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Spinal cord injury

medical indications


Spinal cord injurySpinal cord injury access


Spinal Cord Injury is an injury to the head and the spinal cord caused by trauma or destructive pathologies such as tumors that cause compression and deformity on spinal cord.  Left untreated this can lead to neurovascular deterioration, reduced blood supply and oxygen supply (ischemia and hypoxia), swelling and consequent degeneration of nerve cells (neurons) leading to Paraplegia and Quadriplegia.

HBOT can reverse neuronal damage by providing immediate high oxygen levels to injured nerve tissue. Sufficient oxygen can activate anatomically intact but dormant neurons in the penumbra zone, zone with diminished tissue oxygenation surrounding infarct (dead) cells.  HBOT relieves ischemia of the grey matter of the spinal cord and reduces swelling of the white matter.  Increased oxygen levels in the cerebral spinal fluid correct biochemical disturbances at the immediate and distal sites of spinal cord injury including metabolic enzymatic disturbance, therefore reducing secondary spinal cord degeneration.

The key element in preventing neurovascular deterioration in SCI is early HBOT implementation. Further HBO therapy in later rehabilitation will speed up neuromuscular recovery.

Although SCI fits under “investigative condition” category and may not be covered by insurance, many hospitals around the world especially in Asia (ref Asamoto et al. 2000, Lee et al.  1989) are using HBOT as an initial treatment in acute patients and later as addition to rehabilitation in chronic patients.

Early oxygen therapy provides protection against progressive degeneration of post traumatic spinal cord injury.

Symptoms

Rational for use of hyperbaric oxygen

Cost / benefits analysis

In acute, early SCI neurovascular damage of the spinal cord results in decreased blood flow (ischemia) and reduced oxygen supply (hypoxia) causing swelling and inflammation that further reduce blood supply. This vicious circle causes further progressive neuronal damage. Early oxygen therapy provides protection against progressive degeneration of post traumatic spinal cord injury Shorter hospital stay and faster rehabilitation.
Inability to exercise due to excess concentrations of lactate, pyruvate and ammonia cause spasticity and fatigue Improves metabolic circulatory function which reduces muscle spasm and increases muscle strength. Increases capacity for exercise and reduces fatigue Improved neuromuscular function and faster recovery
headaches Improves CSF (cerebral spinal fluid) dynamics, reduces intracranial pressure (ICP) and neurovascular deterioration. This would reduce migraine and cluster headache attacks and pains Improved quality of life
Immobility can cause pressure sores (decubitus ulcer) - open wound caused by pressure on the skin. Speeds up wound healing by promoting micro circulation and fibroblastic function of collagen synthesis A few sessions of HBO can turn a hypoxic/ischemic non-healing wound into a healing wound. Cost of wound dressing alone can reach $4000-$5000 per year.
Inflammation – caused by reduced blood flow, leads to accumulation of toxic substances (ammonia and lactate). Consequent swelling further impairs blood supply causing pain. Improved blood supply reduces inflammation and swelling which cause pain. Improved quality of life
Bacterial infection promotes ischemia and hypoxic development which interferes with local perfusion. Hypoxia limits antibiotics therapeutic function. Prevents and treats infection by: having direct bacteriostatic effect (kills most bacteria), improving function of white blood cells (phagocytosis), improves function of antibiotics. Improved circulation in the wound bed allows for successful skin grafting.
Deep bone infection - osteomyelitis Improves removal of necrotic (dead) bone, facilitates formation of a new bone tissue(osteogenesis)   and strengthens the existing bone structure If not responding to antibiotics osteomyelitis can cause death. (Christopher Reeves??)
Muscle weakness and pain Relives pain by removing excess of ammonia, lactate and pyruvate. Reduces muscle spasm and increases muscle strength. Increases exercise capacity and range of movement, reduces weakness and fatigue Faster recovery. Effect magnified when combined with physiotherapy and electrical stimulation.
Peripheral nerve damage Facilitates nerve regeneration

Improves sensitivity and decreases parasthesia (“pins and needles” sensation
Faster recovery. Results even better when combined with functional electrical stimulation.
Central nerve damage – loss of control, inability to make a movement Improved brain oxygenation and circulation. Improved permeability of blood brain barrier (BBB). Activation of the unaffected (dormant) neurons in the penumbra zone. Faster recovery due to improved control of movement combined with  improved neuromuscular function.
Bowel problems such as constipation, diarrhea and impaction that can lead to perineal fissure, fistulas and other complication. Soiled skin can be source of infection. Regulates motility.

Enhances closure of perineal fistulas and fissures. Prevents infections by improving skin microcirculation and strengthening immune system.
Reduced/avoided hospital stay.
Bladder dysfunction (incontinence) – susceptibility to infection is due to retention of urine and frequent need for catheterization (causing bacteria that are normally on the skin to be pushed into the bladder) Reduces bladder spasticity (muscle tension). Increases bladder capacity and improves bladder control of emptying. Urinary urgency and frequency is reduced. Prevents infections. Reduced possibility of infections and open wounds (pressure sores).
Respiratory problem – reduced vital capacity, impaired cough reflex (aspiration pneumonia) Increases vital capacity. Prevents respiratory tract infections. Improved quality of life.


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References:


  1. Asamoto S, Sugiyama H, Doi H, Iida M, Nagao T, Matsumoto K. Hyperbaric oxygen (HBO) therapy for acute traumatic cervical spinal cord injury.Spinal Cord. 2000 Sep;38(9):538-40.
  2. Lee HC, Niu KC, Chen SH, Chang LP, Lee AJ.Hyperbaric oxygen therapy in clinical application. A report of a 12-year experience. Zhonghua Yi Xue Za Zhi (Taipei). 1989 May;43(5):307-16
  3. Maeda N (1965) Experimental studies on the effect of decompression procedures and hyperbaric oxygenation for the treatment of spinal cord injury. J Natl Med Assoc 16:429-447
  4. Hartzog JI, Fischer RG, Snow C (1969) Spinal cord trauma: effects of hyperbaric oxygenation. Proc Ann Clin Spinal Cord Injury Conf 17:70-71.
    Locke GE, Yashon D, Feldmann RA (1971) Ischemia in primate spinal cord injury. J Neurosurg 34:614
  5. Yeo (1977) A study of the effects of hyperbaric oxygen on the experimental spinal cord injury. July 30, 1977 Medical Journal of Australia pg.145-147.
  6. Yeo JD (1976) Treatment of paraplegic sheep with hyperbaric oxygenation. Med J Austr 1:538-540.
  7. Higgins AC, Pearlstein RD, Mullen JB (1981) Effect of hyperbaric therapy on long tract neuronal conduction in acute phase of spinal cord injury. J Neurosurg 55:501-510.
  8. Sukoff MH (1982) Use of hyperbaric oxygen therapy for spinal cord injury. Neurochirurgia 24:19.
  9. Geldert JB, Fife WP, Bowers DE, Deschner SH, Welch DW (1983) Spinal cord transection in rats: the therapeutic effects of dimethyl sulfoxide and hyperbaric oxygen therapy. Ann NY Acad Sci 911: 218-233
  10. Neubauer RA, et al. Cerebral oxygenation and the recoverable brain. Neurol Res, 20 Suppl 1: S33-6, 1998
  11. Hart GB, Strauss MB (1984) Vital capacity of quadriplegia patients treated with hyperbaric oxygen therapy. J Am Paraplegia Soc: 113-114.
  12. Kieper NR (1987) the use of Hyperbaric Oxygen Therapy in the rehabilitation of spinal cord injured patients due to decompression sickness. In Kindwall EP (ed) Proceedings of the 8th international congress on hyperbaric medicine. Best, San Pedro, Ca
  13. Eltorai I, Hart GB, Strauss MB.Osteomyelitis in the spinal cord injured: a review and a preliminary report on the use of hyperbaric oxygen therapy.Paraplegia. 1984 Feb;22(1):17-24
  14. Yeo JD.The use of hyperbaric oxygen to modify the effects of recent contusion injury to
    the spinal cord.Cent Nerv Syst Trauma. 1984 Winter;1(2):161-5.
  15. Gamache FW Jr, Myers RA, Ducker TB, Cowley RA. The clinical application of hyperbaric oxygen therapy in spinal cord injury: a
    preliminary report.Surg Neurol. 1981 Feb;15(2):85-7
  16. Asamoto S, Sugiyama H, Doi H, Iida M, Nagao T, Matsumoto K.Hyperbaric oxygen (HBO) therapy for acute traumatic cervical spinal cord injury. Spinal Cord. 2000 Sep;38(9):538-40.
  17. K.K. Jain: Textbook of hyperbaric medicine: Ch 13: Hyperbaric Oxygen Therapy in Infections, Hogrefe& Huber Publishers, Inc., 3rd Ed.13: 189 –211, 1999
  18. K.K. Jain: Textbook of hyperbaric medicine: Ch 14:Hyperbaric Oxygen Therapy in Wound Healing, Plastic Surgery, and Dermatology, Hogrefe& Huber Publishers, Inc., 3rd Ed.14: 213–241, 1999
  19. Eric P. Kindwall, MD: Hyperbaric Medicine Practice: Ch 17:Wound Management: Best Chronic Wound Care Practices for The Hyperbaric Practitioners, Best Publishing Company, 2nd Ed: Ch 17:395-429,1999
  20. Eric P. Kindwall, MD: Hyperbaric Medicine Practice: Ch 33:Enhancement of Healing in Selected Problem Wounds, Best Publishing Company, 2nd Ed: Ch 33:813-850,1999
  21. Eric P. Kindwall, “The use of Hyperbaric Oxygen in Treatment of Osteomyelitis” Hyperbaric Medical Practice 1999; 23:604 –613
  22. Halm M, Zearley C.:Assessment and follow-up of problem wounds in the hyperbaric oxygen setting.Ostomy Wound Manage. 1991 Nov-Dec;37:51-9
  23. Mader JT, Adams KR, Wallace WR, Calhoun JH:Hyperbaric oxygen as adjunctive therapy for osteomyelitis.Infect Dis Clin North Am. 1990 Sep;4(3):433-40. Review
  24. Brown RB, Sands M. Infectious disease indications for hyperbaric oxygen therapy.Compr Ther. 1995 Nov;21(11):663-7. Review
  25. Tompach PC, Lew D, Stoll JL.Cell response to hyperbaric oxygen treatment.Int J Oral Maxillofac Surg. 1997 Apr;26(2):82-6
  26. Marmo M, Contaldi G, Luongo C, Imperatore F, Tufano MA, Catalanotti P, Baroni A, Mangoni G, Stefano S, Rossi F[Effects of hyperbaric oxygenation in skin and pulmonary infections caused by Pseudomonas aeruginosa].Minerva Anestesiol. 1996 Sep;62(9):281-7
  27. Boykin JV Jr, Crossland MC, Cole LM.Wound healing management: enhancing patient outcomes and reducing costs.J Healthc Resour Manag. 1997 May;15(4):22, 24-6.
  28. Molnar GE. Cerebral palsy. In Molnar GE (ed): Pediatric Rehabilitation, Baltimore. Williams & Wilkins. 1985,481-533. 
  29. Kudrjavcev T. Schoenberg BS,  Kurland LT. Groover, RV. Cerebral Palsy: Trends in incidence and changes in concurrent neonatal mortality: Rochester. Mn, 1985 - 1970. Neurology 1983; 33:1433-1438.
  30. Bozynski MEA, Nelson MN, Genaze D, Rosati-Skertich, C, Matalon. TAS. Vasan, U, Naughton, PM. Cranial ultrasonographyand the prediction of cerebral palsy in infants weighing < 1200 grams at birth. Developmental Medicine and Child Neurology 1988; 30:342-348. 
  31. Biether JK, Cummins 5K, Nelson KB. The California cerebral palsy project Pediatric Perinatology and Epidemiology 1993; 6:339-351.
  32. Stempien LM. Gaebler-Spira D. Rehabilitation of children and adults with cerebral palsy. In: Physical Medicine and Rehabilitation. Braddon. RL, Buschbacher. R, Dumitra, D, Johnson. EW. Matthews, D, Sinaki, M.eds., Saunders, 1996, pp.1113-1132.
  33. Katz RT, Rymer WZ. Spastic hypertonia: Mechanisms and measurement. Archives of Physical Medicine and Rehabilitation 1989; 70:144-155.
  34. Lance JW. Symposium Synopsis. In: Feldman RG, Young RR, Koella WP Spasticitv:Disordered Motor Control. (Eds).Chicago: Yearbook Publishers: 1980. p. 485-494.
  35. Krageloh-Mann ~ Hagberg G, Meisner C, Schelp B, Haas G, Eeg-Olofsson KE, Hagberg B, Michaelis R. Bilateral spastic cerebral palsy - A comparative study between southwest Germany and western Sweden. I Clinical patterns and disabilities. DevelopmentalMedicine and Child Neurology 1993; 35:1031-1047. 
  36. Kudrjavcev T, Schoenberg BS, Kurland LT, Groover RV. Cerebral palsy: Survival rates, associated handicaps, and distribution by clinical subtype. Rochester, MN 1950 - 1976. Neurology 1985; 35:900-903. 
  37. Park TS, Owen JH. Surgical management of spastic diplegia in cerebral palsy. The New England Journal of Medicine 1999 326:745-749. 
  38. Peacock WJ, Staudt LA. Spasticity in cerebral palsy and the selective dorsal rhizotomy procedure. Journal of Child Neurology 1990; 5:179-185. 
  39. Herndon WA, Troup P, Yngve DA, et al. Effects of neurodevelopmental treatment on movement patterns of children with cerebral palsy. Journal of Pediatric Orthopedics 1987; 7:395-400.
  40. Mayo N. The effect of physical therapy for children with motor delay and cerebral palsy: A randomized clinical trial. American Journal of Physical Medicine and Rehabilitation 1991; 70-258-267. 
  41. Palmer FB, Shapiro BK, Wachtel RC, Allen, MC, Hiller JE. Harryman SE. Mosher BS. - Meinert CL, Capute AJ. The effects of physical therapy on cerebral palsy. A controlled trial in infants with spastic diplegia. The New England Journal Medicine 1988: 318:803-808
  42. Machado JJ. Reduction of spasticity, clinicallv observed in patients with neurological diseases, submitted .to hyperbaric oxygen-therapy specially children with cerebral palsis. Transcripts from the annual meeting of the Undersea and Hyperbaric Medicine conference, 1969.