Abdominal Sepsis: Causes, Why Does It Happen? Treatment, Mortality Level and Study

What is Abdominal Sepsis about?

Severe sepsis and septic shock

First of all, before talking about abdominal sepsis, we should talk about infections.

Infections, if they are often benign but not treated early and appropriately, can become complicated dramatic states that have long been called septicemia.

This term reflects the massive invasion of the organism by microbes with the risk that the body’s defenses are overwhelmed.

However, it is inaccurate because it does not take into account the different phases of the evolution of the infection.

New terms have emerged for abdominal sepsis, which are severe sepsis and septic shock, but their definitions do not always cover all infections that can be complicated by serious infectious diseases and death.

The clinical picture of these urgent infectious states usually represents a sudden alteration of the general state, in the course of a fever (or equivalent), which can be complicated by an attack on the main functions of the organism or even with a state of shock.

The fulminant purple coloration, due to the meningococcus, is a “particular body paint” whose evolution has the appearance of an extensive necrotic purple spot.

It is a disease associated with significant morbidity and mortality rates due to its implications in the damage and death of organs and tissues located in the abdominal area.

The results of prospective trials have often overestimated the corollaries of patients with severe peritonitis.

However, the results of published clinical trials may not be representative of the true morbidity and mortality rates of these infections.

Patients who have perforated appendicitis are usually more represented in clinical trials.

In addition, patients with intra-abdominal infection enrolled in clinical trials often have a greater chance of cure and survival.

In fact, the eligibility criteria of the trials often restrict the inclusion of patients with diseases that would increase the mortality rate of patients with intra-abdominal infections.

After excluding patients with perforated appendicitis, they found that the cure rate between patients who had intra-abdominal infections and enrolled in clinical trials was much higher than that of patients who were not enrolled (79% vs. 41% ) and that the mortality rate was much lower 10% versus 33%).

Epidemiological studies of patients with intra-abdominal infections including severely ill subjects have shown higher mortality rates.

In the CIAO study, the overall mortality rate was 7.7%. When analyzing the subgroup of patients with severe sepsis or septic shock at hospital admission, the mortality rate reached 32.4% (89/274). In patients with severe sepsis or septic shock in the immediate postoperative period, the mortality rate was 42.3% (110/266).

Why does abdominal sepsis occur? – Causes

Abdominal sepsis represents the systemic inflammatory response of the host to bacterial or yeast peritonitis.

In the case of gram-negative, gram-positive and anaerobic peritonitis bacteria, including the common intestinal flora, such as Escherichia coli, Klebsiella pneumoniae, streptococcus SPP. and Bacteroides fragilis, these enter through the peritoneal cavity.

Sepsis of abdominal origin is initiated by the external membrane component of gram-negative organisms (for example, lipopolysaccharide, lipid A or endotoxin), or gram-positive organisms (eg lipothyotic acid or peptidoglycan), as well as anaerobic toxins .

This leads to the release of proinflammatory cytokines such as tumor necrosis factor and interleukins.

This necrosis and the interleukins lead to the production of toxic mediators, including prostaglandins, leukotrienes, platelet activating factor and phospholipase A2, which damage the endothelial lining, which leads to an increase in capillary leaks.

Cytokines lead to the production of adhesion molecules on endothelial cells and neutrophils. The interaction between neutrophils and endothelial cells leads to increased endothelial damage through the release of neutrophil components.

Activated neutrophils release nitric oxide, a potent vasodilator that leads to septic shock. Cytokines also alter the natural modulators of coagulation and inflammation, activated protein C and antithrombin. As a result, multiple organ failure can occur.

Early detection and timely therapeutic intervention can improve the prognosis and overall clinical outcome of septic patients. However, early diagnosis of sepsis can be difficult.

Determining which patients show signs of infection during an initial evaluation, if they have it now, or later develop a more serious disease is not an easy or simple task.

Abdominal sepsis is a complex multifactorial syndrome that can evolve in conditions of variable severity. If left untreated, it can lead to functional impairment of one or more vital organs or systems.

The severity of the disease and the inherent risk of mortality increase from sepsis to severe sepsis and septic shock to multiorgan failure.

Diagnosis of abdominal sepsis

The causes of a severe septic syndrome are very numerous and you can only indicate a procedure based on a careful and repeated clinical examination. If respiratory and visceral sepsis is the most frequent, the examination must be complete in order not to miss the purpuric lesions, for example.

This approach is based on the search for indexes of contact with the healthcare environment, a history of invasive maneuvers or the presence of foreign bodies.

The environment, the underlying pathologies and the risk factors of infection and immunosuppression are met.

There are also recent symptoms, more or less modulated according to the recent intake of drugs.

The clinical examination focuses on the search for signs in the home and this research is followed with an imaging.

Microbiological samples

Blood cultures are collected in the vicinity (2 blood cultures per hour), as well as any microbiological sample taken according to clinical signs.

Sometimes, the difficult collection of urine will often lead to the taking of urine samples that will allow diuresis control.

Often, the digestive sample is not possible to achieve outside the intensive care unit. Cutaneous / mucosal / oral swabs are often forgotten at the beginning of treatment, and their interpretation is complex.

On the other hand, a fistula with purulent discharge should be taken.

Suspicion of meningitis or meningoencephalitis can cause a lumbar puncture (after a possible brain scan image in the second case).

Treatment of abdominal sepsis

The recognition of severe sepsis syndrome or abdominal sepsis requires the rapid introduction of a series of measures at the same time that the clinical examination continues.

The isolation is not systematic, but simple protection measures should be implemented and measures should be reinforced in case of suspicion of a multidrug-resistant germ.

Close supervision must be carried out taking into account the opinion of the rescuer for a transfer.

The delay between emergency care and the ICU is often long for many reasons, hence the value of close cooperation between services.

This transfer is essential in case of septic shock or in case of significant hypotension before filling since it is necessary to resort to a vasopressor treatment.

Remember, finally, that in the case of symptoms such as those indicated here, it is always best to go to your personal doctor or, failing that, to a guaranteed medical entity.

Mortality level

Previous studies have shown that mortality rates increase dramatically in case of severe sepsis and septic shock.

Severe sepsis may be a reasonable approximation of the “inflection point” between stable and critical clinical conditions in the management of intra-abdominal infections. Severe sepsis is defined as sepsis associated with at least one acute organ dysfunction, hypoperfusion or hypotension.

It is well known that hypotension is associated with an increased risk of sudden and unexpected death in patients admitted to a hospital with non-traumatic diseases.

Therefore, identifying patients with early severe sepsis and correcting the underlying microvascular dysfunction can improve patient outcomes.

If left uncorrected, microvascular dysfunction can lead to global tissue hypoxia, direct tissue damage and, ultimately, organ failure.

Recently updated international guidelines for the treatment of severe sepsis and septic shock. These guidelines are the cornerstone for the management of severe sepsis and septic shock, but do not focus on the specific context of intra-abdominal infections.

Although sepsis is a systemic process, the physiopathological cascade can vary from organ to organ.

Currently, there is little data on systemic and local responses during peritonitis in humans and their correlation with patient outcomes.

In this sense, and based on findings of high concentrations of cytokines in the peritoneal compartment, some evidence suggests that intra-abdominal sepsis can result in a cytokine-mediated inflammatory response that is initially compartmentalized in the peritoneal cavity.

Models with animals have shown that peritonitis is associated with a significant and prolonged peritoneal inflammatory response that correlates negatively with the survival outcome.

It has been reported that the levels of selected peritoneal cytokines are significantly different between the animals that survived compared to those that died after a septic challenge.

The plausibility of peritoneal compartmentalization of the initial inflammatory response during peritonitis was highlighted in a recent prospective cohort study of patients with secondary generalized peritonitis.

The results of this study showed a large gradient between peritoneal fluid and plasma cytokine concentrations, with no correlation between peritoneal and plasma levels, suggesting that plasma levels may increase only after saturation of the tissues within the abdominal compartment. .

The inflammatory response in patients with sepsis depends on the causative pathogen and the host (genetic characteristics and coexisting diseases), with differential responses at the local, regional and systemic levels.

The inflammatory response of the host probably changes over time in parallel with the clinical course.

Sepsis, in the early stages of the inflammatory process, should be considered a local / peritoneal disease.

In advanced stages, severe sepsis and septic shock should be considered as a systemic disease, and patients who are extremely unstable and exhibit high mortality rates should be managed more aggressively.

Special cases with regard to Abdominal Sepsis or Peritonitis

In certain patients, peritonitis can quickly lead to an excessive inflammatory response, and early mechanical and aggressive peritoneal control is crucial to stop the septic process.

In those patients, the inability to control or interrupt the local inflammatory response is associated with poor results.

In contrast, in patients with ongoing sepsis, several laparotomies may be required. In these circumstances, the open abdomen allows the surgeon to perform the posterior laparotomies more efficiently and prevents the onset of abdominal compartment syndrome that can further worsen the systemic disease.

The review focuses on the treatment of patients with severe sepsis or septic shock in the specific context of severe peritonitis.