What is distributive shock, its etiology, pathophysiology, signs, symptoms, diagnosis, treatment, and potential complications?

Distributive Shock: Definition, Etiology, Pathophysiology, Diagnosis, and Management

Distributive shock is characterized by an insufficient intravascular volume of blood secondary to pathological vasodilation, resulting in abnormal distribution of microvascular blood flow and metabolic distress despite potentially normal or elevated cardiac output. 1, 2

Definition & Pathophysiology

• Distributive shock represents one of the four major shock categories (alongside hypovolemic, cardiogenic, and obstructive) and is characterized by vasoplegia with relative volume deficiency, causing a mismatch between oxygen supply and demand at the tissue level 2, 3
• The pathophysiological hallmark is peripheral vasodilation leading to decreased systemic vascular resistance, resulting in relative hypovolemia despite potentially normal or even elevated cardiac output 1
• Microcirculatory dysfunction occurs at the capillary level, creating heterogeneous flow patterns and shunting that leads to regional tissue dysoxia despite seemingly adequate macrocirculatory parameters 4
• Myocardial depression is common, particularly in septic shock, with up to one-third of patients developing right ventricular systolic dysfunction 1

Etiology

• Septic shock is the most common cause of distributive shock, resulting from systemic inflammatory response to infection 5, 3
• Other causes include:
  • Anaphylactic shock (severe allergic reaction) 3
  • Neurogenic shock (loss of sympathetic tone following spinal cord injury) 3
  • Adrenal insufficiency (inadequate cortisol production) 6
  • Pancreatitis (inflammatory condition of the pancreas) 1
  • Toxic shock syndrome (bacterial toxin-mediated) 6
  • Burns (extensive thermal injury) 1
  • Drug-induced vasodilation (anesthetic agents, calcium channel blockers) 6

Signs & Symptoms

• Hypotension refractory to fluid administration is the cardinal feature 1
• Warm, flushed skin due to peripheral vasodilation (in contrast to cold extremities seen in other shock types) 3
• Tachycardia as a compensatory mechanism to maintain cardiac output 1
• Altered mental status due to cerebral hypoperfusion 1
• Decreased urine output (<0.5 mL/kg/hr) reflecting renal hypoperfusion 7
• Elevated serum lactate levels indicating tissue hypoxia and anaerobic metabolism 1
• In septic shock specifically: fever or hypothermia, leukocytosis or leukopenia, and signs of infection 1

Diagnosis & Evaluation

• Clinical diagnosis based on hemodynamic parameters:

  • Hypotension (systolic BP <90 mmHg or MAP <65 mmHg) 1
  • Tachycardia (heart rate >100 bpm) 1
  • Normal or elevated cardiac output/cardiac index 1
  • Decreased systemic vascular resistance 1, 3

• Laboratory assessment:

  • Serum lactate levels (>2 mmol/L suggests tissue hypoperfusion) 1
  • Complete blood count, comprehensive metabolic panel, coagulation studies 5
  • Blood cultures and other infection workup in suspected sepsis 1

• Hemodynamic monitoring:

  • Echocardiography to assess cardiac function and rule out other shock types 1
  • Central venous pressure monitoring may help guide fluid therapy 1
  • Arterial line for continuous blood pressure monitoring 1
  • Advanced hemodynamic monitoring (when available) to assess cardiac output and systemic vascular resistance 5

Interventions & Treatments

• Initial resuscitation:

  • Fluid resuscitation with balanced crystalloids (20 mL/kg initial bolus in pediatric patients) is the first step, with subsequent reassessment 1
  • Early recognition and treatment of the underlying cause (antibiotics for sepsis, epinephrine for anaphylaxis, etc.) 5, 3

• Vasopressor therapy:

  • Norepinephrine is the first-line vasopressor after adequate fluid resuscitation in distributive shock 1
  • If hypotension persists, vasopressin (up to 0.03 UI/min) can be added to reduce norepinephrine requirements 1, 7
  • Dopamine is only recommended in hypotensive patients with bradycardia or low risk for tachycardia 1
  • Phenylephrine should be reserved for salvage therapy 1

• Management of myocardial dysfunction:

  • When evidence of myocardial depression and decreased perfusion persists despite adequate fluid resuscitation and vasopressors, consider adding dobutamine to norepinephrine or using epinephrine as a single agent 1
  • Recent evidence suggests epinephrine may be more effective than dopamine in pediatric septic shock for resolution of shock in the first hour 1

• Supportive care:

  • Mechanical ventilation may be required for respiratory failure 1
  • Continuous renal replacement therapy for acute kidney injury or fluid overload 1
  • Glycemic control, stress ulcer prophylaxis, and venous thromboembolism prevention 5

Potential Complications

• Multiple organ dysfunction syndrome affecting respiratory, renal, hepatic, hematologic, and neurologic systems 5
• Acute respiratory distress syndrome (ARDS) 1
• Acute kidney injury requiring renal replacement therapy 1
• Disseminated intravascular coagulation 6
• Adrenal insufficiency (especially in septic shock) 6
• Persistent shock despite appropriate therapy, leading to death 5

Red Flags & CVICU Tips

• Failure to improve with appropriate fluid resuscitation and vasopressors should prompt reassessment for alternative or additional shock types 5
• Beware of myocardial depression in septic shock, which may require addition of inotropic support 1
• Monitor for signs of fluid overload during resuscitation (pulmonary edema, increasing oxygen requirements) 1
• Use ultrasound when possible to help determine shock etiology and guide management 1
• Target a MAP of 65 mmHg as the standard goal, but individualize based on patient's baseline blood pressure and comorbidities 1
• Complement hemodynamic targets with other markers of perfusion (lactate clearance, urine output, mental status) 1
• In pediatric patients, tachycardia may be the earliest sign of shock before hypotension develops 1
• Vasoactive drugs have a narrow therapeutic window and can cause life-threatening complications; they require precise therapeutic targets, close monitoring, and should be weaned as soon as possible 7