Description
The prognosis of sepsis syndromes varies and spans a clinical spectrum. The most serious consequence of sepsis, septic shock, has a high death rate. An inciting substance triggers the activation of both the pro-inflammatory and anti-inflammatory immune systems, leading to septic shock. This takes place in tandem with the activation of neutrophils, monocytes, and macrophages, which engage with the endothelium via pathogen recognition receptors and cause further cytokine, protease, kinin, reactive oxygen species, and nitric oxide involvement. The endothelium is the main location of this reaction, and in addition to microvascular damage, it also triggers the complement and coagulation cascades, which worsen the vascular damage and cause capillary leakage. The clinical signs and symptoms of sepsis and the progression from sepsis are caused by this series of events.
Summary Listen
- Sepsis is defined as life-threatening organ dysfunction caused by infection and a dysregulated host response, often assessed using the SOFA score (Sequential Organ Failure Assessment). Septic shock, a subset of sepsis, requires both hypotension necessitating vasopressors to maintain adequate mean arterial pressure (MAP) and a lactate level exceeding 2 mmol/L, despite sufficient fluid resuscitation.
- Fluid resuscitation in septic shock involves four phases: rescue, optimization, stabilization, and de-resuscitation. The initial "rescue" phase prioritizes rapid administration of 30 ml/kg of crystalloid for hypotension or lactate levels above 4 mmol/L. Subsequent fluid boluses should be guided by evidence of hypoperfusion and fluid responsiveness, avoiding over-resuscitation.
- Hypoperfusion can be assessed by monitoring lactate levels, aiming for a decrease of at least 20% every 2-4 hours. Capillary refill time (CRT) is also a simple, bedside indicator, with a normal CRT (less than or equal to 3 seconds) suggesting adequate perfusion. Fluid responsiveness, meaning an increase in cardiac output with fluid bolus, can be assessed using static parameters (heart rate, blood pressure, CVP, IVC diameter) and dynamic parameters (pulse pressure variation, stroke volume variation, IVC diameter variation, passive leg raising test).
- Balanced crystalloids, like Ringer's lactate or Plasma-Lyte, are preferred over normal saline for initial resuscitation. Albumin can be considered in patients requiring large crystalloid volumes. Vasopressors should be initiated early, alongside fluid resuscitation, to reverse hypotension.
- Norepinephrine is the first-line vasopressor, targeting a MAP of 65 mmHg. Vasopressin can be added as a second-line agent at a fixed dose of 0.03 units/minute, particularly if the patient remains hypotensive despite norepinephrine or has low diastolic blood pressure, tachycardia, or arrhythmias. Epinephrine can be used as a second-line agent if the patient has low heart rate, low cardiac output, digital or mesenteric ischemia, or severe cardiac dysfunction.
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About the Speakers
Dr. Ripenmeet Salhotra
Senior Consultant Critical Care, Amrita Hospital, Faridabad
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