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Septicaemia and septic shock
Bacteria in the blood can produce a wide spectrum of clinical entities from mild physiological abnormalities to septic shock.
· Bacteraemia is a transient asymptomatic presence of organisms in the blood.
· Septicaemia is used to describe organisms multiplying in blood causing symptoms. There is a systemic inflammatory response syndrome (SIRS) clinically defined by pyrexia, tachycardia, and leucocytosis. The term sepsis syndrome refers to the additional presence of inadequate organ function/perfusion (confusion, hypoxaemia, raised lactate or oliguria).
· Septic shock refers to the presence of severe sepsis with associated hypotension and organ dysfunction despite adequate fluid resuscitation.
Risk factors for development of sepsis include increasing age, immunodeficiency, liver damage and malignancy. Specific causes include
· direct introduction of bacteria into the blood stream via peripheral or central intravenous line (Staph. epi-dermidis),
· gastrointestinal perforation, rupture or ischaemia leading to bacterial translocation (E. coli, Streptococcus faecalis, anaerobic organisms),
· bacteraemia arising from the urinary tract including pyelonephritis, renal abscess, acute prostatitis (E. coli,
· Klebsiella aerogenes, Proteus mirabilis),
· overwhelming pneumococcal infection in patients with impaired or absent splenic function (Streptococ-cus pneumoniae),
· meningococcaemia from a respiratory source may also result in sepsis with or without associated meningitis (Neisseria meningitidis),
· patients with surgical site infections (Staph. aureus, E. coli, anaerobes) and
· burns (Staph. aureus, Streptococci, Pseudomonas).
The normal mechanisms involved in overcoming infection become detrimental when the infection is generalised. Bacteria cell wall components such as lipopolysaccharide (gram-negative bacteria), peptidoglycan (gram-positive and gram-negative bacteria) and lipoteichoic acid (gram-positive bacteria) cause the pro-duction and release of proinflammatory cytokines from macrophages, monocytes and neutrophils. These include interleukin (IL)-1, IL-5, IL-6, IL-8, IL-11, IL-15 and tumour necrosis factor (TNF)-α. Complement activation causes further tissue damage and widespread activation of the coagulation cascade results in disseminated intravascular coagulation (DIC). Hypotension results from widespread induction of nitric oxide causing a generalised vasodilation. Cellular damage may occur through a combination of ischaemia, direct cytopathic damage and apoptosis.
The systemic inflammatory response syndrome is defined as follows:
· Temperature over 38˚C or less than 36˚C.
· Heart rate over 90 beats per minute.
· Respiratory rate over 20 breaths per minute or PaCO2 more than 4.3 kPa.
· WBC over 12 × 109/L or less than 4 × 109/L, or >10% immature (band) forms.
Organ hypoperfusion may manifest as altered mental state, lactic acidosis or oliguria. Systemic hypotension is defined as a systolic blood pressure below 90 mmHg or a reduction of more than 40 mmHg from baseline. Patients may go on to develop multiorgan dysfunction including acute respiratory distress syndrome, disseminated intravascular coagulation, hepatic failure, renal failure and confusion or coma.
Blood and where appropriate, urine, stool, pus and CSF should be sent for culture prior to starting treatment whenever possible. Full blood count, glucose, urea and electrolytes, liver function tests, arterial blood gases and coagulation screen should be sent and repeated regularly until the patient is stable.
Aggressive resuscitation is essential. Airway patency and oxygenation must be maintained and may require the use of an oropharyngeal airway or endotracheal intubation. Blood pressure support involves aggressive fluid replacement via wide bore canulae with careful monitoring. CVP measurement allows assessment of fluid resuscitation, and the response of the CVP to fluid challenge helps guide further resuscitation.
Refractory hypotension despite adequate volume replacement requires the use of inotropic agents such as adrenaline, noradrenaline, dopamine or dobutamine in an intensive care setting.
Identification and management of underlying causes may require surgical intervention or the removal of indwelling catheters or lines.
Antibiotic therapy should be based on local guidelines and chosen on the basis of presumed infection source until the results of microbiological investigations are known. Septicaemia originating in skin and soft tissue infections requires flucloxacillin and benzylpenicillin. If methicillin resistant Staph. aureus (MRSA) is suspected vancomycin or teicoplanin should be used. Septicaemia following intestinal perforation should be treated with cefuroxime, gentamicin and metron-idazole. Septicaemia from the urinary tract should be treated with a cephalosporin and gentamicin. If Pseudomonas infection is suspected piperacillin or ciprofloxacin are effective.
Other treatments such as immunoglobulin, anticytokine antibodies, recombinant protein C and nitric oxide synthetase inhibitors are under investigation. Steroids and nonsteroidal anti-inflammatory agents have not been shown to be of benefit.
The reported mortality from septicaemia ranges from 15 to 50% depending on the severity of sepsis and the general status of the patient prior to the illness.
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