Distributive Shock (Adult)

Overview

Distributive shock is characterized by profound systemic vasodilation leading to maldistribution of blood flow and inadequate tissue perfusion despite normal or elevated cardiac output.[1] Unlike hypovolemic or cardiogenic shock, the primary problem is loss of vascular tone rather than volume depletion or pump failure.

Clinical Pearl: The hallmark of distributive shock is "warm shock"

• hypotension with warm, flushed peripheries and bounding pulses, reflecting vasodilation. This distinguishes it from "cold shock" seen in hypovolemic and cardiogenic states.[2]

The four major subtypes of distributive shock:

Additional causes:

• Adrenal crisis (adrenal insufficiency)
• Thyroid storm (thyrotoxicosis)
• Pancreatitis-induced SIRS
• Post-cardiopulmonary bypass vasoplegia
• Severe liver failure
• Transfusion reactions

Exam Detail: MRCP/FRACP frequently test differentiation between shock types using hemodynamic profiles. Key distinguishing feature of distributive shock: low SVR with normal/high cardiac output. FRCEM emphasizes rapid recognition and cause-specific treatment.

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Epidemiology

Incidence by Subtype

Risk Factors

Septic shock:

• Extremes of age, immunocompromise, chronic disease, indwelling devices

Anaphylactic shock:

• Prior anaphylaxis, atopy, beta-blocker use (impairs epinephrine response)

Neurogenic shock:

• Cervical/high thoracic spinal cord injury, spinal anaesthesia

Drug-induced:

• Vasodilator medications (nitrates, calcium channel blockers, ACE inhibitors)
• Anaesthetic agents (propofol, opioids)
• Poisoning (cyanide, carbon monoxide, hydrogen sulfide)

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Aetiology and Pathophysiology

Common Pathway

All distributive shock subtypes share:[1,2]

1. Systemic vasodilation → Decreased systemic vascular resistance (SVR)
2. Relative hypovolemia → Blood pooling in dilated venous capacitance vessels
3. Maldistribution of blood flow → Some tissues overperfused, others underperfused
4. Hypotension → Despite normal/increased cardiac output
5. Tissue hypoperfusion → Anaerobic metabolism, lactate production
6. Organ dysfunction → If prolonged

Hemodynamic Profile

Classic distributive shock hemodynamics:

Subtype-Specific Pathophysiology

Septic shock:[7]

• PAMPs trigger TLR activation → Cytokine storm (TNF-α, IL-1β, IL-6)
• Excessive nitric oxide (NO) production → Vasodilation
• Endothelial dysfunction → Capillary leak, third-spacing
• Myocardial depression → Septic cardiomyopathy (30-50%)
• Mitochondrial dysfunction → Cytopathic hypoxia

Anaphylactic shock:[8]

• IgE-mediated mast cell/basophil degranulation
• Histamine, tryptase, prostaglandins, leukotrienes released
• Vasodilation + increased vascular permeability
• Bronchospasm, laryngeal edema
• Mixed distributive + hypovolemic shock (up to 35% plasma volume loss in 10 min)

Neurogenic shock:[5]

• Disruption of sympathetic outflow (T1-L2 spinal cord)
• Loss of vasomotor tone → Vasodilation
• Loss of cardiac sympathetic innervation (T1-T4) → Bradycardia
• Unopposed vagal tone
• Most common with cervical and upper thoracic SCI

Clinical Pearl: Neurogenic shock is distinguished by the combination of hypotension + bradycardia. Other shock types produce compensatory tachycardia. This "warm, hypotensive, bradycardic" presentation is pathognomonic for loss of sympathetic tone.[5]

Drug-induced/toxic:[6]

• Direct vasodilator effect (nitrates, CCBs)
• Mitochondrial toxins (cyanide, CO, H₂S) impair cellular respiration
• Histamine release (vancomycin, opioids)
• Anaesthetic agents (propofol, volatile anaesthetics)

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Clinical Presentation

General Features

Common to all distributive shock:

• Hypotension (SBP > 90 mmHg or MAP > 65 mmHg)
• Warm, flushed skin (early "warm shock")
• Wide pulse pressure, bounding pulses
• Tachypnoea
• Altered mental status
• Oliguria (despite adequate volume)

Differentiation by Subtype

Septic Shock Presentation

Symptoms:

• Fever, chills, rigors (or hypothermia in elderly/immunocompromised)
• Symptoms of infection source (cough, dysuria, abdominal pain)
• Confusion, altered mental status

Signs:

• Hypotension refractory to initial fluid resuscitation
• Tachycardia, tachypnoea
• Warm, flushed peripheries (early)
• Cool, mottled peripheries (late/refractory)
• Signs of infection source

Laboratory:

• Lactate greater than 2 mmol/L despite resuscitation
• Leukocytosis or leukopenia
• Elevated procalcitonin
• Organ dysfunction markers (creatinine, bilirubin, coagulopathy)

Anaphylactic Shock Presentation

Symptoms:

• Sudden onset after allergen exposure (minutes to 1-2 hours)
• Pruritus, flushing, sense of impending doom
• Throat tightness, difficulty breathing
• Abdominal pain, nausea, vomiting

Signs:

• Urticaria (90%), angioedema (lips, tongue, uvula)
• Stridor, hoarse voice (laryngeal edema)
• Wheeze (bronchospasm)
• Hypotension, tachycardia
• GI symptoms (nausea, vomiting, diarrhea)

Biphasic reaction:

• 5-20% develop recurrence 1-72 hours after initial resolution
• Risk factors: severe initial reaction, delayed epinephrine

Neurogenic Shock Presentation

Context:

• Acute spinal cord injury (cervical > thoracic)
• Spinal anaesthesia (high block)
• Intracranial pathology (rarely)

Clinical triad:

1. Hypotension
2. Bradycardia (or relative bradycardia)
3. Peripheral vasodilation with warm, dry skin

Associated findings:

• Flaccid paralysis below level of injury
• Sensory loss
• Urinary retention
• Poikilothermia (inability to regulate temperature)
• Priapism (autonomic dysfunction)

Clinical Pearl: In trauma, always consider concurrent hemorrhagic shock. Neurogenic shock alone rarely causes lactate greater than 4 mmol/L or requires massive transfusion. If present, search for occult bleeding.[5]

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Investigations

Initial Investigations (All Subtypes)

Subtype-Specific Investigations

Septic shock:

• Blood cultures ×2 (before antibiotics)
• Urine culture, sputum culture, wound cultures
• Procalcitonin
• CXR, CT as indicated for source

Anaphylactic shock:

• Serum tryptase (within 1-4 hours of onset, peak at 1 hour)
• IgE levels (outpatient follow-up)
• Allergen-specific testing after recovery

Neurogenic shock:

• Spinal imaging (CT, MRI)
• Assess level and completeness of injury
• Rule out hemorrhagic shock in trauma

Drug-induced:

• Drug levels where available
• Toxicology screen
• Carbon monoxide level, lactate (for cellular toxins)

Hemodynamic Monitoring

Invasive monitoring indications:

• Refractory shock requiring multiple vasopressors
• Unclear etiology
• Guiding fluid and vasopressor therapy

Parameters:

• Arterial line (continuous BP, ABG sampling)
• Central venous catheter (CVP, ScvO₂, vasopressor delivery)
• Advanced monitoring (cardiac output, SVR) in refractory cases

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Management

General Principles

Immediate priorities for all distributive shock:[1,2]

1. Recognize shock - Hypotension with warm peripheries, tachycardia (except neurogenic)
2. Establish access - Large-bore IV ×2, consider central venous access
3. Identify cause - History, examination, targeted investigations
4. Treat specific cause - See subtype-specific management
5. Supportive care - Oxygen, monitoring, organ support

Septic Shock Management

Hour-1 Bundle:[9]

1. Measure lactate
2. Blood cultures before antibiotics
3. Broad-spectrum antibiotics within 1 hour
4. Fluid resuscitation (30 mL/kg crystalloid - individualize)
5. Vasopressors if hypotensive during/after fluids (target MAP ≥65 mmHg)

Vasopressor therapy:

• Norepinephrine first-line (0.05-1 µg/kg/min)
• Vasopressin 0.03 units/min as adjunct
• Epinephrine if additional agent needed
• Consider angiotensin II for refractory cases

Source control:

• Identify and drain abscesses
• Remove infected devices
• Surgical debridement if needed

Adjunctive therapy:

• Hydrocortisone 200 mg/day if refractory to fluids + vasopressors

Anaphylactic Shock Management

Immediate treatment:[10]

1. Epinephrine (adrenaline) IM - FIRST-LINE:

• Dose: 0.5 mg (0.5 mL of 1:1000) IM, anterolateral thigh
• Repeat every 5-15 minutes if needed
• Do NOT delay for IV access or other treatments

2. Position:

• Supine with legs elevated (if tolerated)
• Avoid sitting/standing (can precipitate cardiac arrest)

3. Remove trigger:

• Stop infusion of suspected drug
• Remove bee stinger

4. Fluids:

• Aggressive IV crystalloid (1-2 L rapidly)
• Up to 35% plasma volume may extravasate

5. Adjunctive medications:

• Salbutamol nebulized for bronchospasm
• Antihistamines (chlorphenamine 10 mg IV) - second-line
• Hydrocortisone 200 mg IV - prevents biphasic reaction

Refractory anaphylaxis:

• Epinephrine infusion 0.1-1 µg/kg/min IV
• Glucagon 1-5 mg IV if on beta-blockers
• Vasopressin or norepinephrine if refractory

Clinical Pearl: IM epinephrine is first-line for anaphylaxis because it is faster and safer than IV in the acute setting. IV epinephrine risks arrhythmias and should be reserved for refractory cases with continuous monitoring.[10]

Neurogenic Shock Management

Immediate priorities:[5]

1. Spinal immobilization:

• Maintain alignment pending imaging
• Avoid secondary cord injury

2. Fluid resuscitation:

• Judicious fluids (250-500 mL boluses)
• Avoid over-resuscitation (risk of pulmonary edema)

3. Vasopressor therapy:

• Norepinephrine first-line (α-agonist restores vascular tone)
• Target MAP 85-90 mmHg for acute SCI (higher target than other shock types)
• Phenylephrine alternative (pure α-agonist)

4. Bradycardia management:

• Atropine 0.5-1 mg IV for symptomatic bradycardia
• Consider temporary pacing for refractory bradycardia

5. Temperature regulation:

• Poikilothermia common - active warming/cooling as needed

Specific considerations:

• Exclude concurrent hemorrhagic shock in trauma
• Early neurosurgical consultation
• High-dose methylprednisolone controversial (not routinely recommended)

Drug-Induced/Toxic Shock Management

General approach:[6]

1. Stop offending agent
2. Supportive care with fluids and vasopressors
3. Specific antidotes where available:
   • Calcium chloride for CCB toxicity
   • Glucagon for beta-blocker toxicity
   • Hydroxocobalamin for cyanide
   • Methylene blue for refractory vasoplegic shock

Methylene blue:[11]

• Mechanism: Inhibits NO-mediated vasodilation
• Dose: 1-2 mg/kg IV over 15-30 minutes
• Indications: Refractory vasodilatory shock, post-cardiopulmonary bypass vasoplegia
• Contraindication: G6PD deficiency

Adrenal Crisis Management

Recognition:

• Known adrenal insufficiency or chronic steroid use
• Hypotension refractory to vasopressors
• Hyponatremia, hyperkalemia, hypoglycemia

Treatment:[12]

• Hydrocortisone 100 mg IV bolus, then 50 mg IV q6h (or 200 mg/day continuous)
• Aggressive fluid resuscitation (0.9% saline)
• Dextrose for hypoglycemia
• Do NOT wait for cortisol results before treating

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Complications

Complications of Distributive Shock

Subtype-Specific Complications

Anaphylaxis:

• Biphasic reaction (5-20%, up to 72 hours later)
• Refractory anaphylaxis requiring prolonged resuscitation
• Anaphylaxis-related myocardial infarction (Kounis syndrome)

Neurogenic shock:

• Autonomic dysreflexia (after acute phase)
• Deep vein thrombosis (high risk, prophylaxis essential)
• Pressure ulcers

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Prognosis

Outcomes by Subtype

Prognostic Indicators

Poor prognosis:

• Delayed recognition and treatment
• Refractory to multiple vasopressors
• Multi-organ dysfunction
• Persistent lactate elevation
• Elderly, immunocompromised

Good prognosis:

• Early recognition and cause-specific treatment
• Rapid lactate clearance
• Single organ dysfunction
• Younger age, fewer comorbidities

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Prevention

Primary Prevention

Septic shock:

• Vaccination, infection control, antibiotic stewardship

Anaphylactic shock:

• Allergen avoidance, carrying epinephrine auto-injector
• Desensitization for essential medications

Neurogenic shock:

• Spinal cord injury prevention (safety measures)

Drug-induced:

• Careful medication dosing, monitoring
• Avoid drug interactions

Secondary Prevention

Anaphylaxis survivors:

• Epinephrine auto-injector prescription and training
• Allergist referral
• Medical alert identification
• Anaphylaxis action plan

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Key Guidelines

1. Surviving Sepsis Campaign 2021: International Guidelines for Management of Sepsis and Septic Shock[9]
2. EAACI 2021: Anaphylaxis Guidelines[10]
3. AANS/CNS 2013: Management of Acute Cervical Spine and Spinal Cord Injuries[5]
4. ESC 2021: Acute and Chronic Heart Failure (vasoplegia management)[11]

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Exam Scenarios

SBA Question 1

Scenario: A 35-year-old man with a C5 spinal cord injury from a diving accident presents with BP 75/45 mmHg and HR 52 bpm. His peripheries are warm and dry. What is the most likely diagnosis?

A) Hypovolemic shock from occult hemorrhage
B) Cardiogenic shock from cardiac contusion
C) Neurogenic shock
D) Septic shock from aspiration pneumonia
E) Obstructive shock from tension pneumothorax

Answer

Answer: C) Neurogenic shock

The clinical triad of hypotension + bradycardia + warm peripheries following high spinal cord injury is pathognomonic for neurogenic shock.[5]

Key differentiating features:

• Bradycardia (not tachycardia as in other shock types)
• Warm, dry peripheries (vasodilation from loss of sympathetic tone)
• Context of cervical spinal cord injury

Hypovolemic shock would cause tachycardia and cold peripheries. Always exclude concurrent hemorrhage in trauma, but the bradycardia and warm peripheries favor neurogenic shock.

SBA Question 2

Scenario: A 45-year-old woman develops urticaria, facial swelling, wheeze, and hypotension (BP 70/40 mmHg) 5 minutes after receiving IV penicillin. What is the most appropriate first-line treatment?

A) Chlorphenamine 10 mg IV
B) Hydrocortisone 200 mg IV
C) Adrenaline 0.5 mg IM (1:1000)
D) Salbutamol 5 mg nebulized
E) Normal saline 1 L IV bolus

Answer

Answer: C) Adrenaline 0.5 mg IM (1:1000)

Intramuscular epinephrine is the first-line treatment for anaphylaxis and should be given immediately.[10]

Key points:

• IM route preferred over IV (faster onset, safer without cardiac monitoring)
• Anterolateral thigh is optimal injection site
• Repeat every 5-15 minutes if needed

Antihistamines and steroids are adjunctive but NOT first-line. Fluids and bronchodilators are important but should not delay epinephrine.

SBA Question 3

Scenario: Which hemodynamic profile is most consistent with distributive shock?

A) Low cardiac output, high SVR, high CVP
B) High cardiac output, low SVR, low-normal CVP
C) Low cardiac output, low SVR, low CVP
D) Normal cardiac output, high SVR, high CVP
E) Low cardiac output, normal SVR, low CVP

Answer

Answer: B) High cardiac output, low SVR, low-normal CVP

Distributive shock is characterized by:[1,2]

• Low SVR (systemic vasodilation)
• High/normal cardiac output (hyperdynamic response)
• Low-normal CVP (relative hypovolemia from venodilation)

Option A describes cardiogenic shock (high SVR, high CVP, low CO). Option E describes hypovolemic shock (low CVP, low CO, compensatory high SVR).

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Viva Scenario

Examiner: "You are called to resus to see a 28-year-old woman who has collapsed after eating at a restaurant. She has diffuse urticaria, lip swelling, and audible wheeze. Her BP is 65/40 mmHg, HR 135 bpm, RR 28, SpO₂ 88% on room air. Talk me through your management."

Candidate approach:

Immediate recognition: "This is anaphylactic shock - life-threatening allergic reaction with cardiovascular and respiratory compromise. I would initiate immediate treatment following anaphylaxis guidelines."

Immediate actions (within first 5 minutes):

"FIRST - Adrenaline IM:

• 0.5 mg (0.5 mL of 1:1000) IM into anterolateral thigh
• This is first-line and should not be delayed for any other intervention
• I would prepare to repeat in 5 minutes if no improvement

Simultaneously:

• High-flow oxygen 15 L/min via non-rebreather mask
• Position supine with legs elevated (if tolerated - not if respiratory distress)
• Stop any ongoing allergen exposure
• Call for senior help
• Large-bore IV access ×2

IV fluid resuscitation:

• 500 mL crystalloid bolus rapidly, repeat as needed
• May need 2-4 L due to capillary leak

Bronchospasm management:

• Salbutamol 5 mg nebulized with oxygen
• Consider ipratropium 500 mcg nebulized"

Examiner: "Despite IM adrenaline and 2 L of fluid, her BP is now 70/45 mmHg. What next?"

Candidate: "This is refractory anaphylaxis. I would:

1. Repeat IM adrenaline - second dose of 0.5 mg IM

2. Prepare IV adrenaline infusion if still no response:

   • 1 mg adrenaline in 100 mL saline = 10 mcg/mL
   • Start at 0.1 mcg/kg/min (approximately 5-10 mL/hour for 70 kg)
   • Titrate to BP, with continuous cardiac monitoring

3. Continue aggressive fluids - another 1-2 L crystalloid

4. Consider adjuncts:

   • Chlorphenamine 10 mg IV
   • Hydrocortisone 200 mg IV (prevents biphasic reaction)

5. Prepare for airway intervention:

   • Her SpO₂ is 88% with wheeze and lip swelling
   • Prepare difficult airway equipment
   • Early anaesthesia/ENT involvement
   • Consider awake intubation if laryngeal edema suspected

6. If on beta-blockers:

   • Glucagon 1-5 mg IV (bypasses beta-receptor blockade)"

Examiner: "She stabilizes with IV adrenaline infusion. What is your post-acute management?"

Candidate: "After stabilization:

1. Observation: Minimum 6-12 hours (some guidelines suggest 24 hours for severe reactions) due to risk of biphasic reaction

2. Tryptase level: Send serum tryptase within 1-4 hours of symptom onset to confirm anaphylaxis

3. Discharge planning:

   • Prescribe epinephrine auto-injector (2 devices)
   • Teach patient how to use it
   • Provide anaphylaxis action plan
   • Medical alert bracelet recommendation

4. Allergy referral: Outpatient allergist follow-up for:

   • Allergen identification (likely food given restaurant setting)
   • Specific IgE testing
   • Consider food challenge testing
   • Discuss avoidance strategies

5. Documentation: Complete documentation of reaction, triggers, and treatment for future healthcare encounters"

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Patient Explanation (Layperson Level)

"You are experiencing a type of shock called 'distributive shock.' This happens when your blood vessels relax too much throughout your body, causing your blood pressure to drop dangerously low.

There are several causes:

1. Severe allergic reaction (anaphylaxis): Your immune system overreacts to something you ate, touched, or received as medication. This causes widespread swelling and vessel relaxation. Treatment: adrenaline injection is life-saving.

2. Severe infection (septic shock): An infection has spread and triggered massive inflammation throughout your body. Treatment: antibiotics and medications to raise blood pressure.

3. Nerve injury (neurogenic shock): Damage to your spinal cord has disconnected the nerves that normally keep your blood vessels squeezed tight. Treatment: medications to tighten blood vessels.

What we're doing to help:

• Medications through your vein to tighten your blood vessels and raise blood pressure
• Fluids to fill up your circulation
• Treating the cause (antibiotics for infection, adrenaline for allergy, etc.)
• Close monitoring in intensive care until you're stable

With quick treatment, most people recover from distributive shock. The key is recognizing it early and treating the underlying cause."

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