1 / 22

HYDROGEN SULFIDE : Does Hyperbaric Oxygen work?

HYDROGEN SULFIDE : Does Hyperbaric Oxygen work?. Case of the week December 12, 2003 Rob Hall MD. H2S Knock-down case of the week!. How is H2S toxic?. Inhibits cytochrome oxidase Thus inhibits oxidative phosphorylation Anaerobic metabolism can ’ t keep up! -------------> CELLULAR HYPOXIA

imani-key
Download Presentation

HYDROGEN SULFIDE : Does Hyperbaric Oxygen work?

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. HYDROGEN SULFIDE:Does Hyperbaric Oxygen work? Case of the week December 12, 2003 Rob Hall MD

  2. H2S • Knock-down case of the week!

  3. How is H2S toxic? • Inhibits cytochrome oxidase • Thus inhibits oxidative phosphorylation • Anaerobic metabolism can’t keep up! • -------------> CELLULAR HYPOXIA • EARLY DEATH • Respiratory paralysis due to toxic effect at the respiratory centers

  4. Permanent Neurologic Sequelae • Prolonged coma • Recurrent seizures • Chronic vegatative states • Tremors • Cognitive impairment

  5. Why might HBOT be effective? • Increased oxygen delivery to tissues • Increased oxyhemoglobin which increases the auto-oxidation of sulfide

  6. What are the TEXTBOOK recommendations for HBOT? • Haddad. 1998. • “May be beneficial in patients in whom CNS symptoms do not resolve spontaneously or with prompt nitrite therapy” • Ford. • “Should be used in neurologically compromised or acidemic patients refractory to conventional therapy” • Goldfrank 2003 • “All patients should receive HBOT if readily available; transport solely for HBOT is unnecessary”

  7. H2S and HBOT…… So what is the evidence??

  8. 1) Vicas. Vet Hum Toxicol 1989 • 30 yo male • H2S contaminated petroleum • Unconcscious on arrival in ED • 3 HBO treatments 13 hr post exposure • 2 further HBO treatment • Increased LOC, memory, verbal interaction, problem solving • Persistent retrograde amnesia

  9. 2) Al-Mahesneh. Vet Hum Toxicol 1989 • Acute exposure to known high [H2S] • Comatose, unresponsive, F/D pupil on arrival in the ED • Flown to hyperbaric chamber (?delay) • HBOT for 3 hours • NO improvement • Patient died at 56hrs after exposure

  10. 3) Snyder. Am J Emerg Med 1995 • Construction pit on of New Jersey coast • Two men knocked – down, several other rescuers knocked down, 1 Dead on scene • Worker 1 • GCS 3 on arrival, sent for HBO • 12 hour delay until HBOT started

  11. 3) Snyder. Am J Emerg Med 1995 • Day1 • One session of 2ATA for 45 min • GCS 3 -> 5 • Day 2 • Two sessions of 1.5 ATA for 90 min each • Day3 – 7 • Two sessions of 1.0 ATA for 90 min each • Day 3 GCS 7, Day 5 GCS 11, Day 7 GCS 15 • Day 8-16 • One session of 1.0 ATA for 90 min

  12. 3) Snyder. Am J Emerg Med 1995 • Persistent Neurological Sequelae • Slow speech, flat affect, inability to concentrate, impaired visual memory, easily distractible, confabulation • Neurologic Sequelae unchanged at 12 and 18 months

  13. 4) Schneider. Occ Med 1998 • 27yo male • Building a sewer system in New Jersey • Rescuer died at the scene • GCS 3 on arrival at ED • Transfer for HBOT 10hrs after exposure • 2 ATA for 45 min bid X “several” days • Regained consciousness on day 5 • GCS 11 on day 7 then improved to 15 • Similar neurological sequelae to last case noted at one month and 4yrs post incident

  14. Neuroimaging • CT head was normal in this case on day of exposure • MRI was normal at 17 months despite persistent neurological sequelae • PET scan at 3 years showed marked decrease in perfusion to thalamus, basal ganglia and abnormal metabolic patterns in the temporal and parietal lobes

  15. NOTE • Normal CT or MRI of brain does not preclude permanent neurologic sequelae!

  16. 5) Smilkstein. J Emerg Med 1985 • 34 yo male • Oil pump waste collection tank • GCS of 7 on arrival to ED • HBOT started 10hrs after exposure • Total of 12 HBOT treatments over 6 days • #1: 2.5 ATA for 45 min • #2: 2.0 ATA for 75 min • #3-12: 2 ATA for 90-120 min • Outcome: stepwise improvement, awake/alert by 48hrs, slight difficulty with complex tasks persisted

  17. 6) Harefuah. 1994 • Another Case report of H2S treated with HBOT • Hebrew!

  18. The RATS have the last word!Bitterman. Tox Appl Pharm 1986 • Rat model: several groups with 20 rats each • LD 75 dose of intraperitoneal sodium sulfide • Various treatments after sulfide injection • Group 1: no treatment • Group 2: sodium nitrite + room air • Group 3: 100% oxygen • Group 4: HBOT at 2 ATA • Group 5: sodium nitrite + 3 ATA HBOT • Various treatments before sulfide injection • Group 7: HBOT 3 ATA • Group 8: sodium nitrite and HBOT 3ATA

  19. The RATS have the last word!Bitterman. Tox Appl Pharm 1986 pretreatement rescue treatments

  20. The RATS have the last word!Bitterman. Tox Appl Pharm 1986 • Conclusions from the rats • Methemoglobinemia alone not beneficial • Oxygen beneficial • HBOT + methemoglobinemia beneficial

  21. SUMMARY: H2S and HBOT • 6 Case reports: 5 +ve, 1 -ve • Case reports have significant delay from exposure to HBOT: does this matter? • 1 Animal model • NO case series • NO controlled trials

  22. Summary • HBOT may have a role in the management of H2S toxicity but it’s efficacy is LARGELY UNKNOWN

More Related