TREATING SEPSIS

Introduction

Severe sepsis (1) (2)is characterized by stimulation of a series of inflammatory cascades leading to extensive cardiovascular derangement, the most overt signs of which are hypotension due to vasoplegia, relative hypovolemia, and widespread dysfunction of the microvasculature (“capillary leak”) (3). Simultaneously, there is activation of the coagulation cascades (4;5) , the formation of intravascular thrombus, and subsequent tissue injury and multi-organ dysfunction.

The two major priorities in management of septic patients are 1). To maintain delivery of oxygen to the tissues, by way of optimization of cardiac output and peripheral resistance, and 2) To modulate the procoagulation response. It is essential to obtain maximal results from minimal interventions. In particular, it is important to avoid using excessive amounts of catecholamines, in under-resuscitated patients.

In this tutorial we will explore a typical strategy for the resuscitation and treatment of a patient in septic shock. We will use a specific model for the temporal approach to these patients. There are nine steps, listed below and represented in figure 1:

Step A  = Airway:  ensure that the airway is protected; if not intubate the patient.

Step B = Breathing: address oxygenation and ventilation, administer oxygen and, if intubated, commence mechanical ventilation.

Step C = Circulation: restore circulating volume with  fluid resuscitation, invasive monitoring and vasopressors if necessary:.

Step D = Diagnosis / Detective work: obtain a history, examine the patient and make a “best 

guess” as to the source.

Step E = Empiric therapy: start empiric antimicrobials, and activated Protein C if indicated.

Step F = Find and control the source of infection

Step G = Gut: feed it to prevent villus atrophy and bacterial translocation

Step H = Hemodynamics: assess adequacy of resuscitation and prevention of organ failure.

Step I =  Iatrogenic: avoid hospital acquired injuries (DVT, line sepsis, pressure sores) and

address other supportive issues – analgesia, sedation and psychospiritual welfare, control blood sugar and think about adrenal insufficiency.

Step J = Justify your therapeutic plan and reassess

Step KL = Keep Looking. Have we adequately controlled the source? Are there secondary sources of infection/inflammation.

Step MN = Metabolic and Neuroendocrine control. Tight control of blood sugar. Address adrenal insufficiency. Think about early aggressive dialysis in renal failure.

Using this method will remove the panic factor from clinical situations. This type of methodology has been extremely successful in Advanced Cardiac Life Support (ACLS) and Advanced Trauma Life Support (ATLS).

Learning Objectives

• To learn a methodical approach to resuscitating the patient in septic shock
• To learn about empiric antibiotic strategies, vasoactive drugs and activated Protein C

References

(1)   Bone RC. Toward an epidemiology and natural history of SIRS (systemic inflammatory response syndrome). JAMA 1992; 268(24):3452-3455.

(2)   Bone RC, Sibbald WJ, Sprung CL. The ACCP-SCCM consensus conference on sepsis and organ failure. Chest 1992; 101(6):1481-1483.

(3)   Balk RA. Pathogenesis and management of multiple organ dysfunction or failure in severe sepsis and septic shock. Crit Care Clin 2000; 16(2):337-52, vii.

(4)   Faust SN, Heyderman RS, Levin M. Coagulation in severe sepsis: A central role for thrombomodulin and activated protein C. Crit Care Med 2001; 29(7):S62-S68.

(5)   Kidokoro A, Iba T, Fukunaga M, Yagi Y. Alterations in coagulation and fibrinolysis during sepsis. Shock 1996; 5(3):223-228.

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