Category: Toxicology
Keywords: Carbon Monoxide, Hyperbaric (PubMed Search)
Posted: 9/26/2025 by TJ Gregory, MD
(Updated: 9/29/2025)
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Carbon Monoxide Poisoning (COP) is a major toxicologic pathology and a common case in the Emergency Department and pre-hospital setting. History is a key component in assessment with the standard diagnostic test being blood gas analysis of Carboxyhemoglobin (COHb).
Standard pulse oximeter devices are not capable of differentiating oxyhemoglobin from carboxyhemoglobin, leading to the classic pearl that pulse ox may be falsely reassuring in COP.
In recent years, devices capable of differentiating oxyhemoglobin from COHb have been developed and are fielded in many hospitals and EMS agencies.
This meta-analysis reviews diagnostic accuracy of pulse CO-oximetry (spCO) devices in comparison to a reference standard COHb blood test. Six studies (1734 patients) were included.
This analysis found that spCO testing has a low sensitivity and high specificity.
Pooled sensitivity 0.65 (95% CI 0.44–0.81)
Pooled specificity 0.93 (95% CI 0.83–0.98)
Pooled LR+ 9.4 (95% CI 4.4 to 20.1)
Pooled LR- 0.38 (95% CI 0.24 to 0.62)
The authors conclude that the low sensitivity precludes use of spCO as an effective screening tool for COP or substitute for COHb. Conversely, we can recognize the utility of the high specificity in identifying patients who do have clinically significant toxicity. Indeed, the authors discuss potential applications for triage and transport to a hyperbaric oxygen chamber for those who are found to have elevated readings.
Technology advancement and refinement will be interesting to follow. In the meantime, don’t skip the COHb lab just because spCO measurement is reassuring.
Category: Critical Care
Keywords: hyperbaric, dive medicine, evaluation, (PubMed Search)
Posted: 8/31/2025 by TJ Gregory, MD
(Updated: 12/4/2025)
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You've encountered it at ABEM General Hospital, but now a SCUBA diver actually comes into your ED and you're concerned for DCS. What next?
Evaluation:
Symptom nature and timing are key in detailed history. Transient neurocognitive symptoms at depth suggest nitrogen narcosis or oxygen toxicity. Neurological symptoms within 10 minutes of surfacing suggest AGE. Widely variable symptoms within 24 hours of surfacing suggest DCS. Symptom onset greater than 24 hours suggests alternative diagnosis (still discuss with Hyperbaric Medicine or DAN).
Thorough physical exam. DCS may manifest only as localized pain. Look for marine envenomation or trauma to the area.
Neurological exam including detailed sensation and ataxia/balance - get the patient on their feet!
Unbiased differential. E.g. DCS may cause chest pain or SOB, but divers still have heart attacks. SCUBA setting may raise alert for AGE, but divers still have strokes. People go to the tropics to dive, but they also eat local fish (Scombroid and Ciguatera for a future pearl).
Management:
Early consult to Hyperbaric Medicine. In settings with no such team available, a good resource is the Divers Alert Network (DAN) Emergency Hotline at 1-919-684-9111
100% O2 via NRB or highest available delivery. You're not titrating to spO2, you're creating a diffusion gradient for tissue inert gas washout.
IV access and isotonic Fluids. PO if tolerable and unable to obtain IV access.
NSAIDs unless otherwise contraindicated. No special regimen. Standard dosing Ibuprofen or Naproxen are fine. Toradol is ok if limitations to PO.
Horizontal positioning in bed for AGE. Trendelenburg is not recommended.
Manage end organ effects as applicable. E.g. Spinal DCS may yield bladder retention requiring foley
Give consideration to activity specific considerations: hypothermia, restrictive clothing, etc
IV lidocaine has mixed evidence for neuroprotection in AGE. Discuss with Hyperbaricist before starting.
Pre-hospital considerations:
Transport should occur via ground or pressurized air transit capable of 1.0 ATA (sea level) cabin pressure. If non-pressurized aircraft transport is absolutely necessary, maintain continuous oxygen supplementation and altitude less than 2000 feet. This also applies to the inter-hospital setting.
O2 delivery by best means available to include SCUBA regulator mouthpiece or even a rebreather apparatus if present.
PO fluids if tolerable and no IV available.
https://pubmed.ncbi.nlm.nih.gov/8378877/
[Clinical aspects, pathophysiology and therapy of decompression sickness]Abstract The primary treatment of decompression illnesses (arterial gas embolism and all types of decompression sickness) is recompression therapy, combined with hyperbaric oxygen breathing. It is essential to initiate treatment as soon as the symptoms arise. However, prior to hyperbaric oxygen therapy--particularly with any delay in starting recompression--specific supportive therapy for ...pubmed.ncbi.nlm.nih.gov
Decompression Sickness - Injuries; Poisoning - MSD Manual Professional Edition
Decompression Sickness - MSD ManualsSymptoms and Signs of Decompression Sickness Severe symptoms may manifest within minutes of surfacing, but in most patients, symptoms begin gradually, sometimes with a prodrome of malaise, fatigue, anorexia, and headache. Symptoms occur within 1 hour of surfacing in approximately 50% of patients and by 6 hours in 90%. Rarely, symptoms can manifest 24 to 48 hours after surfacing, particularly ...www.msdmanuals.com