Decompression Sickness (Type II)

Decompression Sickness (Type II): A Comprehensive Clinical Guide

Decompression Sickness (DCS), historically known as "the bends" or "caisson disease," represents a systemic pathological condition caused by the formation of inert gas bubbles (primarily nitrogen) in the blood and tissues. While Type I DCS is generally characterized by mild, localized manifestations, Type II DCS involves the central nervous system (CNS), the cardiopulmonary system, and the inner ear. It is a medical emergency that requires rapid identification and hyperbaric intervention to prevent permanent neurological deficit or mortality.

1. Clinical Definition and Etiology

Definition

Decompression Sickness (Type II) is defined as a multi-system dysbaric injury occurring when ambient pressure decreases too rapidly, causing dissolved inert gases (nitrogen) to come out of solution and form bubbles within the body. Type II specifically refers to "serious" DCS, involving the spinal cord, brain, vestibular system, or cardiopulmonary systems.

Etiology and Predisposing Factors

The primary trigger is the violation of decompression protocols during ascent from a high-pressure environment. However, susceptibility is highly variable. Key risk factors include:
* Physiological: Age, obesity (adipose tissue acts as a nitrogen reservoir), dehydration, and patent foramen ovale (PFO).
* Environmental: Cold water exposure, heavy exertion during or after diving, and altitude exposure immediately post-dive.
* Diving Profile: Rapid ascent rates, omission of decompression stops, repetitive diving, and high depth-time exposures.

2. Pathophysiology: The Mechanics of Injury

The pathophysiology of Type II DCS is a complex interplay of mechanical, biochemical, and vascular insults.

The Bubble Effect

1. Mechanical Obstruction: Bubbles act as emboli, blocking microvasculature and causing ischemia in the spinal cord (white matter) and brain.
2. Endothelial Damage: Bubbles physically damage the vascular endothelium, triggering an inflammatory cascade.
3. Biochemical Cascade: The bubble-blood interface acts as a foreign surface, activating platelets, leukocytes, and the complement system. This leads to capillary leakage, hemoconcentration, and further perfusion deficits.
4. Autochthonous vs. Embolic: Bubbles may form locally within the myelin sheaths of the spinal cord (autochthonous) or travel from the venous circulation to the arterial side via intracardiac shunts (paradoxical embolism).

3. Clinical Staging and Presentation

Type II DCS is categorized by the organ system involved. Clinical presentation is often rapid, occurring within 1–6 hours of surfacing.

Clinical Classification Table

Detailed Symptomatology

• Spinal Cord Involvement: The most common form of Type II DCS. It typically affects the thoracic or lumbar segments, presenting as girdle-like pain, lower extremity weakness, and bladder/bowel incontinence.
• Cerebral Involvement: Rare but severe. Symptoms mimic a stroke, including cognitive impairment, focal motor deficits, and potential seizures.
• Vestibular/Inner Ear: Often misdiagnosed as middle ear barotrauma. Patients experience severe vertigo, nausea, and vomiting.
• Cardiopulmonary ("Chokes"): Caused by massive venous gas emboli overwhelming the pulmonary filter. This leads to pulmonary hypertension, right heart strain, and potential cardiovascular collapse.

4. Differential Diagnosis

Distinguishing Type II DCS from other diving-related injuries is essential for treatment.

• Arterial Gas Embolism (AGE): Usually occurs immediately upon surfacing (within 10 minutes). Rapid onset of loss of consciousness or focal neurological deficits.
• Inner Ear Barotrauma: Often associated with ear pain during descent; vertigo is usually transient.
• Spinal Cord Infarction/Stroke: Non-diving related etiologies must be considered if the patient has underlying cardiovascular disease.
• Migraine with Aura: Can mimic transient cerebral DCS symptoms.

5. Diagnostic Evaluation and Testing

Diagnosis of Type II DCS is primarily clinical. However, diagnostic tests are used to rule out secondary causes and assess damage.

Key Diagnostic Tests

1. Neurological Examination: A baseline must be established immediately, including GCS, cranial nerves, motor strength, and sensory mapping.
2. Imaging:
   • MRI (Brain/Spine): The gold standard for identifying spinal cord edema or infarction.
   • CXR/CT Chest: If "Chokes" (pulmonary DCS) is suspected, to rule out pneumothorax or pulmonary edema.
3. Cardiac Evaluation: Echocardiography (Bubble Study) to screen for a Patent Foramen Ovale (PFO), which increases the risk of paradoxical embolism.
4. Laboratory Analysis: CBC (hemoconcentration), electrolytes, and potentially D-dimer (though non-specific).

6. Treatment Protocols

Immediate Field Management

• Oxygen: 100% High-flow normobaric oxygen via non-rebreather mask.
• Hydration: Oral rehydration if conscious; IV fluids (isotonic crystalloids) if indicated to manage hemoconcentration.
• Positioning: Supine position. Avoid elevation of the head.
• Evacuation: Immediate transport to a facility with a hyperbaric chamber.

Definitive Treatment: Hyperbaric Oxygen Therapy (HBOT)

HBOT is the cornerstone of treatment, utilizing the US Navy Treatment Tables (typically Table 6).
* Mechanism:
* Mechanical Reduction: Boyle’s Law dictates that increased pressure reduces bubble volume.
* Diffusion Gradient: Breathing 100% oxygen increases the nitrogen gradient, accelerating inert gas washout.
* Anti-inflammatory: Reduces edema and inflammation in the CNS.

7. Risks, Contraindications, and Prognosis

Contraindications to HBOT

• Untreated Pneumothorax: Must be treated with a chest tube prior to compression.
• Certain Medications: Doxorubicin, Cisplatin, or Disulfiram (rare).

Long-Term Prognosis

Prognosis depends on the time to treatment (the "Golden Hour").
* Early Intervention: Full recovery is common if treatment begins within 6 hours.
* Delayed Intervention: Residual deficits, including chronic neuropathic pain, bladder dysfunction, or cognitive impairment, are significantly more likely.
* Psychological Impact: Post-traumatic stress or anxiety regarding future diving activity is common.

8. Frequently Asked Questions (FAQ)

1. How long after a dive can Type II DCS occur?
While most symptoms appear within 6 hours, some can manifest up to 24–48 hours post-dive, especially after flying or altitude exposure.

2. Is Type II DCS always fatal if untreated?
Not always, but it carries a high risk of permanent disability. Untreated "Chokes" or severe CNS DCS can lead to death.

3. Does being physically fit prevent Type II DCS?
Fitness helps, but physical fitness does not guarantee immunity. Dehydration and fatigue are often greater risk factors than baseline fitness.

4. Can I go back to diving after a Type II DCS incident?
This is a complex decision. A full neurological and cardiac evaluation (including PFO screening) is required. Most specialists recommend a minimum of 6–12 months of cessation, depending on the severity of the initial injury.

5. What is the role of the PFO in Type II DCS?
A Patent Foramen Ovale allows venous blood (potentially containing nitrogen bubbles) to bypass the lungs and enter the systemic arterial circulation, leading to brain or spinal cord injury.

6. Why is hydration so important?
Dehydration reduces blood volume and viscosity, worsening bubble formation and impeding the clearance of inert gas from tissues.

7. Is pain the primary symptom of Type II DCS?
No. Type I DCS is characterized by pain. Type II is characterized by neurological deficit or systemic dysfunction. If a diver has pain plus neurological weakness, it is classified as Type II.

8. What is the "Golden Hour" for DCS?
The window of opportunity to begin recompression to minimize permanent nerve cell damage and secondary inflammatory processes.

9. Can I take aspirin for DCS symptoms?
Aspirin is often recommended in the field for its anti-platelet effect (to mitigate the inflammatory cascade), but it should not delay transport to a hyperbaric facility.

10. Do I need a referral for a hyperbaric chamber?
In an emergency, one should call the Divers Alert Network (DAN) or the nearest emergency department for immediate coordination with a hyperbaric physician.

9. Conclusion

Decompression Sickness (Type II) remains one of the most critical pathologies in diving and aerospace medicine. The transition from minor physiological stress to catastrophic neurological injury can occur within minutes. As clinicians, maintaining a high index of suspicion and ensuring immediate access to hyperbaric oxygen therapy is paramount. Through diligent adherence to decompression protocols, proper hydration, and an understanding of individual risk factors (such as PFO), the incidence of this potentially debilitating condition can be effectively mitigated.

Disclaimer: This guide is intended for educational purposes for healthcare professionals and diving safety officers. It does not replace professional medical advice, diagnosis, or treatment. Always consult with a hyperbaric medicine specialist in the event of a suspected diving injury.