We need you! See something you could improve? Make an edit and help improve WikSM for everyone.

Decompression Sickness

From WikiSM
Jump to: navigation, search

Other Names

  • Decompression Illness (DCI)
  • Decompression Sickness (DCS)
  • The "Bends"
  • The "Staggers"
  • The "Chokes"
  • Decompression Stress

Background

  • This page refers to decompression sickness (DCS), a disease process where dissolved nitrogen comes out of solution and forms bubbles in blood and tissue

History

  • First reported by Pol in 1854[1]

Epidemiology

  • Decompression Illness
    • Overall incidence estimated to be about 0.03%
    • Varies by divers: scientific diver (0.015%), recreational diver (0.01-0.019%), US navy divers (0.03%), commercial divers (0.095%)[2]
    • Of 441 cases of DCI reported to Divers Alert Network (DAN), only 3.9% were classified as possible AGE[3]

Pathophysiology

  • See: Dive Medicine Main
  • General
    • Cause by intra- or extravascular bubbles formed as a result of decompression
    • Symptoms start soon after surfacing, nearly all within 24 hours of surfacing
    • However, secondary effects can cause delayed onset up to 24 hours
    • Clinical manifestation range from trivial to fatal
  • Terminology
    • Decompression Illness (DCI): broad term encompassing all disease processes related to decompression
    • Decompression Sickness (DCS): intra- or extravascular bubbles formed as a result of decompression
    • Arterial Gas Embolism (AGE): severe form of DCI in which gas bubbles are introduced into the arterial circulation
    • Decompression Stress: undefined term, need update
  • Diving type
    • Recreational divers typically experience pain or very mild neurological symptoms (numbness, parasthesia)

Etiology

  • Depth
    • Generally requires at least 6 m and is uncommon at depths less than 10 m[4]
    • Rarely, can occur after ascent from a depth as shallow as 1.0 to 1.5 m if underlying pulmonary disease
  • Pressurized gas saturation
    • Super saturation of inert gas occurs
    • Due to partial pressure of the gas being respired at high pressure during compression
  • Super saturation
    • This process occurs during ascent
    • Sum of dissolved gas tensions (O2, CO2, N2, He) and water vapor exceeds local absolute pressure
    • Thus the gases begin bubble formation and increase in size in the extra- and intravascular space
    • Essentially, rate of ambient pressure reduction exceeds rate of inert gas washout
  • Mechanical effects of bubbles
    • Distortion of tissues causing pain
    • Vascular obstruction causing stroke-like signs and symptoms
  • Endothelial damage of bubbles
    • Capillary leak
    • Extravasation of plasma
    • Hemoconcentration
    • Decreased effect of vasoactive compounds
    • Hypotension in severe cases
    • Platelet activation and deposition[5]
    • Consequences of vascular occlusion (ischemia-reperfusion injury, apoptosis)

Type I (Pain only DCS)

  • General
    • Involves joints and extremities with cutaneous symptoms
    • Joints most commonly involved: shoulder, elbow, knee
  • Skin and lymphatics
    • Pruritus, stinging, paresthesias, hot/cold sensations
    • Fine scarletiniform rash from nitrogen movement through sweat glands
    • Cutis marmorata - marbling rash, purplish-bluish discoloration, otherwise common and normal in infants
    • Pitting edema, peripheral swelling from lymphatic blockage

Type II (Serious DCS)

  • General
    • Multiple joints may qualify as type II
    • Presence of a PFO or right-to-left cardiac shunt is present in up to 30% of the population, may facilitate venous to arterial embolization
  • Spinal cord
    • Signs and symptoms often trace to a single location in the cord, note skip lesions may be present
    • Ascending paralysis
    • Limb weakness, parasthesias, paralysis
    • Urinary retention, fecal incontinence, priapism
  • Vestibular "staggers"
    • Vertigo
    • Hearing loss
    • Tinnitus
    • Distinguished from otic barotrauma, which occurs during descent
  • Pulmonary "chokes" (cardiorespiratory DCS)
    • Cough
    • Hemoptysis
    • Dyspnea
    • Substernal chest pain
    • Pulmonary edema

Type III (Type II + Arterial Gas Embolism)

  • General
    • Presents with neurological dysfunction
    • Arterial Gas Embolism is present
    • Symptoms can resolve spontaneously

Risk Factors

  • Demographic
    • Female gender
    • Lower BMI
    • Advanced age
  • Medical
    • Previous DCI
    • Dehydration
    • History of PFO
  • Sports/ Occupation
    • Diving
    • Water immersion (vs dry hyperbaric chamber exposure)
    • Rapid ascent in flying or military operations
    • Hypobaric medicine training
    • Aviation
    • Astronaut/ Spaceflight
    • Compressed air worker
  • Diving-related/ environmental
    • Cold temperature
    • Dive depth
    • Dive time
    • Exercise after decompression

Differential Diagnosis

Differential Diagnosis Dive Medicine

Clinical Features

Clinical manifestations of decompression illness[6]
  • History
    • Consider DCI in any symptom arising shortly after decompression
    • Symptoms that occur during descent or at depth are not due to DCI (unless there was a recent previous dive)
    • Symptoms typically begin shortly after surfacing
      • Within in 1 hr (42%), 3 hrs (60%), 24 hrs (98%)[7]
      • CNS cases present more rapidly; 56% within 10 mins[8]
      • Some symptoms can be delayed for days[9]
      • Delayed presentation should strongly be considered in someone who subsequently traveled by air or ascended to altitude
    • Common symptoms include pain (68%), numbness or parasthesia (63%), constitutional (41%), dizziness/ vertigo (41%) and motor weakness (19%)
    • Constitutional symptoms include malaise, fatigue, headache, transient periarticular discomfort
    • joint pain is more common in the arms of recreational divers, knees in saturation divers
    • Vestibulo-cochlear manifestations more common after deep heliox diving
    • New onset altered mental status, seizure, confusion, focal cortical signs should suggest AGE
  • Physical Exam
    • A careful neurological examination is critical for all divers with suspected DCI
    • Physical exam is often normal, may be limited to pain or parasthesia
    • Rash can be present
    • Lymphedema of the trunk
    • Hypoesthesia and truncal ataxia are common and can be missed
    • Objective neurological findings can include weakness, paralysis, seizure, change in mentation
  • Special Tests

Evaluation

  • Primarily a clinical diagnosis
    • No clearly diagnostic imaging or laboratory findings
  • Imaging
    • Imaging is not diagnostically useful to include/ exclude
    • Should not delay recompression unless strong suspicion of non-DCI related causing of symptoms
    • Bubbles are rarely detectable with radiograph in joints affected by pain
    • Bubbles are rarely noted on CT or MRI Brain or of the spine

Radiographs

Sphygmomanometry

  • Pain can improve if BP cuff is inflated above the joint to 150 to 200 mm Hg

Laboratory

  • Consider if unclear diagnosis
    • Point of care glucose
    • Complete blood Count
      • Hemoconcentration can occur due to endothelial leak
    • Creatine Kinase
      • Can help distinguish AGE from DCS (high in AGE)
    • Metabolic Panel
    • Lactate
    • PIT/PTT
    • Blood Gas
    • Ethanol level
    • Urine Toxicology Screen

Other Neurological Testing

  • Can typically be delayed until after recompression therapy
    • Including audiometry, electronystagmography for inner ear DCI

Ultrasound

  • Echocardiography
    • Valuable into research of venous gas emboli
    • Not needed for DCI, should not delay treatment

Classification

  • Type I
    • Pain
    • Cutaneous manifestations
    • Constitutional symptoms
  • Type II
    • Neurological manifestations include numbness, tingling, paresthesia, weakness, paralysis, mental or motor abnormalities
  • Type III

Management

Nonoperative

  • Indications
    • All cases
  • ABCs
    • Manage patient ABCs
    • BLS or ACLS as indicated
  • Oxygen Therapy
    • Denitrogenation with oxygen is first line treatment, pure oxygen washes inert gases from lungs
    • Administer 100% non rebreather regardless of Sp02
    • Continue for at least 2 hours after symptom resolution
  • Position
    • Maintain patient in supine position
    • Trendelenburg not recommended (i.e. head down position to avoid arterial bubbles from traveling to cerebral circulation)[10]
  • Hyperbaric Oxygen Therapy (HBOT)
    • Effective even in delayed presentation or delay in initiating HBOT
    • If suspicious for Type II/III, recommend immediate recompression
    • If delayed, may recompress up to 14 days after symptom onset[11][12]
    • The time beyond which recompression is not useful is not currently known
  • Hydration
    • In patients requiring IV fluids, isotonic crystalloid solutions are recommended
    • Adequate hydration decreases bubble formation after decompression[13]
    • Take care to avoid fluid overload, which can contribute to cerebral, spinal cord and pulmonary edema
  • Elevation related DCS
    • Descent to ground level ASAP
  • Contact Divers Alert Network (DAN) Emergency Hotline at 1-919-684-2948
    • Similar function as to poison control
  • Transportation
    • Recommend ground transportation if practical
    • If air transport, max 1000 ft with pressured cabin to 1 ATA
  • NSAIDS
    • Tenoxicam decreased the number of recompressions to achieve symptom resolution but did not change the final outcome in an RCT[14]
    • Aspirin has been recommended for its anti-platelet effect but has not been formally studied
  • Medication Adjuncts
    • Lidocaine often administered with type II or III DCS
    • High dose steroids worsen outcomes and are not recommended[15]
  • Perfluorcarbon emulsions
    • Probably helps by enhancing tissue oxygenation and inert gas transport from tissue to lungs in animal studies[16]
    • Human trials are pending
  • Venous Thromboembolism Prophylaxis
    • Consideration should be made in patients with leg immobility
  • Avoid
    • Nitrous oxide (may increase size of bubbles by inward diffusion)

Prevention

  • See: Preventing injuries in Dive Medicine
  • Reduced risk of DCI:
    • Avoid breath holding
    • Avoid rapid ascent
    • Do not dive with active pulmonary infections or disease
  • Oxygen therapy
    • High oxygen concentration can help eliminate inert gases before decompression
    • High oxygen partial pressure gases may decrease inert gas absorption at depth
  • Decompression Stops
    • Greatly reduced frequency of DCI
    • Delay ascent to surface, allow inert gases to be eliminated in dissolved form
  • Detection of Patent Foramen Ovale
    • Estimates of relative risk of serious DCI from PFO range from 2.5 to 6.6 (need citation)
    • However, absolute risk of neurological DCI is small (< 0.02%), which makes routine screening unnecessary[17]

Rehab and Return to Play

Rehabilitation

  • No clear rehabilitation guidelines

Return to Play/ Work

  • Observe for a period after treatment near a decompression chamber
    • 2 hours for mild symptoms
    • 6 hours for severe symptoms
  • US Navy recommends patients be within 1 hour travel time for 24 hours following recompression
  • Flight
    • Patients who were recompressed with complete relief should not fly for at least 72 hours
  • Resumption of diving
    • For recreational divers, typically allowed 4 weeks after treatment with complete recovery
  • Assessment of Patent Foramen Ovale
    • Recommended for patients with severe or recurrent DCI
    • Detection should warrant counselling about future diving

Complications and Prognosis

Prognosis

  • General
    • One study showed that nearly 50% of patients still had impairments at an average of 6.1 years[18]
  • Recompression treatment
    • Results in complete resolution in most cases, mild residual symptoms in a few cases, severe residual symptoms rarely

Complications

  • Chronic Sequelae includes
    • Impaired urination
    • Impaired defication
    • Sexual dysfunction

See Also

References

  1. ↑ Pol B, Watelle TJJ. Mémoire sur les effets de la compression de l’air appliquée au creusement des puits à houille. Ann Hyg Pub Med Leg 1854;2:241-279.
  2. ↑ Vann RD, Ugoccioni DM. DAN's Annual review of recreational scuba diving injuries and fatalities based on 1998 data. Durham, NC: Divers Alert Network, 2000.
  3. ↑ Pollock NW. Annual diving report: 2008 edition. Durham, NC: Divers Alert Network, 2008.
  4. ↑ US Navy diving mannual, revision 06; 15 April 2008.
  5. ↑ Bosco, G., et al. "Environmental stress on diving-induced platelet activation." Undersea & hyperbaric medicine 28.4 (2001): 207.
  6. ↑ Tawar, Ashish, and P. Gokulakrishnan. "Decompression illness." Journal of Marine Medical Society 21.2 (2019): 112.
  7. ↑ Navy Department. US Navy Diving Manual. Revision 6. Vol 5: Diving Medicine and Recompression Chamber Operations. NAVSEA 0910-LP-106-0957. Washington, DC: Naval Sea Systems Command, 2008.
  8. ↑ Francis TJ, et al. Central nervous system decompression sickness: latency of 1070 human cases. Undersea Biomed Res. 1988; 15:403–417.
  9. ↑ Freiberger JJ, et al. The relative risk of decompression sickness during and after air travel following diving. Aviat Space Environ Med. 2002; 73:980–984.
  10. ↑ Moon RE, ry sl. Guidelines for treatment of decompression illness. Aviat Space Environ Med. 1997; 68:234–243.
  11. ↑ Marx et al. Rosen's Emergency Medicine - Concepts and Clinical Practice. 8th Ed. 2013. Ch 143. Pg. 1925.
  12. ↑ Edmonds C et al. Diving and Subaquatic Medicine, Fifth Edition. 2015. Decompression Sickness: Treatments. Pg 173.
  13. ↑ Gempp, Emmanuel, et al. "Preventive effect of pre-dive hydration on bubble formation in divers." British journal of sports medicine 43.3 (2009): 224-228.
  14. ↑ Bennett, M. H., S. J. Mitchell, and A. Dominguez. "Adjunctive treatment of decompression illness with a non-steroidal anti-inflammatory drug (Tenoxicam) reduces compression requirement." Undersea Hyperb Med 30.3 (2003): 195-205.
  15. ↑ Moon, Richard E. "Adjunctive therapy for decompression illness: a review and update." Diving Hyperb Med 39.2 (2009): 81-7.
  16. ↑ Zhu, J., et al. "Intravenous perfluorocarbon emulsion increases Nitrogen washout after venous gas emboli in rabbits." Undersea Hyperb Med 34.1 (2007): 7-20.
  17. ↑ Bove, Alfred A. "Risk of decompression sickness with patent foramen ovale." Undersea & hyperbaric medicine 25.3 (1998): 175.
  18. ↑ Vann RD, et al. Decompression illness. Lancet. 2011; 377(9760):153-164.
Created by:
John Kiel on 30 June 2019 23:02:01
Authors:
Last edited:
25 July 2022 20:53:45
Category:

Retrieved from "https://wikism.org/w/index.php?title=Decompression_Sickness&oldid=17300"