Treatment Protocol Guidelines
The following hyperbaric medicine treatment protocol is based upon the recommendations of the Hyperbaric Oxygen Committee of the Undersea and Hyperbaric Medical Society. Clinical protocols and/or practice guidelines are systematically developed statements that help physicians, other practitioners, case managers and clients make decisions about appropriate health care for specific clinical circumstances.
Protocols allow health providers to offer evidence-based, appropriate, standardized diagnostic treatment and care services to patients undergoing hyperbaric oxygen therapy (HBOT). Evidence-based medicine offers clinicians a way to achieve improved quality, improved patient satisfaction, and reduced costs. This discussion covers Decompression Illness and Arterial Gas Embolism. Utilization Review should be initiated when clinical decisions result in deviation from or modification of treatment protocols. This includes any course of treatment at or above the recognized threshold limits.
Medical Necessity
Medicare.gov defines “medically necessary” as “health-care services or supplies needed to prevent, diagnose, or treat an illness, injury, condition, disease, or its symptoms and that meet accepted standards of medicine.”
The following condition meets coverage indications per the National Coverage Determination (NCD) 20.29.[1] Continued HBOT without documented evidence of effectiveness does not meet the Medicare definition of medically necessary treatment. Thorough re-evaluation should be made at least every 30 days for documentation of response to therapy.
TREATMENT PROTOCOL
| Decompression Illness |
Sample Physician Order: Initial | Sample Physician Order: follow-up | $ ICD-10 Crosswalk | Treatment Tables V & VI | Emergent Indication
|
| Arterial Gas Embolism | Sample Physician Order: Initial | Sample Physician Order: follow-up | $ ICD-10 Crosswalk | Treatment Tables V & VI | Emergent Indication
|
Background
| - Decompression Illness (DCI) arises from the generation of bubbles of inert gas in tissue and/or blood in volumes sufficient to interfere with organ function. This state can be caused by rapid decompression during ascent from diving, flying after diving, or a hyperbaric/hypobaric chamber exposure. Bubble formation occurs when the rate of decompression exceeds the rate at which diffusion and perfusion reduce the tissue inert gas partial pressure. HBOT is the standard of care for definitive treatment of altitude-induced cases that do not respond to ground level O2, and for DCI after diving.
- Gas embolism occurs when gas bubbles (regardless of source) enter arteries or veins. There are numerous causes for arterial gas embolism (AGE) outside of diving, some of which are iatrogenic accidents during invasive procedures. AGE may occur due to a pulmonary bleb rupture during normal scuba ascent, asthma exacerbation with air trapping, concussive blast injury (in or out of the water), inadequate mechanical ventilation, penetrating chest trauma, inadequate chest tube placement, bronchoscopy lung biopsy, and orogenital sex where air is forced into the vagina. AGE usually produces a sudden onset of stroke-like manifestations, such as impaired consciousness, confusion, seizures, and focal neurological deficits.
- Decompression illness (DCI) is associated with a reduction in ambient pressure surrounding the body. DCI encompasses two diseases, decompression sickness (DCS) and arterial gas embolism (AGE). DCS results from bubbles in body tissues causing local damage.[2]
- Because it may not be possible to differentiate clinical DCS from AGE related to a rapid decrease in ambient pressure, the term “decompression illness” DCI is often used to describe DCS or both.
- Small amounts of venous gas embolism (VGE) should not be confused with arterial gas embolism. VGE is often tolerated without signs of DCI due to filtration by pulmonary capillaries.[3] VGE rarely needs to be treated in the hyperbaric chamber.
- The Ideal Gas Law applies in bubble disorders (see topic "Gas Laws And The Therapeutic Effects of HBOT"). There are primarily 2 treatment pressures for DCI/AGE: 2.8 ATA and 6 ATA, with different breathing gases as determined to avoid oxygen toxicity. Boyle's law applies for gas volume: At 2 ATA the volume is 50% the size at 1.0 ATA, and at 3 ATA the volume is 1/3 or 66% smaller than at 1.0 ATA.
- The radius of the bubble is a bit more complicated, as the equation for bubble radius is V = 4/3(pi)r^3 (and we are solving for radius). When the volume of the bubble is 100 units, the radius is 2.8. As we increase pressure to 6 ATA, the volume now becomes 12.5 and the radius is 1.4. So, it takes 6 ATA to make a 50% smaller radius of a bubble. Hence, the difference between a U.S. Navy Treatment Table 6 at 2.8 ATA and a Table 6A at 6 ATA.
- Among divers, decompression sickness appears to be significantly more common than arterial gas embolism. In two recent case series, comprising 3018 cases, only 6.5% were diagnosed as arterial gas embolism.[4]
|
|
Goals of HBOT
|
- Reduce bubble size (diameter and volume) and restore blood flow to end-organ tissues. The key is to make sure that the bubbles stay in a 'round' configuration. This means that the bubble is not impeded in travel. Once the bubble becomes oblong, it has been impeded in flow and the clotting/inflammatory cascade from WBCs is released.
- Increase diffusion gradient for inert gas from the bubble (e.g., replaces inert nitrogen in the bubble with oxygen). Overwhelming the nitrogen gas in a bubble with high concentrations of oxygen in plasma is called a countercurrent diffusion principle.
- Oxygenate ischemic end-organ tissue
- Decrease cerebral edema and inflammation
|
|
Diagnosis
|
- Presumptive diagnosis of DCI is made on the basis of signs and/or symptoms within 24 hours after a dive or altitude exposure.
- Common manifestations include paresthesias, hypesthesia, joint pain, skin rash, and malaise.
- In mild DCI, patients may present with limb pain, constitutional symptoms, subjective sensory symptoms, or rash, with clinical stability for 24 hours or more and a normal neurological exam.
- More severe manifestations include motor weakness, ataxia, dyspnea, urinary and fecal incontinence, shock, lower extremity (girdle) paralysis, and death.
- Cerebral Arterial Gas Embolism (CAGE) my occur in conjunction with DCI although this is rare. It almost always requires a pneumothorax or pulmonary barotrauma.
- A diagnosis of gas embolism is usually made by a history of susceptible events and focal neurologic deficits, frequently with a loss of consciousness or collapse.
- Be aware that the diagnosis of DCI and CAGE are generally diagnoses of EXCLUSION. We try to rule out all other causes before assigning a diagnosis of DCI and/or CAGE.
- Imaging to detect intravascular gas is not necessary to make the diagnosis due to low diagnostic sensitivity. Absence of intravascular gas should not prevent treatment. Diagnostic imaging is indicated if other pathologies with similar manifestations need to be ruled out.
Table 1. Differential Diagnosis of DCS in Divers [4]
Diving Condition and Key Features
| Differential Diagnosis
| | Inner ear DCS: cochlear symptoms are less common (33%) than vestibular symptoms (92%); symptoms begin during ascent or early after surfacing (within 60 min in 85% of cases); vertigo is typically sustained. | Inner ear barotrauma |
| Vestibular migraine |
| Alternobaric vertigo |
| Benign paroxysmal positional vertigo |
| Seasickness | | Sinal DCS: symptoms usually evolve relatively rapidly (within 1-2 hr after surfacing) | Epidural hematoma or abscess |
| Transverse myelitis, Guillain-Barre syndrome, MS | | Cardiopulmonary DCS: onset within 30 min after surfacing; provocative dives (e.g. >25m, rapid ascent, omitted decompression) | Immersion pulmonary edema |
| Near drowning |
| Myocardial infarction | | Musculoskeletal DCS: may be multifocal | Musculoskeletal injury | | Constitutional DCS (fatigue, malaise, headache) | Viral or bacterial infection |
| Carbon dioxide retention |
|
|
Hyperbaric Criteria
|
- All symptomatic patients with a history of decompression due to diving or violation of decompression tables
- Mild DCI can be adequately treated without recompression if HBOT not available or contraindicated, however, recovery may occur at a slower rate
- With mild DCI or DCI at a remote location, some operators will attempt in-water recompression with SCUBA tanks for various air/O2 mixtures. This is NOT recommended or supported.
- Patients with diagnosis consistent with DCI due to sudden altitude decompression that do not respond to 1 ATA O2 may be candidates for recompression.
- Diagnosis of AGE, even if symptoms spontaneously resolve shortly after onset (particularly after administration of first aid oxygen). HBO is recommended even in the absence of symptoms, as secondary deterioration can occur later.
|
|
Evaluation
|
- Patients should be on high-flow 100% oxygen by mask, endotracheal tube (ET)/ nasotracheal tube (NT) tube during evaluation
- Supine positioning, continuous monitoring. (In the past, there were recommendations about Trendelenburg position, on the side, etc. These have been debunked and are no longer used.)
- History:
- Complete dive history: exposure profile with the time, duration, depth and ascent rate of the dive(s)
- In the face of CAGE, a history of exposure to a potential cause of arterial embolism with symptoms.
- Past medical history: risk factors (age, obesity, dehydration, aerobic or anaerobic exercise performed within 4 hours of completing the dive)
- Physical examination:
- Neurological examination (Never delay HBOT for a formal neurology consult). A reasonably accurate neurological examination can be performed by a trained undersea and hyperbaric medicine physician. In a multiplace chamber, this may be performed while in the chamber and compressing.
- Mild DCI: musculoskeletal pain only, skin bends, lymphatic bends. There should be no evidence of neurologic signs.
- Severe DCI: Occurs when there are neurologic signs and symptoms with gross neurologic losses documented.
- Neurological symptoms: numbness; paresthesia, altered sensation (e.g., tingling), muscle weakness, impaired gait, difficulty walking, problems with physical coordination or bowel/bladder control, paralysis, a change in mental status (e.g., confusion or lack of alertness)
- There can be cardiopulmonary DCI called "chokes." This occurs when the lung filtration system for bubbles is overloaded and forces an airlock in the right atrium. Symptoms include dry cough; chest pain behind the sternum, and breathing difficulty.
- Diagnosis of inner ear DCI is complicated and may be overlooked. This primarily occurs in the setting gas switching ( isobaric counter diffusion), usually switching a nitrogen containing gas to a helium containing gas (e.g., Trimix, with a bottom gas of Helium). Symptoms include new onset ringing in the ears, hearing loss, vertigo or dizziness, nausea, vomiting, impaired balance, and gait disturbance.
- STAT chest x-ray: chest radiography prior to HBOT in selected cases may be useful to exclude pneumothorax which will require a tube thoracostomy placement before recompression.
- Electrocardiogram (ECG): Substernal chest pain should include a rule out MI diagnosis and appropriate laboratory tests.
- Lab work to consider. Do not delay treatment while results are pending.
- Arterial Blood Gas (ABG)
- Complete Blood Count (CBC)
- Comprehensive Metabolic Panel (CMP)
- Fibrinogen
- Partial Thromboplastin Time (PTT); Prothrombin Time (PT)
|
|
Treatment
|
- NOTE!!! If you, or your facility, are not DCI experts and capable of supporting critically ill patients in your hyperbaric chamber environment, do NOT start therapy for these patients. They must be evacuated to a facility that can adequately treat and support the patient during recovery.
- If you have a clinical question about a DCI diagnosis, we recommend that you call Divers Alert Network (DAN) immediately. [1-919-684-9111]
- HBOT is the standard of care and should be instituted as soon as possible. Complete resolution of DCI is most likely to result from early hyperbaric treatment.
- Gas bubbles have been thought to persist for several days. HBOT can be administered after delays of hours to days while still achieving some resolution of DCI signs and symptoms. No one knows how long after an episode occurs that HBOT can be used. Some papers show delays of up to a week or more.
- Treatment tables will be decided by the hyperbaric physician based on history of pressure exposure and physical examination findings.
- Airway management
- Monitor blood pressure & ECG
- Hydration:
- 500 cc bolus of a balanced salt solution or normal saline. Avoid IV fluids with glucose at this time.
- Maintain aggressive intravenous fluid therapy to achieve a urinary output of 1-2 cc/kg/hr.
- If the patient is awake/alert and can manage his/her airway, oral hydration is acceptable.
- You must provide a way for the patient to urinate during the long treatment table for DCI. If necessary, you may need to place a Foley catheter and bag system for urine management, especially in a monoplace chamber.
- In patients with AGE caused by pulmonary barotrauma, there may be a coexisting pneumothorax that could develop into a tension pneumothorax during chamber decompression. Therefore, placement of a chest tube in patients with pneumothorax prior to HBOT is recommended.
Initial Treatment:
- Immediate compression to 2.8 ATA (26.7 psi, 60 fsw) breathing 100% oxygen
- A U.S. Navy Treatment Table 5 for mild DCI has been used in the past. This is not recommended procedure now. Treat all patients with a US Navy Table 6 for initial therapy.
- Initiate the U.S. Navy Treatment Table 6 for all DCI
- The hyperbaric physician may repeat parts of the neurological exam at pressure, during air breaks in order to assess response and whether to prolong the treatment table.
- If clinical response is not optimal, consider extensions at 2.8 and/or 1.9 ATA according to the expertise of the resources available.
- Lidocaine may be used as an adjunct treatment for AGE but may not be beneficial for DCI. We recommend consultation with DAN before starting this regimen.[4]
Repetitive HBOT: - Where residual neurological deficits remain after the initial treatment, re-treat after a 4-8 hour interval. Without evidence of full resolution of symptoms, a repeated U.S. Navy Treatment Table 6 is the treatment of choice. (Even with experienced hyperbaric physicians, a call to DAN and agreement on a treatment plan is a wise choice in complicated cases.)
- 2.0 ATA x 120 minutes, with 5-10 minute air breaks or 2.4 ATA x 90 minutes, with 5-10 minute air breaks may be needed for slight residual treatments until there is maximal resolution of symptoms.
- There is no universal agreement as to how many tailing treatments or when to stop, but we generally say to treat the patient one more time after maximal response to HBOT has been achieved or the patient remains symptom free.
- Enoxaparin 30 mg SQ every12h or dalteparin 5000 IU SQ every 24h if the patient is paralyzed. Full neurologic precautions should be undertaken for paralyzed patients and preventing catastrophic clot formation.
- Aspirin or corticosteroids are not recommended
- Lidocaine infusions have shown some benefit for DCI, but it is not routinely used. We recommend consultation with DAN before starting this regimen.
- Avoid hyperthermia during treatment
Post Compression Treatment: - Consider hospital admission after treatment with Table 6
- The patient must remain within 30 minutes in a recompression facility for a period of 6 hours.
- The patient must remain within 60 min travel time of chamber for 24 hrs.
- The patient must be accompanied during that timeframe as symptoms do recur and need to be immediately addressed.
|
|
Follow-Up
|
- Neurology consultation/evaluation immediately post-treatment and with persistent cognitive changes.
- Consider cardiology consult/referral in cases of suspected Patent Foramen Ovale (PFO)
- Return to diving decisions should be made on the basis of clinical assessment, preferably with evaluation by a diving medicine physician.[5]
- Provide written DCI discharge instructions
|
|
Treatment Threshold
|
Until complete resolution of symptoms or lack of improvement on two consecutive treatments establishes the endpoint of treatment, typically no more than one to two treatments but in some cases may reach five to ten. Utilization/peer review should occur after 10 treatments. (DCI - preferably in conjunction with recommendations from Divers Alert Network physicians)
|
|
Coding
|
Refer to the ICD-10 Guideline for the appropriate ICD-10 code for Decompression Illness Refer to the ICD-10 Guideline for the appropriate ICD-10 code for Arterial Gas Embolism
|
|
Comments
|
- If diabetes mellitus, blood glucose should be checked within an hour prior to treatment and immediately post-HBOT
|
Primary Sources: Whelan and Kindwall [6]
, Weaver[7][8][9][10],
Huang [11]
DOCUMENTATION
[NOTE: Every time a patient with decompression illness and/or arterial gas embolism presents, you must perform a thorough diving medical evaluation and physical examination. The next crucial step is to call Divers Alert Network and discuss the case with the diving medical technologist and physician on call before putting this patient into a hyperbaric chamber and treating with a TT6. If you have never treated a DCI patient, and you have never been a graduate of the NOAA diving medical officer training course, please arrange transport of this patient to a hyperbaric facility that can manage diving medical accidents. This is not a case where you can learn on the job.]
History
- Complete dive history: exposure profile with the time, duration, depth and ascent rate of the dive(s)
- In the face of CAGE, a history of exposure to a potential cause of arterial embolism with symptoms.
- Past medical history: risk factors (age, obesity, dehydration, aerobic or anaerobic exercise performed within 4 hours of completing the dive)
For a decompression illness history of present illness (HPI), the following format is acceptable:
"Mr. Jones was SCUBA diving the past three days with friends. He completed 4 dives per day. His diving gas was air every dive. He tells me that his dives averaged 70 feet of seawater pressure for 40 - 50 minutes per dive. Some were deeper and some were more shallow. He had an average of 45 minute surface intervals between dives with 2 dives before lunch and an hour or two break then 2 or 3 dives in the afternoon. Unfortunately, he did not bring his dive computer or printouts of his diving for my review." (NOTE: This behavior is common, as the diver does not want you to see the actual computer log. Divers tend to under-estimate depth and time exposure.)
"He complains of constant pain in his right shoulder that radiates to the right chest wall. Exertion and range of motion in that joint does not exacerbate the pain. It is constant and rated as 7 of 10. His last dive was 3 hours ago. In addition to shoulder pain, he has noted weakness of his bilateral legs and he cannot urinate. The boat captain put him on O2 by mask and terminated the day's diving with a return to the dock. The boat ride to the dock took 90 minutes, and transportation to the hyperbaric facility took an hour or so by ambulance."
Physical examination
- Neurological examination (Never delay HBOT for a formal neurology consult). A reasonably accurate neurological examination can be performed by a trained undersea and hyperbaric medicine physician. In a multiplace chamber, this may be performed while in the chamber and compressing.
- Mild DCI: musculoskeletal pain only, skin bends, lymphatic bends. There should be no evidence of any neurologic signs.
- Severe DCI: Occurs when there are neurologic signs and symptoms with gross neurologic losses documented. (This man cannot walk and cannot urinate.)
"This patient has constant pain in the shoulder and chest wall that crosses multiple dermatomes. It is no worse with range of motion. In addition, he demonstrates a weak squeeze on the right (4+) with the left normal (5+). Index and thumb, 5th finger and thumb allow easy pull through loss of strength.
He demonstrates long-tract dysfunction with rapid alternating movements not synchronized. He is unable to perform a heel-shin test or Romberg due to weakness in both lower extremities.
He has been unable to urinate and fails to feel the urge to urinate.
His bilateral legs show deep tendon reflexes of 1+ bilaterally. He has some sensation loss following the L3, L4, and L5 dermatomes bilaterally. He has no sensation on the tip of his penis and he fails the anal wink test. (Absence of response in the sacral cord segments.)"
(NOTE: You must carefully report the entire neurologic examination. We have included some of the pertinent findings for this particular case.)
Impression
"Mr. Jones has presumed severe decompression illness based on his history of provocative dives with inadequate surface intervals. He is unable to move his lower extremities at this time. He has physical findings consistent with neurological decompression illness. We have elected to call Divers Alert Network in order to confirm our findings and will start this patient on a US Navy Treatment Table 6 within the next hour."
Plan
Decompression Illness and Arterial Gas Embolism
Hyperbaric oxygen treatment is the cornerstone of treatment for AGE/VGE/DCI and should be instituted as soon as possible in the treatment course. Treatment tables will be decided by the hyperbaric physician. Most treatment of DCI will be prescribed in conjunction with consultation from Divers’ Alert Network (DAN).
Risk and Benefit of Hyperbaric Oxygen Therapy
- Please refer to topic "Documentation HBO: Risks and Benefits"
Indication for Hyperbaric Oxygen Therapy (HBOT)
Decompression Illness
Decompression illness (DCI) arises from the generation of bubbles of inert gas in tissue and/or blood in volumes sufficient to interfere with organ function. This state can be caused by rapid decompression during ascent from diving, flying after diving, or a hyperbaric/hypobaric chamber exposure. Bubble formation occurs when the rate of decompression exceeds the rate at which diffusion and perfusion reduce the tissue inert gas partial pressure. There are a variety of clinical expressions of DCI, the most serious of which causes neurologic deficits as evidenced on the physical examination. The diagnosis of DCI is a diagnosis of exclusion and depends greatly upon the history and physical examination of the diver.
A wide variety of hyperbaric regimens have been described in the medical literature. These vary in treatment pressure, time at pressure, partial pressure of oxygen, and use of other mixed gases. There have been no broad scientific studies in a prospective, randomized controlled fashion. However, the following points are generally accepted: 1) Complete resolution occurs when patients are treated early in the disease process, and 2) the US Navy oxygen treatment tables (TT6) with initial recompression to 60 fsw have been the most widely used treatments and have a high degree of success. Recompression and hyperbaric oxygen administration has 3 main effects: 1) bubble compression, 2) oxygenation of compromised tissues, and 3) an anti-inflammatory effect.
Arterial Gas Embolism
Gas embolism occurs when gas bubbles (regardless of source) enter arteries or veins. Arterial gas embolism (AGE) was classically described during submarine escape training, caused by pulmonary barotraumas during free ascent after breathing compressed gas at depth. AGE commonly occurs when a pulmonary bleb ruptures during normal SCUBA ascent, asthma with air trapping, a concussive blast injury (in or out of the water), mechanical ventilation, penetrating chest trauma, chest tube placement, or bronchoscopy. Venous gas embolism (VGE) is more rare and can occur after compressed gas diving. A large amount of venous bubbles overcome the pulmonary arterial capillary network and are passed to the left side of the heart. There are numerous causes for gas embolism outside of diving, some of which are iatrogenic accidents during invasive surgical procedures. Hyperbaric oxygen remains the definitive treatment for gas embolism. Indications for treatment include neurological or cardiac manifestations of gas embolism in any procedure at risk. Effects of gas bubbles can persist for many days, so a trial of hyperbaric oxygen treatments should be started on any patient with symptoms, even days after the event. Recompression and hyperbaric oxygen administration has 3 main effects: 1) bubble compression, 2) oxygenation of compromised tissues, and 3) an anti-inflammatory effect.
[NOTE: For Arterial Gas Embolism, there are some subtle differences. Usually, an AGE is a result of an accident in the operating room with gas being introduced into the bloodstream (at one atmosphere pressure). The signs and symptoms of AGE are frequently identical to DCI but with a much more rapid onset.]
Sample Order
- See Sample Physician Order Decompression Illness - Initial Visit
- See Sample Physician Order Decompression Illness - Follow Up
- See Sample Physician Order Arterial Gas Embolism - Initial Visit
- See Sample Physician Order Arterial Gas Embolism - Follow Up
CLINICAL EVIDENCE AND RECOMMENDATIONS
Hyperbaric Oxygen Therapy for Decompression Illness
- 1CFor patients with a history of decompression and signs/symptoms of decompression illness, we recommend HBOT as first-line treatment to improve DCI-related clinical manifestations (Grade 1C).
- Rationale: HBOT is thought to reduce bubble volume, increase the diffusion gradient for inert gas from the bubble into the surrounding tissue, improve oxygen delivery to ischemic tissues, and reduce edema of the central nervous system.[9] The recommendation of HBOT as primary treatment for DCI is based on expert consensus opinion, animal and retrospective clinical studies (evidence level C).[9][12][13] Much like the randomized controlled trials (RCTs) for parachute use, HBOT has the same distinction for use as primary treatment modality for DCI. In other words, there are no RCTs, nor could there be, since HBOT is the de facto treatment for this diagnosis, hence any trial is unethical. There have been multiple clinical trials about using a variety of adjunctive drugs in addition to HBOT with outcomes studies. These are beyond the scope of this review.
- Note: for mild DCI (i.e. pain only) following diving with no neurological manifestations, treatment with administration of normobaric oxygen may be sufficient. However, for more serious cases of DCI after diving, or for altitude-induced cases refractory to normobaric oxygen, HBOT remains the standard of care. [9][14] Time from decompression to HBOT treatment greater than 24 or 48h has been shown to be as effective as earlier treatment.[14][15]
Hyperbaric Oxygen Therapy for Arterial Gas Embolism
- 1C For all patients with AGE or symptomatic venous gas embolism, we recommend HBOT as first-line treatment to improve AGE-related clinical manifestations (Grade 1C).
- Rationale: HBOT is thought to reduce bubble volume, increase tissue oxygenation and reduce edema of the central nervous system.[10][16][17] Evidence supporting HBOT as first-line treatment for AGE is mainly derived from retrospective studies and expert opinion (evidence level C).[18][19][20] No RCTs comparing HBOT with no HBOT for treatment of AGE have been conducted. Since HBOT is the de facto treatment for this diagnosis, any trial would be considered unethical.
- Note: shorter interval between embolism and HBOT is associated with a higher probability of better outcomes.[18] HBOT is also recommended for patients who appear to have spontaneously recovered from AGE-related manifestations, as those tend to deteriorate after apparent recovery.[21]
- It is possible that the gas bubbles may persist for several days. That might explain why even delayed treatment with HBOT is successful in some cases. The best treatment remains to opt for HBOT as soon as possible after the event.
APPENDIX
Summary of Evidence
Hyperbaric Oxygen Therapy for Arterial Gas Embolism
(back to text)
Retrospective studies
- In a retrospective review of 656 published AGE cases in 1991, Dutka et al. found that 78% of patients who received HBOT (n=515) fully recovered, compared to only 56% of patients who did not receive HBOT (n=141) [19]
- In a 2003 case series (n=19), Berson reported that after 5 treatments, 26% of patients fully recovered, 58% improved, and only 5% had no change (11% were not assessable due to medically-induced paralysis) [20]
- In a 2016 case series (n=45), Beevor found that good neurological outcome (Glasgow 7 or 8) was achieved in 60% of the patients [18]
Hyperbaric Oxygen Therapy for DCI
(back to text)
Retrospective studies
- A 2020 retrospective study of patients treated for decompression illness (DCI) at the Geneva hyperbaric chamber between 2010 and 2016 found 64 with neurological and 28 with mild DCI. The majority of mild cases had musculoskeletal symptoms, while neurological cases primarily had spinal or vestibular symptoms. Despite no single factor predicting a negative outcome, severe DCI was associated with a high rate of persisting deficits. A Boussuges score > 7 indicated an unfavorable outcome in spinal DCI with 90% sensitivity.[22]
- A 2022 retrospective study included 546 DCI patients treated in Finland in the years 1999-2018 and investigated factors associated with recompression delay and outcome. Treatment outcome was defined as fully recovered or presence of residual symptoms on completion of HBOT. The symptoms, use of first aid oxygen, number of recompression treatments needed and characteristics of the study cohort were also addressed. Authors found that delayed HBOT (> 48 h) remained effective with final outcomes similar to those treated within 48 h. Cardio-pulmonary symptoms were associated with a shorter treatment delay (median 15 h vs 28 h without cardiopulmonary symptoms, P < 0.001), whereas mild sensory symptoms were associated with a longer delay (48 vs 24 h, P < 0.001). A shorter delay was also associated with only one required HBOT treatment (median 24 h vs 34 h for those requiring multiple recompressions) ( P = 0.002). Tinnitus and hearing impairment were associated with a higher proportion of incomplete recoveries (78 and 73% respectively, P < 0.001), whereas a smaller proportion of cases with tingling/itching (15%, P = 0.03), nausea (27%, P = 0.03), motor weakness (33%, P = 0.05) and visual disturbances (36%, P = 0.04) exhibited residual symptoms. Patients with severe symptoms had a significantly shorter delay than those with mild symptoms (median 24 h vs 36 h respectively, P < 0.001), and a lower incidence of complete recovery. Authors concluded that delayed HBOT remains an effective and useful intervention. A shorter delay to recompression is associated with fewer recompressions required to achieve recovery or recovery plateau. [23]
CATEGORY A CONTINUING EDUCATION CREDIT
This topic has been reviewed and approved by the National Board of Diving and Hyperbaric Medical Technology (NBDHMT) for one (1) Category A Credit.
To claim the credit:
- 1. Read the topic
- 2. Answer the examination and course critique questions.
- Take the quiz via SurveyMonkey
- 3. Receive the certificate by e-mail. A passing score of 70% is required (please allow up to 8 business days for processing)
For more information on Category A continuing education credits see blog post " Hyperbaric Certification and Continuing Education for Technicians & Nurses".
REVISION UPDATES
| Dates | Description |
| 10/23/24 | Expanded/updated Section 'Treatment Protocol' |
1/8/20
| Added section 'Category A Continuing Education Credit'
|
| 11/17/19 | Added sections 'Clinical Evidence and Recommendations' and 'Appendix' |
