Toxicology – Hyperbaric Oxygen Therapy (HBOT)

Core Concept

Hyperbaric oxygen therapy (HBOT) delivers nearly 100% oxygen while the patient is exposed to pressure greater than normal atmospheric pressure inside a hyperbaric chamber.

In toxicology, its principal established role is in selected patients with carbon monoxide (CO) poisoning.

Older literature proposed HBOT for several other poisonings, but many of these indications have weak or uncertain evidence and are not routine modern practice.

Basic Principle

At normal atmospheric pressure, most oxygen is transported bound to hemoglobin, with only a small amount physically dissolved in plasma.

Increasing ambient pressure while breathing nearly 100% oxygen markedly increases the amount of dissolved plasma oxygen.

This can temporarily improve oxygen delivery even when normal hemoglobin-mediated oxygen transport is impaired.

Hyperbaric vs Normobaric Oxygen

Normobaric oxygen

High-concentration oxygen administered at approximately normal atmospheric pressure.

This is the immediate treatment for suspected significant CO poisoning.

Hyperbaric oxygen

High-concentration oxygen delivered at elevated ambient pressure.

HBOT provides:

• Much higher dissolved plasma oxygen
• More rapid CO elimination
• Very high tissue oxygen tensions

However, the need for HBOT depends on the clinical situation rather than simply the presence of CO exposure.

Hyperbaric Chambers

Two broad designs are used.

Monoplace chamber

• Usually accommodates one patient
• Entire chamber may be pressurized with oxygen
• Direct physical access to the patient during treatment is limited

Multiplace chamber

• Accommodates multiple people
• Chamber is usually pressurized with air
• Patients receive oxygen through masks, hoods, or airway systems
• Trained clinical personnel may remain inside with critically ill patients

The available chamber type can influence whether an unstable patient can safely undergo treatment.

Carbon Monoxide Poisoning

CO causes toxicity through several mechanisms.

It binds hemoglobin with high affinity:

CO + hemoglobin → carboxyhemoglobin (COHb)

This:

• Reduces oxygen-carrying capacity
• Interferes with oxygen unloading to tissues

But CO toxicity is more complex than COHb formation alone.

Cellular Effects of Carbon Monoxide

CO also interacts with intracellular proteins such as:

• Myoglobin
• Mitochondrial cytochromes

Consequences may include:

• Cellular hypoxia
• Oxidative stress
• Mitochondrial dysfunction
• Inflammatory injury
• Lipid peroxidation
• Neurologic and myocardial injury

This helps explain why the COHb concentration does not perfectly predict clinical severity.

How Oxygen Accelerates CO Elimination

CO dissociates from hemoglobin over time.

Increasing inspired oxygen accelerates this process.

Therefore:

Room air → slower CO elimination

100% normobaric oxygen → faster elimination

Hyperbaric oxygen → even faster elimination

HBOT also substantially increases dissolved oxygen available to tissues.

Possible Additional Effects of HBOT

Beyond accelerating CO elimination, HBOT may influence secondary injury pathways associated with CO poisoning.

Proposed effects include reduction of:

• Leukocyte-mediated injury
• Oxidative stress
• Lipid peroxidation
• Post-hypoxic inflammatory processes

These mechanisms have been proposed as explanations for potential neurologic benefit.

Immediate Management of Suspected CO Poisoning

Do not delay oxygen while deciding whether HBOT is appropriate.

Initial management includes:

• Removal from the exposure
• High-concentration oxygen
• Airway and ventilatory support when necessary
• ECG
• Neurologic assessment
• Evaluation for myocardial injury when appropriate
• COHb measurement by co-oximetry
• Assessment for associated smoke-inhalation injuries

HBOT consultation can occur simultaneously.

Pulse Oximetry Limitation

Standard pulse oximetry can appear normal or reassuring in significant CO poisoning.

Conventional pulse oximeters cannot reliably distinguish:

• Oxyhemoglobin
• Carboxyhemoglobin

Therefore:

A normal SpO₂ does not exclude CO poisoning.

Co-oximetry is required to measure COHb accurately.

COHb Concentration

COHb helps confirm exposure but should not be interpreted as a direct toxicity score.

The measured concentration can be affected by:

• Time since exposure
• Duration of oxygen therapy before sampling
• Exposure intensity
• Smoking status
• Ventilation

A patient can therefore have serious neurologic or cardiac toxicity despite a relatively modest COHb concentration measured later.

When HBOT Is Considered for CO Poisoning

There is no universally accepted single threshold that determines treatment.

Urgent hyperbaric consultation is particularly reasonable when significant CO poisoning is accompanied by features such as:

• Loss of consciousness
• Persistent or substantial neurologic abnormalities
• Severe altered mental status
• Seizures
• Significant myocardial ischemia or cardiac injury
• Hemodynamic instability
• Severe metabolic acidosis
• Substantial COHb elevation in the appropriate clinical context
• Pregnancy with clinically significant poisoning

The entire clinical picture matters.

Do Not Use COHb Alone

Older recommendations often relied heavily on fixed COHb thresholds.

Modern assessment places greater emphasis on:

• Neurologic condition
• Cardiac involvement
• Loss of consciousness
• Metabolic abnormalities
• Exposure history
• Pregnancy
• Overall severity

Thus:

Treat the patient, not simply the COHb number.

Neurologic Toxicity

Acute CO poisoning can cause:

• Headache
• Dizziness
• Confusion
• Ataxia
• Syncope
• Seizures
• Coma
• Focal neurologic abnormalities

Neurologic findings are important when considering HBOT.

Delayed Neurologic Sequelae

Some patients develop neurologic or neuropsychiatric problems after apparent initial recovery.

Possible manifestations include:

• Cognitive impairment
• Memory difficulty
• Personality or behavioral changes
• Gait abnormalities
• Movement disorders
• Mood symptoms

These can appear after a symptom-free interval.

Whether HBOT reliably prevents delayed neurologic injury remains an area of uncertainty; clinical trials have produced differing results.

Cardiac Toxicity

The myocardium is highly sensitive to CO-related hypoxia.

Possible manifestations include:

• Chest pain
• Ischemic ECG abnormalities
• Elevated cardiac biomarkers
• Dysrhythmias
• Reduced ventricular function
• Cardiogenic shock

Significant myocardial involvement increases concern for severe poisoning and supports early discussion with a hyperbaric specialist.

Pregnancy

Pregnancy deserves special consideration because:

• CO crosses the placenta.
• Fetal hemoglobin binds CO strongly.
• Fetal CO elimination is slower than maternal elimination.
• Maternal COHb does not reliably reflect fetal exposure.

Therefore, clinicians may use a lower threshold for hyperbaric consultation in significant maternal CO poisoning.

Pregnancy itself is not a contraindication to HBOT when clinically indicated.

Smoke Inhalation

A patient exposed to an enclosed-space fire may have several simultaneous problems:

• Carbon monoxide poisoning
• Cyanide toxicity
• Thermal airway injury
• Pulmonary irritant injury
• Burns
• Trauma

HBOT addresses the CO component but does not replace treatment of these other conditions.

Cyanide Poisoning

Older literature proposed HBOT as an adjunct for severe cyanide poisoning.

It is not a primary modern cyanide antidote.

Management instead centers on:

• Airway and ventilation
• High-concentration oxygen
• Hydroxocobalamin
• Supportive cardiovascular care
• Additional antidotal therapy in selected circumstances

HBOT should not delay established cyanide antidotal treatment.

Hydrogen Sulfide Poisoning

HBOT has also been reported in severe hydrogen sulfide poisoning.

However, evidence is limited.

Modern management primarily involves:

• Safe removal from exposure
• High-concentration oxygen
• Ventilatory support
• Cardiovascular support
• Treatment of seizures and other complications

HBOT may occasionally be discussed for exceptionally severe cases, but it is not established routine therapy.

Methemoglobinemia

Methemoglobinemia impairs hemoglobin’s ability to transport and release oxygen effectively.

Standard treatment of clinically significant acquired methemoglobinemia generally involves:

• Removal of the oxidizing agent
• Oxygen
• Methylene blue when appropriate

HBOT is not routine.

It may be considered as an exceptional rescue strategy when severe tissue hypoxia persists and standard treatment is ineffective or unsuitable.

Carbon Tetrachloride and Chloroform

Older reports proposed HBOT for chlorinated hydrocarbon poisoning to reduce hepatic injury.

This is not an established routine modern indication.

Management of these exposures is predominantly supportive and directed toward organ complications.

Severe Anemia

HBOT can dramatically increase dissolved plasma oxygen.

For this reason, it has occasionally been used as a temporary supportive measure in exceptional cases of profound anemia when adequate oxygen-carrying capacity cannot promptly be restored.

This is a specialized nonroutine indication.

Other Established Non-Toxicologic Uses

HBOT also has applications outside poisoning, including selected cases of:

• Decompression sickness
• Arterial gas embolism
• Gas gangrene
• Certain necrotizing infections
• Radiation tissue injury
• Compromised grafts or flaps
• Selected difficult wounds
• Refractory osteomyelitis

Indications depend on current hyperbaric-medicine criteria.

Absolute Contraindication

The major classic absolute contraindication is:

Untreated pneumothorax

During pressure changes, trapped pleural gas can expand and produce life-threatening tension physiology.

A pneumothorax requiring treatment must therefore be appropriately managed before HBOT.

Recent Chest Surgery

Contrary to the older source, recent thoracic surgery is not automatically an absolute contraindication.

Risk depends on factors such as:

• Residual pneumothorax
• Trapped gas
• Surgical anatomy
• Pulmonary condition

The hyperbaric physician should assess these factors individually.

Ear and Sinus Barotrauma

Pressure changes can cause:

• Ear pain
• Middle-ear barotrauma
• Tympanic membrane injury
• Sinus pain
• Sinus barotrauma

Patients must be able to equalize pressure or receive appropriate preventive management.

Middle-ear barotrauma is among the more common HBOT complications.

Pulmonary Barotrauma

Pressure changes can also affect the lungs.

Patients with certain pulmonary disorders, trapped intrathoracic gas, or significant air-space disease require careful assessment.

Pulmonary barotrauma is uncommon but potentially serious.

Oxygen Toxicity

Very high oxygen partial pressures can cause CNS oxygen toxicity.

The most dramatic manifestation is:

• Generalized seizure

An oxygen-toxicity seizure does not necessarily imply permanent neurologic injury, but it requires immediate management of oxygen exposure and patient safety.

Seizure Risk

A history of epilepsy is generally a relative consideration rather than an absolute contraindication.

Other factors that may lower the seizure threshold include:

• Fever
• Certain medications
• Metabolic abnormalities
• Alcohol withdrawal
• Underlying toxicologic illness

Risks must be balanced against the potential benefit of HBOT.

Claustrophobia

Monoplace chambers can provoke:

• Anxiety
• Panic
• Claustrophobia

Preparation and reassurance may help.

Any sedating medication must be used carefully because it can complicate neurologic and respiratory monitoring.

Temporary Visual Changes

Repeated HBOT exposures can produce temporary refractive changes, particularly myopia.

Longer treatment courses can also contribute to ocular effects such as cataract progression.

These issues are more relevant to repeated treatments than to a single emergency session.

Critically Ill Patients

Transporting an unstable poisoned patient to a hyperbaric facility can itself create risk.

The decision must consider:

• Hemodynamic stability
• Airway requirements
• Ventilator compatibility
• Monitoring capability
• Distance and transport time
• Chamber staffing
• Ability to manage deterioration inside the chamber

HBOT should not compromise essential resuscitation.

Monoplace vs Multiplace in Critical Illness

A multiplace chamber may offer an important advantage because trained personnel can remain physically present with the patient.

Monoplace treatment may limit immediate physical access.

Therefore, chamber capabilities matter when treating:

• Intubated patients
• Hemodynamically unstable patients
• Patients requiring continuous interventions

Timing

When HBOT is chosen for acute CO poisoning, early treatment is generally preferred.

However, the decision should not delay:

• High-concentration normobaric oxygen
• Airway stabilization
• Cardiovascular resuscitation
• Treatment of concurrent poisoning or trauma

Monitoring

Depending on illness severity and chamber capabilities, monitoring may include:

• Continuous ECG
• Blood pressure
• Oxygenation
• Ventilation
• Neurologic status
• Airway and ventilator function
• Signs of barotrauma
• Seizure activity

Equipment used inside hyperbaric chambers must meet appropriate safety requirements.

Important Modernization of the Older Source

• HBOT means high-concentration oxygen delivered at greater-than-atmospheric pressure.
• Its principal toxicologic role is selected carbon monoxide poisoning.
• All suspected significant CO poisoning should receive high-concentration oxygen promptly while HBOT is being considered.
• COHb concentration alone does not accurately determine poisoning severity or the need for HBOT.
• Serious neurologic or cardiac manifestations are particularly important in treatment decisions.
• Pregnancy warrants special consideration because fetal CO kinetics differ from maternal kinetics.
• Evidence that HBOT prevents delayed neurologic sequelae is not completely consistent, so treatment decisions remain individualized.
• HBOT is not a substitute for hydroxocobalamin in cyanide poisoning.
• Evidence supporting HBOT for hydrogen sulfide poisoning is limited.
• HBOT is only an exceptional rescue option for severe refractory methemoglobinemia.
• Routine HBOT for carbon tetrachloride or chloroform poisoning is not supported by modern practice.
• Untreated pneumothorax is the major absolute contraindication.
• Recent thoracic surgery is not automatically an absolute contraindication.
• Middle-ear barotrauma is an important common complication.
• CNS oxygen toxicity can cause seizures.
• Transport and chamber limitations must be weighed against potential benefit in unstable patients.
• Historical rigid pressure/time protocols should not be generalized; treatment profiles are determined by experienced hyperbaric teams.

Key Points

• HBOT increases dissolved plasma oxygen by combining high-concentration oxygen with elevated ambient pressure.
• Its main toxicologic application is selected severe carbon monoxide poisoning.
• It accelerates CO elimination and markedly increases tissue oxygen availability.
• CO toxicity involves more than carboxyhemoglobin alone, including mitochondrial, inflammatory, neurologic, and myocardial injury.
• COHb concentration does not correlate reliably enough with severity to determine treatment by itself.
• A normal standard pulse oximeter reading does not exclude CO poisoning.
• Loss of consciousness, major neurologic abnormalities, myocardial injury, severe acidosis, hemodynamic instability, and pregnancy are important factors when considering hyperbaric consultation.
• High-concentration normobaric oxygen should begin immediately and should not be delayed while arranging HBOT.
• HBOT is not routine definitive therapy for cyanide, hydrogen sulfide, chlorinated hydrocarbon poisoning, or methemoglobinemia.
• Untreated pneumothorax is the major absolute contraindication.
• Important adverse effects include ear/sinus barotrauma, oxygen-toxicity seizures, anxiety/claustrophobia, and less commonly pulmonary barotrauma.
• The decision to use HBOT should incorporate poisoning severity, timing, transport risk, chamber capability, and specialist assessment.