Highlights  A novel model to study lamellar signaling events during preferential weight bearing is presented.  Lamellar signaling events related to hypoxia and inflammation were assessed.  Lamellar hypoxia inducible factor-1a was increased in the supporting limb relative to the contralateral hind limb.  No differences in lamellar inflammatory signaling were present between the supporting limb and hind limbs.

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Background: Incisional complications are a common cause of morbidity following laparotomy. Although uncommon, acute abdominal dehiscence (AAD) is a potentially fatal post-operative complication. However, few AAD cases are described in the literature. Objectives:To describe common features of cases of AAD following ventral midline laparotomy, management and outcomes. Study design: Retrospective case series.Methods: Hospital records of horses that underwent a ventral midline laparotomy at nine hospitals in the UK, Ireland and USA over a 10-year period (2009-2019) were reviewed. Data were collected for pre-, intra-and post-operative factors that were considered relevant. Descriptive statistical analysis was performed.Results: A total of 63 cases of AAD were identified. AAD occurred due to tearing of sutures through the linea alba or rupture of the body wall adjacent to the suture line in 46 horses (73%). AAD occurred at a median of 5 days (0.5-70 days) postoperatively and broodmares accounted for 25% of the cases (n = 16). Surgical site infection developed prior to AAD in 28 horses (44%); leakage of peritoneal fluid occurred in 5% of horses prior to AAD being identified. Surgical repair was performed in 27 horses (43%), 10 (16%) were treated conservatively and 26 (41%) were euthanised immediately. Repair was most frequently performed using suture (n = 14), wire (n = 5) or a combination (n = 5). Overall survival to hospital discharge was 39% (24/63). Where surgical repair was performed, 15 horses (56%) survived to hospital discharge; 9 horses (90%) managed conservatively survived to hospital discharge.Main limitations: Follow-up was not performed for all cases following hospital discharge and some data were incompletely recorded in hospital files.

Increased concentrations of activated ERK 1/2 and SAPK/JNK in the acute stages of SRL indicate a possible role of these signalling proteins in lamellar injury. Signalling related to ERK 1/2 and SAPK/JNK 1/2 pathways should be further investigated to determine if these play a detrimental role in laminitis and may be therapeutic targets to be manipulated independently of RDH.

Background Increased intraabdominal pressure, termed intraabdominal hypertension (IAH), is reported as an independent cause of morbidity and mortality in the human ICU but, until recently, has been rarely described in veterinary species outside of experimental models. Failure to identify severe IAH leads to organ dysfunction, termed abdominal compartment syndrome, and rapidly becomes fatal without therapeutic intervention. Although the veterinary community has been slow to address the concept of IAH and associated comorbidities, recent companion and large animal case series and experimental studies suggest IAH may also be common in veterinary species and correlates well with risk factors and grading systems already described in the human literature. Pathophysiology Increasing abdominal pressures exert deleterious local effects through visceral ischemia and reperfusion injury as well as systemic effects on the cardiovascular, pulmonary, renal, and central nervous systems. Even mild grades of IAH increase systemic vascular resistance, impede venous return, increase pulmonary wedge pressure, and decrease pulmonary function. More severe grades cause azotemia, oliguria, decreased coronary blood flow, hypoxia, increased intracranial pressure, and death. Importance Many of the common diseases in veterinary patients are associated with IAH, including gastric dilatation–volvulus, colon volvulus, closed pyometra, hemoperitoneum, ascites, uroperitoneum, and hydrops. Monitoring of the veterinary patient is difficult, but several experimental studies validate both the presence of IAH and the ability to monitor abdominal pressures in large and small animal species. Moreover, prompt recognition of IAH and subsequent treatment is feasible in the veterinary ICU. Key points Increasing abdominal pressures exert deleterious local effects through visceral ischemia and reperfusion injury as well as systemic effects on the cardiovascular, pulmonary, renal, and central nervous systems. Increases in central venous pressure, systemic vascular resistance, pulmonary wedge pressure, and a decreased cardiac output by way of both decreased preload and increased afterload have been documented as a result of intraabdominal hypertension (IAH). Direct diagnosis of IAH is achieved by blind or ultrasound‐guided abdominal needle puncture attached to a water manometer or direct pressure monitoring transducer. Transvesicular measurement of intraabdominal pressure (IAP) is relatively noninvasive, and many patients that would benefit from rapid diagnosis of IAH and abdominal compartment syndrome already have indwelling bladder catheters. Recommendations for interventions are based on the assigned grade of IAH (mild, moderate, severe). Key points If IAH is strongly suspected or diagnosed, abdominal wall compliance may be improved through judicious use of neuromuscular blockers and sedation. Decompression, either minimally invasive or surgical, is absolutely recommended for IAPs consistently above 20 mm Hg, especially in the presence of signs...