Core Topics in General & Emergency Surgery: Companion to Specialist Surgical Practice (83 page)
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Authors: Simon Paterson-Brown MBBS MPhil MS FRCS
Emma Barrow and
Iain D. Anderson
Abdominal sepsis accounts for many of the serious and all too often fatal emergency conditions that the general surgeon is called upon to treat. It may arise primarily from conditions as seemingly simple and routine as appendicitis, to more complicated and serious conditions such as diverticulitis and perforated peptic ulcer disease. Alternatively it may arise as a consequence of complications of surgery, particularly intestinal anastomotic leakage. While, with experience and a few basic principles, even complex cases of abdominal sepsis can be relatively straightforward to manage, not infrequently the diagnosis is obscured and delayed. As a consequence treatment is often complicated and prolonged. Some 80–90% of general surgical deaths follow emergency admission,
1
and much of this morbidity and mortality expresses itself through the processes of abdominal sepsis. Delay to operation is the single most common reason for adverse outcomes and anastomotic leak the single commonest cited complication in fatal cases. These will be recurring themes in this chapter as even with optimal treatment of abdominal sepsis, multiple organ failure (MOF) may ensue. MOF is more likely and often fatal when treatment is slow or suboptimal. In the intensive care unit (ICU), abdominal sepsis constitutes a substantial proportion of the patients with MOF. Given its frequency and severity, a sound understanding of abdominal sepsis must be integral to every general surgeon's professional armamentarium.
This chapter will address the diagnosis and management of abdominal sepsis, including the complex patient in the ICU, where sequelae such as abdominal compartment syndrome, management of the open abdomen and intestinal fistulation can create particular difficulties. The reader is referred to
Chapter 16
for a description of the intensive care management of the surgical patient,
Chapters 6
,
Chapters 8
,
9
,
10
and
13
for more detail on specific causal conditions, and to
Chapter 17
for surgical nutrition.
The systemic inflammatory response syndrome (SIRS) is a clinically defined response (
Box 18.1
) to a variety of insults including trauma, burns, pancreatitis, tissue ischaemia and inflammatory bowel disease. When the cause of SIRS is a proven or suspected infection, it is termed sepsis. The normal response to infection serves to localise and control bacterial invasion. This occurs through the chemotaxis of neutrophils and macrophages, which in turn release inflammatory mediators. When this inflammatory response becomes generalised, sepsis results. This is characterised by systemic vasodilation and resultant hypotension, increased vascular permeability leading to fluid exudate, and microcirculatory dysfunction with decreased capillary flow. These factors ultimately result in tissue hypoxia. Once triggered, the downward spiral of severe sepsis is believed to be independent of the precipitating infectious insult.
Box 18.1
Sepsis definitions
13
Systemic inflammatory response syndrome (SIRS)
SIRS is defined by the presence of two or more of the following clinical findings:
Body temperature > 38 °C or > 36 °C
Heart rate > 90 per minute
Respiratory rate > 20 per minute or PaCO
2
< 4.3 kPa
White cell count > 12 × 10
9
/L or < 4 × 10
9
/L
Sepsis
SIRS plus a documented or suspected infection
Severe sepsis
Sepsis plus clinical evidence of organ dysfunction:
Hypoxia
Oliguria
Hypotension
Confusion
Disturbances to coagulation
Disturbances to liver synthetic function
Septic shock
Sepsis with acute circulatory failure, despite adequate volume resuscitation in the absence of other causes of hypotension
SBP < 90 mmHg
MAP < 60 mmHg
Multiple organ dysfunction syndrome (MODS)
Altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention
Potentially reversible
Affects two or more organ systems
The theory that sepsis is due to an exaggerated, uncontrolled inflammatory response has now been shown to be overly simplistic. There is no single mediator, system or pathway that drives the pathophysiology of SIRS and sepsis. The predominant theories can be summarised as follows:
Uncontrolled systemic cytokine release.
Uncontrolled release of cytokines from macrophages in response to cellular injury is proposed to initiate other mediator cascades and activate neutrophils and platelets. The particular candidate mediators are tumour necrosis factor (TNF) α, interleukin (IL)-1 and IL-6.
2
However, circulating levels of cytokines are highly variable between different studies and indeed within study populations.
3
Numerous trials have been conducted on agents that block the inflammatory cascade: corticosteroids, TNFα antagonists and anticytokine monoclonal antibodies. These have failed to demonstrate a survival advantage.
3
Individual randomised trials in the clinical effectiveness of activated protein C in severe sepsis showed promising results,
3
but a recent Cochrane review concluded no survival advantage
4
and it has now been withdrawn.
Disturbances to coagulation.
During sepsis, significant alterations occur within both the coagulation and fibrinolytic systems. Activation of vascular endothelial cells by inflammatory mediators leads to a prothrombotic state, which can result in disseminated intravascular coagulation (DIC). This leads to reduced end perfusion, and the subsequent consumption of platelets and clotting factors results in prolonged clotting times.
3
,
5
Immunosuppression.
Another emerging theory implicates immunosuppression rather than immunostimulation in the aetiology of sepsis. Patients with sepsis display features of immunosuppression, such as an inability to clear infection and predisposition towards nosocomial pathogens.
3
A proposed mechanism is a shift from T helper cell secretion of inflammatory cytokines such as TNFα, IL-1 and IL-6 to the anti-inflammatory cytokines IL-4 and IL-10.
3
,
5
This pattern of cytokine release has been observed in septic patients in an intensive care setting.
6
,
7
Lymphocyte apoptosis is another postulated pathway.
3
SIRS and sepsis occur commonly amongst surgical patients on the ward, although they are usually resolved by appropriate treatment of the underlying problem. Sometimes the physiological derangement persists and, particularly when it does so beyond 48 hours, outcome is worsened as progression to organ dysfunction is much more likely. Organ dysfunction denotes severe sepsis and the next step is organ failure, which typically carries a mortality of the order of 40%. Mortality, in general, increases with the number of organ systems affected and with the severity of physiological disturbance at onset.
8
While the onset of SIRS does not accurately predict development of sepsis or the multiple organ dysfunction syndrome (MODS), the progression from SIRS to severe sepsis is associated with increasing risk of multiple organ failure.
9
Approximately 30% of septic patients develop at least one organ dysfunction.
10
Therefore, timely recognition of SIRS, particularly if persistent, alerts the clinician to a potentially deteriorating situation at a time when prompt intervention may yet avert catastrophe. By the time the patient with abdominal sepsis has developed shock, the mortality increases from less than 10% to greater than 50%.
11
,
12
The identification and active management of SIRS and early organ dysfunction is therefore an important first step as, once organ dysfunction is under way, the patient is on a slippery slope that can lead them rapidly downwards despite the best treatment. It is essential that the surgeon appreciates that these processes often start insidiously on the ward and that early detection is vital, as management is most successful at this stage. While there are objective criteria that define organ dysfunction, clinical findings are useful pointers. Hypoxia, oliguria, hypotension, deranged liver function tests or clotting, thrombocytopenia, acidosis and confusion are some of the plethora of signs that indicate that a severe systemic derangement is in process.
The importance of detecting the often subtle signs of abdominal sepsis at the earliest stage cannot be overemphasised and while the rate with which organ dysfunction develops in individual patients will vary, the requirement for rapid identification and treatment remains key.
9
SIRS, sepsis and their sequelae are recognised and defined according to a number of clinical criteria;
13
these are summarised in
Box 18.1
. Whilst these specific criteria are not intended as a substitute for clinical acumen, their use facilitates early identification and appropriate treatment of sepsis by even the most junior member of the surgical team. SIRS and sepsis can be adequately managed on the ward, providing there is response to treatment. However, the deteriorating patient or those with severe sepsis are more appropriately transferred to a critical care environment, where invasive arterial and central venous pressure monitoring will guide resuscitation. The benefits of managing such high-risk surgical patients with early critical care input are well recognised.
14
,
15
In 2008, informed by the results of a number of clinical trials, an international campaign was launched,
16
with the intention of improving outcomes in severe sepsis and septic shock by standardising care. The emphasis of the campaign was timely identification and treatment of patients with severe sepsis, using goal-directed strategies (the rationale for this is detailed in
Chapter 16
). Evidence-based guidelines were published in 2004, split into ‘bundles’ of care to be accomplished within certain time frames (
Box 18.2
). A total of 165 sites participated in the campaign, submitting bundle compliance and outcome data on 15 022 patients with severe sepsis. Despite incomplete compliance, a significant reduction in unadjusted hospital mortality (37% to 31% over the 2-year study period) was identified in those centres participating in the campaign.
17
Box 18.2
Surviving Sepsis Campaign bundles
16
Sepsis resuscitation bundle
To be accomplished within the first 6 hours of identification of severe sepsis:
Measure serum lactate
Obtain blood cultures prior to antibiotic administration
Administer broad-spectrum antibiotic, within 3 hours of A&E admission and within 1 hour for current inpatients
In the event of hypotension and/or a serum lactate > 4 mmol/L:
Deliver an initial minimum of 20 mL/kg of crystalloid or an equivalent
Apply vasopressors for hypotension not responding to initial fluid resuscitation to maintain mean arterial pressure (MAP) > 65 mmHg
In the event of persistent hypotension despite fluid resuscitation (septic shock) and/or lactate > 4 mmol/L:
Achieve a central venous pressure (CVP) of > 8 mmHg
Achieve a central venous oxygen saturation (ScvO
2
) > 70% or mixed venous oxygen saturation (SvO
2
) > 65%
Sepsis management bundle
To be accomplished within the first 24 hours of identification of severe sepsis:
Administer low-dose steroids for septic shock in accordance with a standardised ICU policy
Maintain glucose control > 70 but < 150 mg/dL
Maintain a median inspiratory plateau pressure (IPP) < 30 cm H
2
O for mechanically ventilated patients
The goal-directed treatment bundles developed by the Surviving Sepsis Campaign are to be recommended as a standard of care. Their use in the timely identification and management of patients with severe sepsis has been shown to reduce mortality.
17
