DCI Summary

DCI Types

  • DCS: Evolved gas from tissues
  • AGE: Gas in arterial circulation
  • Symptoms: 0-72 hours post-dive

Emergency Management

  • Call Diving Accident Helpline
  • High-flow oxygen (15L/min)
  • IV fluids - low threshold
  • Urgent recompression therapy

Absolute Contraindications

  • NO Entonox (nitrous oxide)
  • Avoid NSAIDs and opioids
  • No flying after diving

Common Presentations

  • Limb/joint pain (toothache-type)
  • Neurological symptoms
  • Girdle pain (back → abdomen)
  • Cutis marmorata rash
  • Audiovestibular symptoms

Risk Factors

  • Deep/long dives
  • Missed decompression stops
  • Multiple dives
  • Exercise during/after dive
  • Dehydration, obesity, age

Inner-Ear Barotrauma

  • Sudden onset during descent
  • Failed ear equalization
  • Vertigo, hearing loss, nystagmus
  • Contraindication to recompression

Critical Actions

  • National Diving Accident Helpline
  • Urgent diving physician consult
  • Chest drain if pneumothorax
  • Lie patient flat (AGE)

Decompression Illness (DCI)

A disease of compressed gas divers, aviators, astronauts and caisson workers where gas bubbles form in tissues and/or blood during pressure decrease

Overview

Decompression illness (DCI) is a disease of compressed gas divers, aviators, astronauts and caisson workers where gas bubbles form in tissues and/or the blood during or after a decrease in environmental pressure. In the United Kingdom (UK) this is most commonly seen in divers.

Two Types of DCI

  • Decompression Sickness (DCS): Caused by nitrogen coming out of solution during ascent
  • Arterial Gas Embolism (AGE): Gas bubbles in arterial circulation causing occlusion

Pathophysiology

Decompression Sickness (DCS)

Caused by nitrogen coming out of solution when a diver ascends from a dive. The inert gas that evolves from the tissues can cause mass effect and inflammatory response.

Mechanisms of Damage:
  • Direct damage (primary):
    • Artery occlusion
    • Damage to vascular endothelium
    • Venous outflow obstruction
    • Breakdown of blood-brain barrier
  • Inflammatory response (secondary):
    • Activation of clotting cascade
    • Platelet and complement activation
    • Leukocyte activation

Arterial Gas Embolism (AGE)

Occurs when nitrogen bubbles escape into arterial circulation through various mechanisms:

Mechanisms:
  • Pulmonary barotrauma: Lung overinflation during ascent
  • Patent foramen ovale: Right-to-left shunt
  • Overwhelming pulmonary filter: Bypass lung filtration

Cerebral AGE (CAGE): Most serious form when gas embolus lodges in cerebral arteries. Symptoms have rapid onset and require swift recompression.

Time Course: DCI can present anytime from 0-72 hours or more after a dive, although majority within 6 hours. Direct bubble effects present quickly; inflammatory responses can cause latent symptoms.

Risk Factors

Dive-Related Factors

  • Deep dive
  • Long dive duration
  • Missed decompression stops
  • Multiple dives
  • Rapid ascent

Individual Factors

  • Increasing age
  • Obesity
  • Dehydration
  • Patent foramen ovale
  • Poor physical fitness

Behavioral Factors

  • Exercise during or after dive
  • Flying/ascending to altitude after diving
  • Alcohol use prior to dive
  • Smoking

Clinical Features

Bubbles can form in or move to most parts of the body, so DCI can present with almost any clinical picture.

Musculoskeletal

  • Limb or joint pain: Often toothache-type pain, usually not worse on movement or palpation
  • Girdle pain: Pain from back spreading to abdomen

Neurological

  • Tingling, numbness, weakness
  • Change in behavior or personality
  • Poor coordination
  • Loss of bowel/bladder control
  • Hearing or vision changes
  • Memory loss, unconsciousness

Other Presentations

  • Chest pain/breathing difficulties: Pneumothorax, coronary gas, pulmonary edema
  • Rash: Cutis marmorata (mottled rash) - may precede neurological DCI
  • Audiovestibular: Hearing loss, balance problems, vertigo, vomiting
  • Constitutional: Malaise, headache, lethargy, apathy

Emergency Management

Immediate Actions
  1. Call National Diving Accident Helpline (or Divers Alert Network)
  2. High-flow oxygen: 15 L/min via non-rebreather mask regardless of saturations
  3. IV fluids: Low threshold for administration
  4. Urinary catheter: If retention suspected
  5. Chest drain: If evidence of pneumothorax

Recompression Therapy

Imperative: Call diving physician immediately. Patients need recompression therapy without delay.

Effects of Recompression

  • Bubble crushing: Increased pressure decreases bubble volume (Boyle's law)
  • Nitrogen flushing: Oxygen replaces nitrogen in bubbles
  • Tissue healing: Hyperbaric oxygen promotes healing

Critical Contraindications

  • NO Entonox: Nitrous oxide is highly soluble and increases inert gas load, worsening DCI symptoms
  • Avoid pain medications: NSAIDs and opioids should be avoided unless long transfer and after discussion with diving doctor

Inner-Ear Barotrauma (IEBT)

Mechanism of Injury

Barotrauma refers to injuries due to pressure changes. Boyle's law: pressure and volume are inversely proportional. Incremental pressure changes are greatest at the surface.

Clinical Features

  • Sudden onset during descent
  • Associated with ear equalization issues
  • Severe vertigo with nausea/vomiting
  • Hearing loss ± tinnitus
  • Nystagmus
  • Ear pain (may be absent)
  • Feeling of ear fullness

IEBT vs Inner-Ear DCS (IEDCS)

Critical distinction: Recompression is contraindicated in IEBT but essential for IEDCS.

Feature Inner-Ear Barotrauma (IEBT) Inner-Ear DCS (IEDCS)
Onset Sudden, during descent Delayed (minutes to hours post-dive)
Trigger Failed ear equalization Failed decompression
Dive Profile Any depth, surface issues Moderate to significant exposure
Associated Findings Middle-ear barotrauma evidence Other DCS manifestations
Treatment Avoid recompression Urgent hyperbaric oxygen

Investigations

DCI is primarily a clinical diagnosis based on thorough history and examination.

Essential Investigations

  • Chest X-ray: Assess for pulmonary barotrauma (pneumothorax, pulmonary edema, subcutaneous emphysema)
  • Neurological examination: Detailed assessment
  • Vital signs monitoring: Continuous assessment

Additional Investigations

  • CT brain (if neurological symptoms)
  • Echocardiogram (bubble study for PFO)
  • Blood tests (inflammatory markers)
  • Audiological assessment