Mortality following dehiscence of sutured anastomosis in a dog

A three-year-old male cross-breed dog with no prior transfusion history presented to a rural clinic for postsurgical acute abdomen.

Four days earlier, jejunal intestinal resection and end-to-end sutured anastomosis was performed after hours at the same clinic, immediately after the dog sustained a pig tusk-induced perforation of the abdominal wall, leading to moderate peritoneal contamination and jejunal bruising of questionable viability.

Four % succinylated fluid gelatin (gelofusine) and lactated Ringer’s fluids were given intraoperatively and postoperatively. Signs were suggestive of mild to moderate systemic hypoperfusion – evidenced by slightly injected mucous membranes, mild tachycardia and slight changes in demeanour. Mucous membrane injection was suggestive of maldistributive hypoperfusion.

Other abnormalities included progressive pyrexia (39.4°C), repeated vomiting and generalised abdominal pain suggestive of peritonitis. Dehiscence of anastomosis was confirmed per laparotomy.

List of problems

A revised problem list included secondary localised (tending to diffuse) peritonitis and non-specific signs compatible with the systemic inflammatory response syndrome (SIRS; American College of Chest Physicians [ACCP] and Society of Critical Care Medicine [SCCM] Consensus Conference Committee, 1992). Intra-abdominal infection was suspected and combined with signs of hypoperfusion, the patient could be categorised as septic (ACCP and SCCM, 1992; Levy et al, 2003).

Contaminated omentum was excised and a second jejunectomy performed for fresh anastomosis. Omentalisation and serosal patching were not performed to support the repair (Volk, 2006) and not all adhesions were broken down, precluding full contamination assessment of the length of the intestinal tract. The pancreas was not grossly inspected, but pancreatitis can result from peritonitis (King, 1994).

The abdomen was flushed with warmed 0.9% sodium chloride and a Penrose drain was placed through a paramedian ventral abdominal incision. Preoperative IM buprenorphine and subcutaneous cefalexin were given and lactated Ringer’s solution, intraperitoneal penicillin G and IV metronidazole were administered intraoperatively. Sodium lactate was continued postoperatively and voluntary enteral feeding with a prescription diet initiated 12 hours postsurgery.

Two days after the second anastomosis, the patient displaced the drain. Abdominal pain had markedly reduced, discharge from the laparotomy wound was minimal and perfusion parameters were normal, but moderate pyrexia remained apparent. Appetite remained good and no emesis occurred until five days after the second anastomosis. At this point, abdominal distension became apparent, vomiting recurred and a third laparotomy was performed.

More marked peritonitis, with widespread fibrinous adhesions and exudate, followed another anastomosis dehiscence and particulate food matter was carefully dissected away from peritoneal linings. A third jejunal enterectomy and end-to-end interrupted suture anastomosis was performed. Supportive treatments were provided as described, except the caudal inch of the laparotomy wound was left open for drainage and covered with sterile gauze.

Abdominal incision seepage became pronounced and haemorrhagic within two days. A revised problem list comprised of severe generalised peritonitis, compatibility with SIRS (Moore and Moore, 2013) and severe sepsis given potential coagulopathy as evidence of single organ dysfunction (Levy et al, 2003; Dellinger et al, 2013; Dickinson et al, 2015; Kenney et al, 2010).

The patient received an unmatched whole blood transfusion of 11ml/kg in an attempt to address potential disorders of primary and secondary haemostasis in the absence of fresh frozen plasma or cryoprecipitate. Two days later, protruding omentum occluded drainage and an abdominal flush was repeated using two litres of warmed 0.9% saline under general anaesthesia.

After 10 days, weight loss accelerated and a degenerative left shift neutrophilia (white cell count 17.4 × 109/L) and severe hypoalbuminaemia (18g/dL) were recorded. The patient remained pyrexic and multifocal subdermal swellings developed on the face.

Depression in demeanour developed and persistent vomiting began. Euthanasia was performed following a diagnosis of fulminant septic peritonitis (Bosscha et al, 1999) with generalised oedema and fibrin deposition so severe it irreversibly interfered with lymphatic drainage of the peritoneum (Swann and Hughes, 2000). Septic shock likely refractory to vasopressor support was possibly impending.

Abdominal sepsis

Septic peritonitis is a life-threatening outcome to the loss of enteric integrity and studies have identified several risk factors associated with leakage following intestinal anastomoses. One retrospective study of risk factors for dehiscence in dogs identified patients with combinations of preoperative peritonitis, intestinal foreign body and serum albumin concentrations less than 2.5g/dL as having a risk of dehiscence (Ralphs et al, 2003).

Another retrospective study focusing on the failure to survive following gastrointestinal surgery found similar risk factors, but included intraoperative hypotension as a risk factor for death (Grimes et al, 2011). The surgeons’ inexperience may have played an important part in this dehiscence.

Studies largely focus on identifying prognostic indicators as the foundation for developing targeted strategies to improve survival in patients with septic peritonitis. The wide variation in mortality rates reported likely reflect the diversity of aetiologies and the multiplicity of interacting factors potentially involved in determining outcome.

Identifying the most salient prognostic factors from this multiplicity in veterinary patients has been rendered difficult by the heterogeneity of the patient population and inclusion criteria employed to compare patients, the retrospective nature of studies, the invariably small number of animals matching inclusion criteria and, perhaps most importantly, a lack of standardised measures of severity render it difficult to make “direct” comparisons between patients and outcomes in and across studies (Bentley et al, 2007; Bosscha et al, 1999).

It is likely the case outcome would have been positive if dehiscence and its sequelae were managed originally properly and expediently. Indeed, good outcomes can be obtained following dehiscence, leading to similar severity of peritonitis.

In one study focusing exclusively on peritonitis secondary to aetiology of gastrointestinal origin, a survival rate of 85% was attained despite 80% of inclusions (n=20) requiring dehiscence correction, 43% of which required correction a second time (Adams et al, 2014).

In another study, three surviving patients with perforating intestinal foreign bodies had multiple surgeries to repair failed intestinal anastomoses during their period of open peritoneal drainage and all survived (Winkler and Greenfield, 2000). Furthermore, signs compatible with multiple organ dysfunction may not have developed in the patient at the time of initial dehiscence, and preoperative organ dysfunction is considered an important predictor of mortality (Ralphs et al, 2003; Mouat et al, 2014; Kenney et al, 2010).

Most outcome studies emphasise the cornerstones of resolution of abdominal sepsis as early diagnosis, thorough source control, attention to adequate abdominal drainage, antibiotic therapy (Dickinson et al, 2015) and intensive medical support of major body systems – particularly to institute rapid correction of the “lethal triad” of coagulopathy, inflammation and cardiovascular instability resulting from abdominal sepsis (Hecker et al, 2014).

The balance between the need for relaparotomy and to correct pathophysiological derangements beforehand presented a particular quandary in this patient and monitoring was not intensive enough for adequate observation of organ functions. The outcome in this case may have been significantly related to failure to establish prompt and adequate abdominal drainage early in the case management.

Nevertheless, the retrospective nature of veterinary studies focusing on drainage make it difficult to draw firm conclusions about relative protective effects of different methods of open drainage (Woolfson and Dulisch, 1986; Mueller et al, 2001; Staatz et al, 2002; Adams et al, 2014) and whether open abdominal drainage confers benefit over intermittent lavage or no drainage at all (Lanz et al, 2001; Dayer et al, 2013).

Surgery survival rates

Survival varies from 52% to 89%, but these were not related to a comprehensive and repeatable determination of severity. The highest recorded survival rates of 85% following the surgical management of septic peritonitis of gastrointestinal origin (Adams et al, 2014) lend support to the value of closed suction drainage using Jackson-Pratt drains as an integral tool. However, the number of animals meeting inclusion criteria was small and a large component of favourable outcomes could be attributed to the careful and skilled resolution of the cause and patient-tailored appropriateness of postoperative management.

Stoma-based diversion techniques reduce the risks of dehiscence in humans (Hyman, 2009) and relaparotomies are integral to source control with persisting sepsis or questionable bowel viability (de Graaf et al, 1996; Hecker et al, 2014). Successful relaparotomy, however, requires extensive “damage control” to ensure “lethal triad” is managed, as relaparotomy may adversely affect the triad.

The development of vacuum-assisted closure techniques in humans permits accelerated sepsis source control while allowing for better timed anastomosis with complex septic intra-abdominal complications in patients with unfavourable preoperative and intraoperative conditions, such as septic shock and organ failure (Perathoner et al, 2010).

Failure to aggressively remove all lavage fluid may also have been significant and vacuum-assisted abdominal drainage techniques have been employed to assist with postoperative management of septic peritonitis in dogs and cats, for the benefits they confer in reducing abdominal contamination, widening relaparotomy intervals and reducing nosocomial infection risk and visceral oedema, thus improving perfusion of visceral organs in the face of peritonitis (Cioffi et al, 2012).

However, conclusions about the merit of the technique cannot yet be drawn due to the study’s lack of robustness. Furthermore, a visceral protective layer was not placed over the viscera (as it is in human medicine) prior to the application of the open-cell reticulated foam, which reduces complications of vacuum-assisted drainage in people (Perathoner et al, 2010). Nevertheless, a 50% survival was attained in this study despite case bias being towards those chosen on the inability to adequately debride and eliminate peritoneal contamination.

Abdominal drainage could influence the progression of hypoalbuminaemia, itself considered a significant risk factor for mortality in many critical abdominal states in human and veterinary medicine (Wahl et al, 1992; Ralphs et al, 2003; Grimes et al, 2011). This patient developed moderately severe hypoalbuminaemia and this could have contributed towards poor anastomosis healing (Harvey, 1990) and acute gastrointestinal injury from altered fluid compartment dynamics (Boller, 2014).

Hypoalbuminaemia below 19g/dL was shown to be a significant predictor of non-survival in the face of septic peritonitis in one study (Bentley et al, 2007), although hypoalbuminaemia could be as much a marker for disease severity (Grimes et al, 2011).

Given the pathogenesis of peritonitis, rates of loss of effective protein from the vasculature could be independent of abdominal drainage, irrespective of the method used. Single-dose lyophilised canine-specific albumin (CSA) has been trialled to counter the progression of hypoalbuminaemia in states of septic peritonitis and, as well as being a replacement therapy, albumin supplementation may help mediate the inflammatory response via modulation of endothelial cell reactivity and contribute to the reduction of further losses (Craft and Powell, 2012).

Although the trial was randomised, it was unable to provide evidence for improving survivorship following the administration of a single postoperative dose of 800mg/kg CSA. More studies are needed to properly assess the merits and risks.

Postoperative diet

Postoperatively, the patient began consuming only 200 calories per day (cal/day), falling well short of resting energy requirements (RER) of 900cal/day. Bodyweight fell by 21% over the morbidity period.

Patients not anticipated to consume their RER for three to five days are at high risk of malnutrition, which may have serious adverse effects on tissue synthesis, immune competence, gut integrity and intermediary drug metabolism (Eirmann and Michel, 2009). Furthermore, the hypermetabolic state and catabolism associated with the release of stress hormones follows the local and systemic inflammatory response induced by sepsis (Liu et al, 2012), which may raise energy expenditure by 30% in septicaemic patients (Wolfe et al, 1982).

Meeting the nutritional requirements of this patient was made difficult by recurrent emesis, a difficulty shared by attempts to employ early enteral nutrition to meet the metabolic demands of many critically ill human patients (O’Leary et al, 2007).

Persistent emesis may have precipitated from an overwhelmed enteric system due to an overzealous, rather than “micro-enteral”, introduction of food and without better understanding of body perfusion status, and electrolyte and acid-base balance, the optimal timing introducing enteral nutrition was hard to ascertain. It is also unknown what benefits, if any, would have been conferred had anti-emetics and/or promotility agents been administered and had a means of evacuating gastrointestinal content been placed.

It is possible persistent emesis may have been inevitable due to failure to address the peritonitis-based causes of enteric dysfunction, even though enteric nutrition is ostensibly tolerated in the setting of ileus and is recommended in clinical management guidelines for conditions where intra-abdominal sepsis may occur in humans (Meier et al, 2002).

No convincing evidence exists to support the optimal timing of early enteral nutrition in veterinary literature
and attempts to initiate enteral feeding by means other than jejunal tube may have initially been contraindicated, despite the strong body of evidence for a protective effect of enteral feeding on gut-mediated immunity, metabolic response to stress, maintenance of microbial diversity and minimisation of bacterial translocation (Martindale and Warren, 2015).

Evidence to guide clinical decisions regarding the optimal nutritional strategy in the face of septic peritonitis is limited (Liu et al, 2012) and, although concerns have been raised about the potential impact of parenteral nutrition on various gastrointestinal endocrine and immunological homeostatic mechanisms, RER could have been provided parenterally in this patient. Failure to meet nutritional needs is hypothesised to be another important contributor to the poor outcome in this case.

Managing peritonitis

Supportive means of managing peritonitis also emphasise sepsis management in a systemic context and, in particular, on minimising its deleterious systemic inflammatory effects, given the importance of the host response to infection as a significant element of the pathophysiology of sepsis (Levy et al, 2003).

To develop an evidence basis for interventions that target sepsis, paradigms need to be developed to accurately define and identify sepsis, and score its severity. No pathognomonic clinical signs of sepsis exist and this patient was only presumed to be in such a state at readmission – given the presence of non-specific signs consistent with SIRS (Levy et al, 2003) difficult to explain without infection.

The predisposition-infection-response-organ failure paradigm used in humans may be a useful foundation for stratifying cases into risk of adverse outcome and expected response to therapy (Levy et al, 2003) that may have veterinary uses (Otto, 2007), but it may have population-based, trial relevance than individual application.

The simple concepts of sepsis, severe sepsis and septic shock remain clinically useful for prognostication and without more intensive diagnostic evaluation to better assess inflammatory, haemodynamic, tissue perfusion and organ dysfunction parameters, it was not possible to ascertain the severity of sepsis in this patient early on or during hospitalisation.

An over-exuberant systemic inflammatory response is a key driver of multi-organ failure in human trauma patients. This is partly because the ensuing immune dysregulation, endothelial dysfunction and immunoparesis predispose towards sepsis, which further aggravates the systemic inflammatory response (Lord et al, 2014).

With the exception of antibiotic therapy, the systemic management of sepsis is largely supportive, because patient populations with sepsis have proven too heterogeneous to identify protective effects without developing better ways to characterise sepsis for targeting therapies (Vincent, 2015).

It is unknown whether antimicrobial therapy in this patient was appropriate; additional studies are needed to assess the significance of appropriate therapy with different forms and severity of sepsis in veterinary patients (Dickinson et al, 2015).

A number of factors may have collectively contributed to the demise of this patient. Failure to detect dehiscence early, aggressively establish early drainage, and counter progression of hypoalbuminaemia and protein catabolism were undoubtedly of paramount importance.

More intensive monitoring of major organ systems and function may have influenced the outcome. To this end, serial evaluation should have included preoperative blood culture, systolic and mean blood pressure, central venous pressure, mixed venous oxygen saturation and arterial partial pressure of oxygen, activated partial thromboplastin time, thrombocyte count, urine output creatinine measures, bilirubin levels, blood glucose and lactate evaluation.

Serial abdominal ultrasound and abdominocentesis, with cytological assessment and comparison of centesis lactate and glucose levels with blood values, may provide additional information about the progression of septic peritonitis.