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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
Permanent Neurologic Sequelae
Prolonged coma Recurrent seizures Chronic vegatative states Tremors Cognitive impairment
Why might HBOT be effective?
Increased oxygen delivery to tissues Increased oxyhemoglobin which increases
the auto-oxidation of sulfide
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”
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
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
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
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
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
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
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
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
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
The RATS have the last word! Bitterman. Tox Appl Pharm 1986
0102030405060708090
100
N +3ATA
3ATA Control N after 1ATA 3 ATA N +3ATA
pretreatement rescue treatments
The RATS have the last word! Bitterman. Tox Appl Pharm 1986
Conclusions from the rats Methemoglobinemia alone not beneficial Oxygen beneficial HBOT + methemoglobinemia beneficial
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