SHADES OF SHOCK 2

4.2 Bacteraemia (septic shock)
Also named, Toxic shock, and Distributive shock.
It is diagnosed more often in surgical practice today.
There are more aged, immune-compromised patients in hospital.
There are more implants and interventions.
There are more post trauma admissions.

*Septic Shock
Septic shock is the second most frequent cause of shock in the surgical patients.
Invasive bacterial infection represents the most common cause of septic shock, with the most likely sites of infection being the lungs, abdomen, and urinary tract.
Bacterial products cause release of cytokines, tumor necrosis factor-alpha (TNF –alpha) and thromboxanes platelet activating factor, prostaglandin’s etc.
The inflammatory milieu induces several circulatory changes
First, myocardial depression is often evident despite an increase in cardiac index. Several factors contribute to cardiac dysfunction, including biventricular dilatation, myocardial hypo-responsiveness to catecholamine, and diastolic dysfunction.
-Together these phenomena result in a significant reduction in ejection fraction and a sub-optimal response to volume infusion that persists for as long as 10 days.
-The increase in cardiac index despite a reduction in myocardial contractility occurs as a result of a profound reduction in vasomotor tone, the principal cause of hypotension in septic shock.
-The reduction in venous tone leads to pooling of blood in large capacitance vessels, effectively reducing circulating blood volume.
-Several microcirculatory changes also occur distinct from change in vasomotor tone.
These also play a role in the manifestations of septic shock.
The mediator environment of sepsis,
-results in activation of the coagulation cascade,
-leading to micro-thrombus formation, leading to capillary plugging.
This micro-vascular occlusive phenomenon induces the opening of arteriovenous shunts, effectively depriving tissues of adequate perfusion.
Several pro-inflammatory mediators also increase neutrophil endothelial adherence and subsequent exit of activated inflammatory cells into the interstitium where they induce tissue injury.
Increased vascular permeability results in edema which effectively increase the distance required to be covered for cellular oxygen delivery and the opening of arterio-venous shunts, induces cellular hypoxia.


Clinical
Early manifestations of severe sepsis, include, tachypnea, tachycardia, oliguria, and changes in mental status.
-Thus, these simple clinical features should be considered evidence of impending shock in those at risk.
-These clinical features may be followed by the onset of fever and leukocytosis.
Early aggressive management is required to minimizing the morbidity and mortality of septic shock.
- The systemic vaso-dilation and increase in micro-vascular permeability result in patients to require large amount of intravenous fluid to restore a normal blood pressure.
- Vasopressors used are dopamine, epinephrine, or nor-epinephrine if there is an inadequate blood pressure response to fluid resuscitation.
- In-patients not responding to fluid infusion or those with underlying cardiac of renal disease, the use of pulmonary artery catheter is indicated.
- The resuscitation process is incomplete without all measures to reverse the infections process as early as possible.
- The correct choice of antibiotic or antibiotic combination is required.
- If the infection source is an abscess or there is a prior soiling of the pleural or peritoneal cavities, then either drainage or control of contamination is mandatory.
- Similarly, necrotic, infected tissue requires aggressive debridement.*
Any questions be sent to drmmkapur@gmail.com
All earlier posts are stored in archives for your access and review