Introduction to Pediatric Hypovolemic Shock

Hypovolemic shock is a life-threatening condition characterized by insufficient tissue perfusion due to decreased intravascular volume. In children, it represents a significant emergency requiring prompt recognition and intervention.

Key Points

• Most common type of shock in pediatric population
• Leading cause of pediatric mortality worldwide
• Common causes: Dehydration, hemorrhage, burns, trauma
• Children can compensate well initially but decompensate rapidly
• Early recognition and aggressive management are crucial for survival

Pathophysiology

Compensatory Mechanisms

• Sympathetic Response:

  Increased catecholamine release leads to:

  • Vasoconstriction of non-essential vascular beds
  • Increased heart rate and contractility
  • Blood flow redistribution to vital organs
• Hormonal Response:

  Activation of renin-angiotensin-aldosterone system:

  • Increased sodium and water retention
  • Vasoconstriction through angiotensin II
  • ADH release for water conservation

Stages of Shock

1. Compensated Shock:

   Vital organ perfusion maintained through compensatory mechanisms

2. Decompensated Shock:

   Failure of compensatory mechanisms leading to organ dysfunction

3. Irreversible Shock:

   Cellular death and organ failure despite intervention

Clinical Presentation

Early Signs (Compensated)

• Mental Status: Anxious, irritable, or agitated
• Vital Signs:
  • Tachycardia (earliest sign)
  • Normal blood pressure
  • Tachypnea
  • Normal or slightly elevated temperature
• Skin Signs:
  • Cool extremities
  • Prolonged capillary refill (>2 seconds)
  • Pale skin

Late Signs (Decompensated)

• Mental Status: Lethargic, confused, or unconscious
• Vital Signs:
  • Hypotension
  • Weak or absent peripheral pulses
  • Bradycardia (very late sign)
• Other Signs:
  • Decreased urine output (<1ml/kg/hr)
  • Mottled skin
  • Weak central pulses

Diagnosis

Initial Assessment

• Primary Survey (ABC):
  • Airway patency
  • Breathing pattern and effort
  • Circulation assessment (pulses, perfusion)
• Volume Loss Estimation:
  • Mild: 3-5% loss
  • Moderate: 6-9% loss
  • Severe: ≥10% loss

Laboratory Studies

• Immediate Studies:
  • Complete blood count
  • Basic metabolic panel
  • Blood gas analysis
  • Coagulation profile
  • Lactate level
  • Type and cross-match
• Additional Studies:
  • Liver function tests
  • Troponin (if cardiac involvement suspected)
  • Blood cultures (if infection suspected)

Imaging

• Chest X-ray
• FAST scan in trauma
• Point-of-care ultrasound for IVC assessment

Management

Immediate Interventions

• Vascular Access:
  • Two large-bore IV lines
  • Consider intraosseous access if IV access fails
  • Central line placement if necessary
• Fluid Resuscitation:
  • Initial bolus: 20mL/kg isotonic crystalloid
  • Reassess after each bolus
  • May need up to 60mL/kg in first hour
  • Consider blood products if hemorrhagic shock

Specific Management Based on Cause

• Hemorrhagic Shock:
  • Blood products (1:1:1 ratio)
  • Damage control surgery if needed
  • Tranexamic acid consideration
• Dehydration:
  • Calculate maintenance needs
  • Replace ongoing losses
  • Correct electrolyte imbalances
• Burns:
  • Parkland formula for fluid replacement
  • Monitor urine output closely
  • Consider albumin after 24 hours

Complications

Early Complications

• Organ Dysfunction:
  • Acute kidney injury
  • Respiratory failure
  • Metabolic acidosis
• Coagulopathy
• Electrolyte imbalances

Late Complications

• Multiple organ dysfunction syndrome
• Neurological sequelae
• Chronic kidney disease

Monitoring & Follow-up

Clinical Monitoring

• Vital Signs:
  • Continuous heart rate monitoring
  • Blood pressure every 5-15 minutes
  • Continuous pulse oximetry
  • Temperature monitoring
• End-organ Perfusion:
  • Urine output (target >1mL/kg/hr)
  • Mental status
  • Capillary refill
  • Skin temperature

Treatment Response Indicators

• Normalization of vital signs
• Improved mental status
• Warm extremities
• Normal capillary refill
• Adequate urine output