Dr. med. Dirk Manski



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Urosepsis: Definition, Diagnosis and Treatment

Review literature: (Hotchkiss and Karl, 2003) (Tauchnitz, 1991).

Definition of Urosepsis

Urosepsis is a systemic reaction of the body (SIRS) to a bacterial infection of the urogenital organs with the risk of life-threatening symptoms including shock.

Systemic inflammatory response syndrome (SIRS)

SIRS (systemic inflammatory response syndrome) is an inflammatory reaction or inflammatory response as a result of a significant infection and damage to the organism. SIRS affects nearly every organ system. For the definition of SIRS, two of the following symptoms must be present:

Definition of sepsis

Sepsis is the presence of SIRS with clinical signs of a bacterial infection. Urosepsis is the presence of SIRS with clinical signs of a bacterial infection involving the urogenital organs.

Septic shock

A septic shock is the sepsis/urosepsis with hypotension (and tachycardia).

Epidemiology of Sepsis

The incidence of severe sepsis is 3/1000.

Etiology and Pathogenesis of Sepsis

Etiology of Urosepsis

Bacterial Infections of the Urogenital Tract:

renal abscess as a cause for urosepsis

Pyelonephritis, renal abscess, infected hydronephrosis, bacterial prostatitis, epididymitis, fournier's gangrene ...
Responsible bacterial organisms: E. coli, Klebsiella, Enterobacter, Serratia, Proteus, Pseudomonas, Enterococcus.

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Other Causes of Sepsis (Differential Diagnosis)

Cardial infections:

Endocarditis. The bacterial spectrum is diverse: Streptococcus viridans, Enterococcus, Staphylococcus, Pseudomonas, Candida ...

Respiratory infections:

Pneumonia, pleural empyema, mediastinitis, lung abscess. Bacterial spectrum: Pneumococcus, Staphylococcus, anaerobes in case of aspiration, enterobacteria, tuberculosis, Candida, Aspergillus, ...

Infections of the digestive tract:

Peritonitis, liver abscess, cholecystitis, cholangitis, necrotizing pancreatitis. Bacterial spectrum: E. coli, Enterobacter, Salmonella, Campylobacter, anaerobes, Enterococcus, Staphylococcus, Candida ...

Infections of the ENT tract:

Tonsillitis, oral cavity floor phlegmone. Bacterial spectrum: Streptococcus pyogenes, Staph. aureus ...

Infections of the CNS:

Meningococcal meningitis (sometimes with Waterhouse-Friedrichsen syndrome).

Dermal infections:

Erysipel, impetigo, dermal abscess. Bacterial spectrum: Streptococcus, Staphylococcus.

Nosocomial infections:

Catheter associated infections (central venous catheters, bladder catheter), implants, wound infection, pneumonia. Diverse bacterial spectrum.

Pathogenesis of Urosepsis

Immune response in sepsis:

Patients with sepsis suffer initially from an excessive immune response, which leads later in the course of sepsis to a status of immunosuppression. One reason for the transition from hyperinflammation to immunosuppression is the exhaustion of proinflammatory cytokines, apoptosis of lymphocytes and the formation of an anergy.

Hyperinflammation due to sepsis:

The presence of bacteria induces an excessive immune reaction that damages the patients organism. Although the responsible cytokines in the immune response are known in part (TNF-α, interleukin 1 and 2, interferon-γ), clinical studies with a blocking of these cytokines did not improve the prognosis.

Immunosuppression due to sepsis:

The following features are characteristic for immunosuppression: lack of delayed hypersensitivity reaction, impaired ability to eliminate the infection and the susceptibility to nosocomial infections. The immunosuppression is accompanied by a reduced secretion of proinflammatory cytokines in response to bacterial antigens (see above). Furthermore, anti-inflammatory cytokines are increased detectable (interleukin 4 and 10). The stimulation of the immune response with interferon-γ leads to an improvement of the prognosis. Signs of immunosuppression in sepsis correlate with a poor prognosis.

Anergy due to sepsis:

Anergy is a state of the immune system not responding to immunogenic stimuli. Anergy is triggered by e.g. apoptosis of lymphocytes.

Genetic risk factors:

A series of genetic changes (mutations, polymorphisms ...) were identified in the context of increased mortality due to infectious diseases and sepsis.

Cellular mechanisms of organ dysfunction with sepsis:

Autopsy studies were not able to identify significant changes in kidney cells, heart muscle cells or liver cells, which could explain the severe organ dysfunction responsible for mortality. This phenomenon of decreased cell function ("cell stunning or cell hibernating") is caused by cytokines and metabolites of sepsis. Organ function may recover to a large extent after survival of sepsis.

Signs and Symptoms of Urosepsis

Local symptoms:

Local symptoms depend on the underlying cause of infection: flank pain, abdominal tenderness, scrotal pain, ....

General symptoms of urosepsis:

Fever, chills, hyperventilation, tachycardia and hypotension are the classic symptoms. Hypothermia indicates a poor prognosis. Further symptoms are impairment of consciousness, confusion, oliguria or anuria.

Diagnosis of Urosepsis

Vital signs:

Heart rate, blood pressure, respiratory rate, urine output, and vigilance are important parameters for assessing the prognosis and for the initiation of intensive care measures.

Blood cultures:

Blood cultures should be done before antibiotic treatment is started. Ideally, several aerobic and anaerobic blood cultures are taken when fever is rising.

Local swabs and urine culture:

Depending on the suspected site of infection: urine culture, pus from abscess, sputum, faeces, wound secretions, cerebrospinal fluid .... Ideally before antibiotic treatment is started.

Laboratory tests:

Blood count, clotting tests with AT III and fibrinogen, CRP, liver tests, creatinine, blood gas analysis. Possibly procalcitonin as a marker for sepsis.

Imaging in Urosepsis:

Ultrasound of the urogenital organs, abdominal CT and chest x-ray. Depending on the clinical situation further imaging such as CCT or echocardiography might be necessary.

Treatment of Urosepsis

Causal Treatment of Urosepsis

If possible, specific treatment of the diagnosed infection should be started as soon as possible:

Antibiotic Therapy for Urosepsis

After obtaining blood cultures and local cultures (see above), a calculated parenteral antibiotic therapy is begun: e.g. Amoxicillin/clavulanic acid in combination with gentamicin, cephalosporins of the 3rd generation or reserve antibiotics such as imipenem or meropenem if a difficult resistance situation is suspected. Anaerobic infections are possible in peritonitis, wound infection or Fournier's gangrene and may require the use of e.g. metronidazole.

Intensive Care Treatment of Urosepsis

Volume and oxygen therapy in sepsis:

Aggressive volume therapy, control for sufficient oxygen carriers and vasopressor therapy at the beginning of urosepsis improve the prognosis. The aim is to achieve a balance between oxygen consumption and oxygen transport within six hours; this is controlled via the normalization of the central venous oxygen saturation, lactate concentration, base excess (BE) and pH. Important is a liberal volume therapy and the transfusion of packed red blood cells in anemia.

Catecholamins:

If the substitution of volume, oxygen and hemoglobin is not effective enough to reach a balance between oxygen consumption and oxygen transport, the administration of vasoactive and positive inotropic agents such as noradrenaline and adrenaline is necessary.

Corticosteroids and sepsis:

Corticosteroids in a physiological dose may advantageous in urosepsis, especially with persistent shock and long-term ventilation. An postulated explanation for the benefit of corticosteroids is a relative steroid deficiency due to reduced sensitivity of the steroid receptor under vasopressor treatment.

Treatment of organ failure:

Mechanical ventilation and renal replacement therapy (hemofiltration) are often necessary.







Index: 1–9 A B C D E F G H I J K L M N O P Q R S T U V W X Y Z



References

Hotchkiss und Karl 2003 HOTCHKISS, R. S. ; KARL, I. E.:
The pathophysiology and treatment of sepsis.
In: N Engl J Med
348 (2003), Nr. 2, S. 138–50

Tauchnitz 1991 TAUCHNITZ, C:
Sepsis.
In: HAHN, H (Hrsg.) ; FALKE, D (Hrsg.) ; KLEIN, P (Hrsg.): Medizinische Mikrobiologie.
Berlin, Heidelberg : Springer, 1991, S. 501–507


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