Emergency surgery during the COVID-19 pandemic: what you need to know for practice.

INTRODUCTION: Several articles have been published about the reorganisation of surgical activity during the COVID-19 pandemic but few, if any, have focused on the impact that this has had on emergency and trauma surgery. Our aim was to review the most current data on COVID-19 to provide essential suggestions on how to manage the acute abdomen during the pandemic. METHODS: A systematic review was conducted of the most relevant English language articles on COVID-19 and surgery published between 15 December 2019 and 30 March 2020. FINDINGS: Access to the operating theatre is almost exclusively restricted to emergencies and oncological procedures. The use of laparoscopy in COVID-19 positive patients should be cautiously considered. The main risk lies in the presence of the virus in the pneumoperitoneum: the aerosol released in the operating theatre could contaminate both staff and the environment. CONCLUSIONS: During the COVID-19 pandemic, all efforts should be deployed in order to evaluate the feasibility of postponing surgery until the patient is no longer considered potentially infectious or at risk of perioperative complications. If surgery is deemed necessary, the emergency surgeon must minimise the risk of exposure to the virus by involving a minimal number of healthcare staff and shortening the occupation of the operating theatre. In case of a lack of security measures to enable safe laparoscopy, open surgery should be considered.

Proceedings of resources for optimal care of acute care and emergency surgery consensus summit Donegal Ireland.

BACKGROUND: Opportunities to improve emergency surgery outcomes exist through guided better practice and reduced variability. Few attempts have been made to define optimal care in emergency surgery, and few clinically derived key performance indicators (KPIs) have been published. A summit was therefore convened to look at resources for optimal care of emergency surgery. The aim of the Donegal Summit was to set a platform in place to develop guidelines and KPIs in emergency surgery. METHODS: The project had multidisciplinary global involvement in producing consensus statements regarding emergency surgery care in key areas, and to assess feasibility of producing KPIs that could be used to monitor process and outcome of care in the future. RESULTS: Forty-four key opinion leaders in emergency surgery, across 7 disciplines from 17 countries, composed evidence-based position papers on 14 key areas of emergency surgery and 112 KPIs in 20 acute conditions or emergency systems. CONCLUSIONS: The summit was successful in achieving position papers and KPIs in emergency surgery. While position papers were limited by non-graded evidence and non-validated KPIs, the process set a foundation for the future advancement of emergency surgery.

Erratum to: The management of intra-abdominal infections from a global perspective: 2017 WSES guidelines for management of intra-abdominal infections.

[This corrects the article DOI: 10.1186/s13017-017-0141-6.].

Erratum to: Antimicrobials: a global alliance for optimizing their rational use in intra-abdominal infections (AGORA).

[This corrects the article DOI: 10.1186/s13017-016-0089-y.].

Erratum to: 2016 WSES guidelines on acute calculous cholecystitis.

[This corrects the article DOI: 10.1186/s13017-016-0082-5.].

2016 WSES guidelines on acute calculous cholecystitis.

Acute calculus cholecystitis is a very common disease with several area of uncertainty. The World Society of Emergency Surgery developed extensive guidelines in order to cover grey areas. The diagnostic criteria, the antimicrobial therapy, the evaluation of associated common bile duct stones, the identification of "high risk" patients, the surgical timing, the type of surgery, and the alternatives to surgery are discussed. Moreover the algorithm is proposed: as soon as diagnosis is made and after the evaluation of choledocholitiasis risk, laparoscopic cholecystectomy should be offered to all patients exception of those with high risk of morbidity or mortality. These Guidelines must be considered as an adjunctive tool for decision but they are not substitute of the clinical judgement for the individual patient.

Routine preoperative laboratory analyses are unnecessary before elective laparoscopic cholecystectomy.

BACKGROUND: We formulated a clinical pathway (CP) for elective laparoscopic cholecystectomy (LC), which included the following preoperative evaluation: history and physical (H&P), right upper quadrant ultrasound (US), and liver function tests (LFTs). We hypothesized that routine LFTs did not alter management beyond that dictated by H&P and US, and could be excluded from the CP. METHODS: The study involved 387 consecutive patients undergoing elective LC. Abnormalities in the preoperative evaluation were compared with the finding of choledocholithiasis or other unexpected outcomes. RESULTS: In 187 (48%) patients, abnormalities were found by H&P (n = 7), US (n = 13), and LFTs (n = 177). Seven patients (2%) had documented choledocholithiasis; two had abnormal H & P; three had abnormal US; and four had abnormal LFTs. No patient with choledocholithiasis had abnormal LFTs but normal H&P and US. CONCLUSIONS: Routine LFTs before elective LC are not cost effective. Before LC H&P and US are warranted, but LFTs do not add any useful information and should not be routinely measured.

Mesenteric lymph is responsible for post-hemorrhagic shock systemic neutrophil priming.

BACKGROUND: Hemorrhagic shock-induced splanchnic hypoperfusion has been implicated as a priming event in the two event model of multiple organ failure (MOF). We have previously shown that early postinjury neutrophil (PMN) priming identifies the injured patient at risk for MOF. Recent in vitro studies have demonstrated that postshock mesenteric lymph primes isolated human neutrophils. We hypothesize that lymphatic diversion before hemorrhagic shock abrogates systemic PMN priming and subsequent lung injury. METHODS: Sprague-Dawley rats (n >or= 5 per group) underwent hemorrhagic shock (MAP 40 mm Hg x 30 min) and resuscitation (shed blood + 2x crystalloid) with and without mesenteric lymphatic duct diversion. Sham animals underwent anesthesia and laparotomy. Whole blood was taken 2 hours after resuscitation, heparinized, and incubated for 5 min at 37 degrees C. Surface expression of CD11b (a marker for PMN priming) was determined by flow-cytometry compared with isotype controls. In addition, lung myeloperoxidase (MPO) was measured for PMN sequestration, and Evans blue lung leak was assessed in the bronchoalveolar lavage fluid in sham, and shock +/- lymph diversion animals. RESULTS: Hemorrhagic shock resulted in increased surface expression of PMN CD11b relative to sham (23.8 +/- 6.7 vs. 9.9 +/- 0.6). Mesenteric lymphatic diversion before hemorrhagic shock abrogated this effect (8.0 +/- 2.6). Lung PMN accumulation, as assessed by MPO, was greater in the lungs of nondiverted (113 +/- 14 MPO/mg lung) versus sham (55 +/- 4 MPO/mg lung, p < 0.05); lymph diversion reduced lung PMNs to control levels (71 +/- 6.5 MPO/mg lung, p < 0.05). Evans blue lung leak was 1.6 times sham in the hemorrhagic shock group; this was returned to sham levels after lymph diversion (p < 0.05). CONCLUSION: Post-hemorrhagic shock mesenteric lymph primes circulating PMNs, promotes lung PMN accumulation, and provokes acute lung injury. Lymphatic diversion abrogates these pathologic events. These observations further implicate the central role of mesenteric lymph in hemorrhagic shock-induced lung injury. Characterizing the PMN priming agents could provide insight into the pathogenesis of postinjury MOF and ultimately new therapeutic strategies.

Hypertonic saline activation of p38 MAPK primes the PMN respiratory burst.

Investigation of hypertonic saline (HTS) modulation of neutrophils (PMN) cytotoxic responses has generated seemingly contradictory results. Clinically relevant levels of HTS attenuate receptor-mediated p38 MAPK signaling, whereas higher levels activate p38 MAPK. Concurrently, HTS exerts a dose-dependent attenuation of the PMN respiratory burst, most notably at concentrations where p38 MAPK is activated. We hypothesized that HTS-mediated p38 MAPK activation augments the PMN respiratory burst on return to normotonicity. We found that although clinically relevant levels of HTS (Na+ > or = 200 mM) did not activate p38 MAPK, higher concentrations (Na+ > or = 300 mM) resulted in activation comparable with that after PAF stimulation. Transient stimulation with high levels of HTS primed the PMN respiratory burst in response to fMLP and PMA. This effect was attenuated by pretreatment with SB 203580, a p38 MAPK specific inhibitor. We conclude that severe osmotic shock primes the respiratory burst via p38 MAPK signaling, further supporting the role of this signaling cascade in PMN priming.

Blunt carotid and vertebral arterial injuries.

Blunt carotid and vertebral arterial injuries are uncommon but have the potential for devastating consequences. The classic presentation is a neurologic deficit unexplained by computed tomographic scan findings. Screening patients based on injury mechanisms and patterns allows the diagnosis and treatment of injuries while they are still asymptomatic, potentially improving neurologic outcomes. The development of a grading scale may help refine treatment guidelines. Accessible grade II, III, and V carotid injuries should be repaired surgically. Anticoagulation should be considered first-line therapy for grade I and IV, and inaccessible grade II and III carotid lesions, and grade I-IV vertebral injuries. Grade V and persistent grade III lesions may be best treated employing endovascular techniques.

Routine intraoperative laparoscopic ultrasonography with selective cholangiography reduces bile duct complications during laparoscopic cholecystectomy.

BACKGROUND: Laparoscopic cholecystectomy (LC) is the preferred treatment for gallstone disease, even in many complicated cases. Perhaps the only downside to LC is a two- to threefold increase in common bile duct (CBD) injuries compared with open cholecystectomy (OC). Intraoperative cholangiography may prevent inj uries, but its routine use remains controversial. Our institution adopted a policy of selective intraoperative cholangiography in 1993. When intraoperative laparoscopic ultrasonography (IOUS) emerged as a viable diagnostic adjunct, it was hypothesized that the routine use of IOUS would facilitate dissection, detect occult choledocholithiasis, and prevent bile duct injuries during LC. STUDY DESIGN: The experience with LC at our university-affiliated teaching hospital was reviewed. Over a 4 1/2-year period (June 1, 1995, to January 31, 2000), two surgeons used IOUS routinely during LC (ultrasonography [US] group, n = 248); three other surgeons did not (non-US group, n = 594). We compared patient data and outcomes between the two groups. Continuous, data are expressed as mean +/- SEM. RESULTS: During the study period, 842 LCs were attempted. Patient age (37+/-1 years) and gender (85% female) did not differ between the groups. In the US group, more patients had acute cholecystitis (p < 0.05). More LCs were performed per year by non-US surgeons than US surgeons (45 versus 37). Despite this, all bile duct complications occurred in non-US cases (2.5% overall): five CBD injuries (0.8%), six bile leaks (1%), and four retained CBD stones (0.7%). In the subgroup of patients with acute cholecystitis, there were fewer conversions to OC in US compared with non-US cases (24% versus 36%, p = 0.09). CONCLUSIONS: IOUS is noninvasive, fast, repeatable, and can corroborate real-time visualization of the operative field. We have found that LC with IOUS is associated with fewer bile duct complications (CBD injuries, bile leaks, and retained CBD stones) than LC without adjunctive imaging. The success rate of LC in cases of acute cholecystitis is slightly higher when IOUS is used as an aid to dissection. In the absence of definitive prospective data, we recommend routine use of IOUS when performing LC, particularly in patients with acute cholecystitis.

Post-hemorrhagic shock mesenteric lymph lipids prime neutrophils for enhanced cytotoxicity via phospholipase A2.

Hemorrhagic shock induced mesenteric hypoperfusion has long been implicated as a key event in the pathogenesis of the adult respiratory distress syndrome (ARDS) and multiple organ failure (MOF). Previous work links post-hemorrhagic shock mesenteric lymph (PHSML) lipids and neutrophil (PMN) priming in the pathogenesis of ARDS. We hypothesize that gut phospholipase A2 (PLA2) liberates proinflammatory lipids following hemorrhagic shock, which are responsible for enhanced PMN cytotoxicity. Mesenteric lymph was collected from rats (n > or = 5) before hemorrhagic shock, during hemorrhagic shock (MAP 40 mm Hg x 30 min), and after resuscitation (shed blood + 2x lactated Ringers). PMNs were incubated with physiologic concentrations (1-5%, v:v) of (a) buffer control, (b) sham (c) pre-shock lymph, (c) PHSML, (d) PHSML lipid extracts, (e) heat-denatured PSHML, and (f) PHSML harvested after i.v. pretreatment with a known PLA2 inhibitor (quinacrine, 10 mg/kg). PMNs were activated with fMLP (1 micromol), and the maximal rate of superoxide production measured by reduction of cytochrome c. Gut morphology was assessed histologically using hematoxalin and eosin (HE) staining. PHSML and PHSML lipid extracts (5%, v:v) primed for enhanced superoxide production compared to buffer controls (2.5-fold and 3.6-fold), sham (2.5-fold) and pre-shock lymph (2.0-fold). Lymph collected after systemic PLA2 inhibition, in contrast, abrogated the PMN priming response. Gut mucosal morphology, at end-resuscitation, was intact on HE staining both with and without PLA2 inhibition. Heat denaturing the PHSML (eliminating cytokines and complement), on the other hand, did not reduce PMN priming. Physiologic concentrations of PHSML lipids prime the PMN respiratory burst. Lymph priming is diminished with systemic PLA2 inhibition, implicating gut PLA2 as a source of proinflammatory lipids that may be central in the pathogenesis of hemorrhagic shock induced ARDS/MOF.

Phospholipase A(2)--derived neutral lipids from posthemorrhagic shock mesenteric lymph prime the neutrophil oxidative burst.

BACKGROUND: Our previous work identified posthemorrhagic shock mesenteric lymph (PHSML) lipids as key elements in polymorphonuclear neutrophil (PMN)--provoked acute lung injury. We hypothesize that gut phospholipase A(2) (PLA(2)) is responsible for the generation of proinflammatory lipids in PHSML that primes circulating PMNs for enhanced oxidative burst. METHODS: Mesenteric lymph was collected from rats (n = 5) before (preshock), during the induction of hemorrhagic shock (mean arterial pressure, 40 mm Hg x 30 minutes), and at resuscitation (shed blood + 2x lactated Ringer's solution). PLA(2) inhibition (quinacrine, 10 mg/kg, intravenously) was given before shock was induced. Extracted lipids were separated by normal phase high-pressure liquid chromatography and resuspended in albumin. PMNs were exposed to a 5% vol:vol concentration of eluted lipids and activated with N-formyl-methionyl-leucyl-phenylalanine (1 micromol/L). Superoxide production was assessed by cytochrome C reduction. RESULTS: High-pressure liquid chromatography--extracted neutral lipids of lymph collected before hemorrhagic shock did not prime the PMN oxidase, whereas isolated neutral lipids of postshock lymph primed PMNs 2.6- +/- 0.32-fold above baseline (P <.05). PLA(2) inhibition returned PHSML neutral lipid priming to baseline levels. CONCLUSIONS: PLA(2) inhibition before hemorrhagic shock abrogates the neutrophil priming effects of PHSML through reduction of the accumulation of proinflammatory neutral lipids. Identification of these PLA(2)-dependent lipids provides a mechanistic link that may have therapeutic implications for postshock acute lung injury.

Avoidance of abdominal compartment syndrome in damage-control laparotomy after trauma.

HYPOTHESIS: Abdominal compartment syndrome (ACS) is a morbid complication of damage-control laparotomy. Moreover, the technique of abdominal closure influences the frequency of ACS. DESIGN: Retrospective cohort study. SETTING: Urban level I trauma center. PATIENTS: We studied 52 patients with trauma who required damage-control laparotomy during the 5 years ending December 31, 1999, and who survived longer than 48 hours. MAIN OUTCOME MEASURES: Abdominal compartment syndrome, acute respiratory distress syndrome (ARDS), and multiple organ failure (MOF). RESULTS: Mean (+/- SD) age was 33 +/- 2 years; 38 (73%) were male. Mechanism of injury was blunt in 29 patients (56%), and mean (+/- SD) Injury Severity Score was 28 +/- 2. Development of ARDS and/or MOF was seen in 23 patients (44%); ARDS and MOF increased mortality from 12% (3/26) to 42% (11/26). Abdominal compartment syndrome was a common complication (17/52), and was associated with an increase in ARDS and/or MOF (12 patients [71%] vs 11 patients [31%] without ACS; P =.02, chi(2) test) and death (6 [35%] vs 8 patients [23%] without ACS). Primary fascial closure (n = 10) at the initial laparotomy was associated with ACS in 8 (80%) (P =.001, chi(2) test) and ARDS and/or MOF in 9 (90%) (P =.01, chi(2) test); skin closure (n = 25), with ACS in 6 (24%) and ARDS/MOF in 9 (36%); and Bogotá bag closure (n = 17), with ACS in 3 (18%) and ARDS/MOF in 8 (47%). CONCLUSIONS: Damage-control laparotomy is associated with frequent complications. In particular, ACS is a serious complication that increases ARDS and/or MOF and mortality. Avoiding primary fascial closure at the initial laparotomy can minimize the risk for ACS.

Evolution of a multidisciplinary clinical pathway for the management of unstable patients with pelvic fractures.

OBJECTIVE: To determine whether the evolution of the authors' clinical pathway for the treatment of hemodynamically compromised patients with pelvic fractures was associated with improved patient outcome. SUMMARY BACKGROUND DATA: Hemodynamically compromised patients with pelvic fractures present a complex challenge. The multidisciplinary trauma team must control hemorrhage, restore hemodynamics, and rapidly identify and treat associated life-threatening injuries. The authors developed a clinical pathway consisting of five primary elements: immediate trauma attending surgeon's presence in the emergency department, early simultaneous transfusion of blood and coagulation factors, prompt diagnosis and management of associated life-threatening injuries, stabilization of the pelvic girdle, and timely insinuation of pelvic angiography and embolization. The addition of two orthopedic pelvic fracture specialists led to a revision of the pathway, emphasizing immediate emergency department presence of the orthopedic trauma attending to provide joint decision making with the trauma surgeon, closing the pelvic volume in the emergency department, and using alternatives to traditional external fixation devices. METHODS: Using trauma registry and blood bank records, the authors identified pelvic fracture patients receiving blood transfusions in the emergency department. They analyzed patients treated before versus after the May 1998 revision of the clinical pathway. RESULTS: A higher proportion of patients in the late period had blood pressure less than 90 mmHg (52% vs. 35%). In the late period, diagnostic peritoneal lavage was phased out in favor of torso ultrasound as a primary triage tool, and pelvic binding and C-clamp application largely replaced traditional external fixation devices. The overall death rate decreased from 31% in the early period to 15% in the later period, as did the rate of deaths from exsanguination (9% to 1%), multiple organ failure (12% to 1%), and death within 24 hours (16% to 5%). CONCLUSIONS: The evolution of a multidisciplinary clinical pathway, coordinating the resources of a level 1 trauma center and directed by joint decision making between trauma surgeons and orthopedic traumatologists, has resulted in improved patient survival. The primary benefits appear to be in reducing early deaths from exsanguination and late deaths from multiple organ failure.

Hypertonic saline attenuation of the neutrophil cytotoxic response is reversed upon restoration of normotonicity and reestablished by repeated hypertonic challenge.

BACKGROUND: Hypertonic saline (HTS) resuscitation, in addition to enhancing hemodynamic recovery, modulates postinjury hyperinflammation in the critically injured. The polymorphonuclear neutrophil (PMN) cytotoxic response, a key element in the pathogenesis of postinjury organ dysfunction, is attenuated under hypertonic conditions. Although plasma Na(+) rises to 180 mmol/L after HTS infusion, baseline levels are reestablished within 24 hours. We hypothesized that HTS attenuation of the PMN cytotoxic response (beta2-integrin expression, elastase release, and O2- production) is reversed upon return to normotonicity, but can be reestablished by repeated HTS challenge. METHODS: Isolated human PMNs were incubated in HTS (Na(+) = 180 mmol/L) for 5 minutes at 37 degrees C then returned to normotonicity by centrifugation and resuspension in isotonic buffer. Stimulated (PAF) beta2-integrin expression was measured by flow cytometry. Stimulated (PAF/fMLP) elastase release and O2- production were measured by cleavage of N-methoxysuccinyl-Ala-Ala-Pro-Val p-nitroanilide and reduction of cytochrome c (Cyt c). Protein tyrosine phosphorylation in PMN cell lysates was assessed by Western blot. RESULTS: Clinically relevant levels of HTS induced tyrosine phosphorylation in resting PMNs and attenuated cytotoxic responses. Reestablishment of normotonicity returned these functions to baseline. A repeated HTS challenge after restoration of normotonicity also induced tyrosine phosphorylation and suppressed the cytotoxic response. CONCLUSIONS: HTS attenuation of the PMN cytotoxic response is reversible but can be reestablished by repeated HTS treatment. This phenomenon may provide the unique opportunity to selectively and temporarily decrease the postinjury inflammatory response when patients are at greatest risk for PMN-mediated tissue damage.