Surgery

Shock

Septic Shock

Bacteremia: - It is the presence of bacteria within the bloodstream.

Sepsis: - - is the systemic response to infection and - It is defined as the presence of SIRS in addition to a documented or presumed infection i.e., infection-induced syndrome involving 2 or more manifestations of SIRS.

Severe sepsis meets the a forementioned criteria and is associated with organ dysfunction, hypoperfusion, or hypotension.

Septic Shock

Severe Sepsis induced hypotension (systolic < 90 mmHg). Disturbance in Oâ‚‚ delivery and Oâ‚‚ consumption. Gram positive (52%), Gram negative (38%) infections.

Common sites of infection:

  • Lung (50-70%), (respiratory)
  • abdomen (20-25%) ,
  • urinary tract (5-7%),
  • skin.

Risk groups:

  • Immunocompromised
  • 65 years or older

  • Infants under 1 year

Pathophysiology

  • Infection- triggers cytokines (TNF-α, IL 1-β) mediated pro-inflammatory response.

  • Peripheral vasodilatation due to NO release

  • Fall in systemic vascular resistance

  • Reflex tachycardia, increased cardiac output (CO)- High output state.

  • Clinically: warm well perfused periphery

  • Low diastolic BP, wide pulse pressure.

Septic Shock- pathophysiology

If septic state persists: Endothelium dysfunction leads to: - Extravasation of fluid - Loss of intravascular volume - Ventricular dysfunction → impairs CO. - Peripheral perfusion falls

Clinically indistinguishable from low output state

Features of warm and cold shock

EARLY WARM SHOCK (WARM shock)
  • Compensated warm phase of shock.

  • Prompt response to fluids and pharmacologic treatment.

  • Toxins increase the body temperature.

  • Arterial blood pressure falls but the cardiac output increases because the left ventricle has minimal resistance to pump against.

  • Adrenergic discharge further Increases the cardiac output. The skin remains pink, warm & well perfused (Cutaneous vasodilatation).

LATE COLD SHOCK (Refractory septic shock)
  • Late decompensated phase.

  • There is hypovolemia with decrease in right heart filling & decreases cardiac output.

  • The knowledge of existence of a septic focus is the only factor that differentiates septic shock from traumatic & hypovolemic shock.

Treatment:

1) Aim of treatment is to:

  • a- control infection and
  • b- improve the hypovolemic state, caused by endotoxin induced peripheral vasodilatation.

2) Blood culture should be done before antibiotic administration.

3) Debridement & drainage of the infection.

4) Antibiotics: combination of 3rd generation cephalosporin, aminoglycoside and metronidazole should be effective against most organisms.

5) Inotrope (Cardiogenic + Septic) use is indicated in severely ill patients to maintain cardiac output.

Truama

Septic shock

  • Delayed arrival
  • Penetrating abdominal injuries
  • Early septic shock- normal circulating volume
  • Tachycardia
  • Warm skin
  • Systolic BP is near to normal
  • Wide pulse pressure