and liver dysfunction predicted distress, and every possible-TRALI case had received antibody-positive product.^[35] Donor strategy protects the TRALI-prone most: the risk reduction concentrated in susceptible populations (OR 0.51) with only a nonsignificant trend elsewhere — so the bleeding surgical patient is exactly who the blood bank policy defends.^[34] At the bedside, split permeability oedema (possible TRALI among the five) from circulatory overload (congestive pattern among the seven) before diuresing or restricting — the massive-transfusion topic owns trigger thresholds, this topic owns the lung-injury fork.^[35]

Management — Aspiration and extubation: rare events, planned airways

Quote the rarity without dismissing it: under a liberal clear-fluid policy (median 63 minutes), 56,995 anaesthetics produced aspiration at 3.7 per 10,000, regurgitation at 25 per 10,000 and aspiration pneumonia at 2.1 per 10,000 — higher than standard-policy reports, trading wellbeing against risk in a discussion, not a decree.^[36] Plan every extubation as PUMA demands: assess hypoxaemia, aspiration and stimulation risk first — every planned extubation is elective — defer when waiting lowers risk — and convert lifelines rather than replacing them when reintubation may be hard.^[37] The pilot physiology belongs here as curiosity, not practice: 69 patients, open-lung versus conventional extubation, 8 PPCs total with better aeration on the open-lung side — feasibility demonstrated, efficacy untested.^[16]

Complications & Pitfalls — the six traps

Routine high PEEP with recruitment — no protection in PROVHILO, PROBESE, iPROVE or the 2026 DESIGNATION close, with hypotension and vasoactive cost every time; use low PEEP guided by driving pressure.^[5]^[6]^[7]^[10]
Routine prophylactic CPAP or HFNC — PRISM and OPERA both null; reserve pressure for treatment, where Jaber applies.^[26]^[27]^[29]
Spontaneous block recovery — an independent PPC risk factor; reverse pharmacologically, with sugammadex by SNaPP.^[21]^[17]
Incentive spirometry alone — two negative RCTs in exactly the believers' populations; prescribe the physiotherapy bundle instead.^[32]^[33]
High-FiO2 prophylaxis by habit — PROXI null across infection and lung endpoints; know the low-FiO2 review claim and its tension with PROXI rather than ventilating by slogan.^[13]^[14]
Delayed escalation — HFNC must not delay NIV or a definitive airway; NIV failure must not delay reintubation.^[31]^[29]

Prognosis & Disposition — the numbers that set expectations

A PPC multiplies 30-day death roughly forty-fold in mixed surgery (19.5 versus 0.5 percent) and carries 21.0 percent death after emergency laparotomy — 46.3 percent when severe.^[2]^[3] Curative NIV improves the reintubation odds without proven mortality gain at 90 days (14.9 versus 21.5 percent, nonsignificant).^[29] Sugammadex-era reversal trims the atelectasis burden without moving pneumonia or death.^[17] The honest disposition sentence: most post-laparotomy desaturation resolves with reversal-correct practice, analgesia, mobilisation and timely NIV — the minority that progresses to ARDS leaves this topic for the ARDS pathway.^[1]

Special Populations — surgical contexts that change the emphasis

Emergency laparotomy: the highest-risk lane — 39.9 percent PPC, frailty and ileus in the risk set, ARISCAT underestimating by context; plan analgesia and rescue before incision.^[3]
Obesity (BMI ≥35–40): PROBESE negativity for routine high PEEP, EXTUBOBESE positivity for prophylactic NIV, bariatric HFNC signals for hypoxaemia — ventilate simply, extubate onto NIV when morbidly obese.^[6]^[30]^[15]
Esophagectomy: 42.7 percent PPC with plateau and driving pressures guilty in both ventilation phases; TEA earns its keep here (fewer pulmonary complications, 2.3 fewer days) at catheter and vasopressor cost.^[12]^[25]
Thoracic resection: single-shot intercostal block contests the epidural default with noninferior pain and better mobility; incentive spirometry adds nothing to physiotherapy.^[24]^[33]
Head-and-neck flap reconstruction: sugammadex protection against respiratory failure persisting to 90 days; age, anaemia, ischaemia and smoking mark the watch list.^[19]
COPD and the elderly: sugammadex pneumonia benefit without mortality gain and with more ICU admission — quote both halves, and note the benefit concentrates in the elderly and academic centres.^[20]

Evidence, Guidelines & Regional Differences — the trials and who led them

ARMA (US ARDS Network, 2000) anchors stretch physiology; ARISCAT (Spain, 2010) anchors risk; PROVHILO (European-led, 30 centres, three continents, 2014), PROBESE (77 sites, 23 countries, 2019), iPROVE (Spain, 2018) and DESIGNATION (Europe, 2026) form the negative PEEP arc; PROXI (Denmark, 2009) anchors oxygen; SNaPP (Australia, Aotearoa New Zealand, Hong Kong, 2026) anchors reversal; MASTER (Australia/UK, 2002) anchors analgesia; PRISM (six countries, 2021), OPERA/BiPOP/Jaber (France, 2015–2016) and EXTUBOBESE anchor support strategy; TRALI donor evidence spans Dutch meta-analysis and Japanese surgical cohorts.^[1]^[2]^[5]^[13]^[17]^[23]^[26]^[34] The PUMA extubation guideline (international, 2026) is recommendation-level consensus, quoted as guidance rather than trial truth.^[37] Regional practice differs in donor strategy, block availability and NIV access — the trial numbers travel, the implementation adapts.^[34]^[24]

Exam Pearls — the one-liners that score

ARISCAT: seven factors, 5 percent events, forty-fold death gradient — then confess the external AUCs below 0.70.^[2]^[4]
High PEEP with recruitment: PROVHILO 40 vs 39, PROBESE 21.3 vs 23.6, iPROVE 46–51 all arms, DESIGNATION 19.8 vs 17.4 — routine recruitment protects nothing.^[5]^[6]^[7]^[10]
Driving pressure: OR 1.16 per unit, the only mediator — PEEP that raises it harms (OR 3.11).^[8]
PROXI: 80 vs 30 percent oxygen — SSI, atelectasis, pneumonia, failure and death all null.^[13]
SNaPP: sugammadex 19.0 vs 21.5 (RR 0.88) via atelectasis; never let block wear off (OR 0.62 with reversal).^[17]^[21]
MASTER: only respiratory failure of eight endpoints improved (23 vs 30) — epidurals are lung therapy.^[23]
PRISM 8.1 vs 8.2 and OPERA null: prophylaxis with pressure prevents nothing — Jaber 33.1 vs 45.5 treats failure.^[26]^[27]^[29]
Spirometry alone: two negative RCTs — prescribe the bundle.^[32]^[33]
TRALI: donor strategy OR 0.61, male-only FFP OR 0.219 against distress — split from overload first.^[34]^[35]
Aspiration under liberal fasting: 3.7 per 10,000 — rare, planned for, PUMA-ruled.^[36]^[37]

Revision summary

Post-laparotomy respiratory failure is five forks — atelectasis, aspiration, transfusion injury, ARDS, hypoxaemia — stratified by seven ARISCAT factors with humble external validity, ventilated intraoperatively with low stretch and low PEEP (routine recruitment never protected), oxygenated without high-FiO2 doctrine (PROXI null), reversed with sugammadex (SNaPP, never spontaneous recovery), kept breathing with epidural or evidence-chosen blocks, mobilised in bundles without spirometry talismans, rescued with curative NIV (Jaber) rather than prophylactic pressure (PRISM/OPERA null), transfused under donor-strategy protection with TRALI split from overload, and extubated by PUMA planning — with ARDS rescue owned next door.^[2]^[5]^[13]^[17]^[23]^[29]^[26]^[34]^[37]^[1]

454 patients with 42.7% PPC (PMID 41713688); quote SNaPP: 3498 patients across 44 hospitals with PPC-or-death 19.0% versus 21.5% (PMID 42263720).^[17] 4793 analysed across 70 hospitals in six countries with composite 8.1% versus 8.2% (PMID 34153272); quote PROXI: 1400 laparotomies across 14 hospitals (PMID 19826023).^[26] 900 at-risk open-abdominal patients at 8 mL/kg tidal volume — high PEEP 12 with recruitment versus low PEEP ≤2 without — PPC 40% versus 39% (RR 1.01), with more hypotension and vasoactive use on high PEEP (PMID 24894577).^[5] 2013 obese patients (BMI ≥35) — high PEEP 12 with recruitment versus low PEEP 4 — PPC 21.3% versus 23.6% (RR 0.93, P 0.23), with less intraoperative hypoxaemia on high PEEP (5.0% versus 13.6%) but no clinical-outcome gain (PMID 31157366).^[6] 1435 at-risk patients — driving-pressure-guided high PEEP with recruitment versus standard low PEEP — PPC 19.8% versus 17.4% (P 0.23), with more hypotension and vasoactive use on high PEEP and more desaturation on low PEEP (PMID 41334859).^[10] 116 obese patients — individualised versus fixed PEEP 5 — any PPC 70.7% versus 75.9% (OR 0.77, P 0.68), physiology improved without clinical translation (PMID 42496731).^[9] 1400 acute or elective laparotomies — 80% versus 30% oxygen during and 2 hours after surgery — SSI 19.1% versus 20.1% (OR 0.94), atelectasis 7.9% versus 7.1%, pneumonia 6.0% versus 6.3%, respiratory failure 5.5% versus 4.4%, 30-day death 4.4% versus 2.9% — no difference anywhere (PMID 19826023).^[13]^[23] 64 patients — early HFNC versus conventional oxygen — hypoxaemia 28.6% versus 80.0% (RR 0.35) and atelectasis 31% versus 77% (RR 0.39), with no severe PPCs in either arm (PMID 30994312).^[15] 15,730 matched UGI-endoscopy patients — failure 3.88% versus 5.79% (ARR 1.91%, NNT 52) with less atelectasis and fewer unplanned ICU admissions on sugammadex (PMID 42317106).^[18] 34,031 matched per arm — pneumonia 1.8% versus 2.1% (HR 0.84) favouring sugammadex but more ICU admissions (HR 1.22), no mortality or exacerbation difference, benefit concentrated in elderly and academic centres (PMID 42629667).^[28] 923 analysed, 64.6% PPCs — pharmacological reversal protected (OR 0.62), so spontaneous recovery stands as an independent PPC risk factor (PMID 32028288).^[21] 888 analysed high-risk major-abdominal patients — epidural-plus-general versus control — any morbidity-or-death 57.1% versus 60.7% (P 0.29) with equal 30-day death — and only respiratory failure of eight system endpoints improved (23% versus 30%, P 0.02), with better pain scores and no major catheter harm (PMID 11965272).^[23] 389 analysed — pain-score failure proportions 20.7% TEA versus 35.5% PVB versus 29.5% ICNB — PVB inferior, single-shot intercostal noninferior, both with less opioid and better mobility (PMID 40560556).^[24] 15 studies with 16,146 patients — TEA cut pain, stay by 2.3 days and pulmonary complications (RD −0.10), at the price of catheter complications and more vasoactive use, with no mortality, reintubation or ICU-stay difference (PMID 40409490).^[25] 293 post-abdominal patients with hypoxaemic failure across 20 ICUs — NIV versus standard oxygen — reintubation 33.1% versus 45.5% (ARR −12.4%, P 0.03), more ventilator-free days, fewer healthcare-associated infections (31.4% versus 49.2%), 90-day death 14.9% versus 21.5% (nonsignificant) (PMID 26975890).^[29] 830 post-cardiothoracic patients — HFNC noninferior to BiPAP on treatment failure (21.0% versus 21.9%) with equal ICU death and more skin breakdown on BiPAP (10% versus 3%) — so choose by tolerance and skin, not by superiority (PMID 25980660).^[28] 585 obese postoperative patients — prophylactic NIV versus oxygen — treatment failure 13.4% versus 23.9% (ARD −10.5) with equal reintubation (8.6% versus 9.9%), benefit concentrated at BMI ≥40 (PMID 41046173).^[28] 387 randomised — physiotherapy-plus-IS versus physiotherapy alone — 30-day PPC 12.3% versus 13.0% with identical pneumonia, ventilation, stay and readmission (PMID 29702071).^[33] Fence ARDS honestly: ARMA proved 6 versus 12 mL/kg PBW cuts ARDS death (31.0% versus 39.8%) with more ventilator-free days — quote it as the physiology anchor, and send proning, rescue and ECMO logic to ards-surgical where it lives (PMID 10793162).^[1]

References38Show

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