Description, Causes and Risk Factors:
$17 billion dollars in the US alone.
Mortality is 20 -- 50%.
2nd leading cause of death in noncoronary ICU's.
10th leading cause of overall death.
Incidence has increased from 1979 (164,000 cases) to 2000 (660,000) -- Annualized increase of 8.7%.
Deaths have increased from 43,579 to 120,491.
Gram positive organisms are the predominant pathogens since 1987
Mortality has decreased from 27% to 17%.
But only 56% go home vs. 78%.
Accounts for about 2% of admissions but 59% require intensive care
Common sites of infection are:
Soft tissues 15%.
Genital tract 10%.
Foreign bodies 5%.
Miscellaneous, including meningococcal 5%.
The sepsis syndrome is a complex systemic inflammatory condition associated with infection. It is not the infective pathogen that directly causes the sepsis syndrome and corresponding high mortality associated with severe sepsis but the host response to that pathogen. To appreciate the current understanding of the syndrome it is useful to divide the complicated pathophysiology into four main areas:
The role of the endothelium (lining of blood vessel).
The disequilibrium of the pro-inflammatory and anti-inflammatory mechanisms.
Activation of the coagulation pathways.
The individual host response.
Following invasion of bacteria, local endothelial cells cause the release of inflammatory mediators and the activation of the clotting cascade. This endothelial action is a part of the normal healthy response of the body to an invading pathogen. In severe sepsis syndrome, however, the endothelial response is no longer a healthy response but a dysfunctional one where, rather than local measured activity, there is an excessive, sustained and generalized activation of the endothelium. This generalized host response can no longer be regulated by local negative feedback mechanisms and results in a severe disequilibrium of inflammatory response, which causes generalized tissue injury, vascular permeability, shock and multiorgan failure.
Symptoms may include:
Fast heart rate.
Hypothermia (very low body temperature).
Warm skin or a skin rash.
Confusion or delirium.
Hyperventilation (rapid breathing).
Decreased urine output.
The early diagnosis of patients withsepsis has been shown to reducemortality rates. It allows prompttreatment with antibiotics and also,where possible, for the removal of thesepsis source. For example, surgicalintervention to remove a portion ofgangrenous gut, or the removal of a skin-tunnelled catheter in people withcancer, can be performed.The difficulty for all nurses andhealthcare teams is that the earlyindications may be subtle anddifficult to recognize. It is also the case that some of the clinical,biochemical and hematological signs of sepsis are also indicators of non-sepsis conditions such aspancreatitis, cerebral hemorrhage or other major shock conditions.Much work over the last 10 years has been concentrated on the earlyrecognition and subsequent earlytherapy for sepsis in an attempt toprevent the systemic symptoms ofgeneralized inflammatory change,tissue damage, increased cellpermeability, shock and organ damage.
Tests may include:
ABG, platelets, liver function tests (LFTs), BUN/creatinine.
White blood count (WBC) is useful to determine the presence of SIRS, either less than 4,000 or greater than 12,000, or a bandemia greater than 10%.
Lactate Measurement. Patients with severe sepsis and septic shock will often exhibit elevations of lactate, as evidence of global hypoperfusion. Lactate levels are highly prognostic of mortality in this population. Arterial lactates do not add significant value over venous and may delay assessment. The key is to run the test as quickly as possible, preferably as point of care testing. Levels above 2.5 mmol/dL are prognostic for higher mortality; levels above 4.0 mmol/L indicate even higher mortality.
Procalcitonin may assist in the risk stratification of sepsis syndromes. Literature suggests that levels are elevated with the presence of systemic bacterial and fungal infections, but not with viral infections. Localized infections and subacute bacterial endocarditis may yield false negatives. Values above 2.0 ng/dL are concerning for severe sepsis and 10.0 ng/dL for septic shock.
Cultures and radiographs may be useful to determine the source and etiology of infection. Blood and urine cultures should be obtained before antibiotic administration. Other cultures, such as cerebrospinal fluid, peritoneal fluid, synovial fluid, abscess material, etc. should be obtained as indicated.
Further diagnostic testing, as noted above, is necessary to elicit the presence of end organ failure and thus severe sepsis.
Critically ill patients should be intubated and arterial and central venous lines and inserted. NG tube and urinary catheter are also required. Patients in this category should be transferred to ICU when stable. Patients who remain hypotensive (MAP <60mmHg) will require monitoring of their cardiac output, stroke volume, pulmonary capillary wedge pressure [PCWP] and SVR [systemic vascular resistance] using Swan Ganz or PiCCO device. Noradrenaline infusion via central line is the first line drug for circulatory support. Dobutamine may be indicated in patients whose cardiac output remains low after volume resuscitation. Renal dose Dopamine has no role. Empirical antibiotic treatment should be started early, after blood cultures, and on the advice of senior colleagues, including microbiologist if possible. Activated Protein c (Xigris) is used in ICU for selected patients with severe sepsis. Other treatments include DVT and stress ulcer prophylaxis, glycemic control (sliding scale insulin) and hydrocortisone 100 mg qds for seven days.
NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.
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