Under Pressure: A Case Report of a Diver's Close Encounter With the Bends

Abstract

Generalized barotrauma, also referred to as decompression sickness (DCS), is a condition that occurs when there is a sudden shift in atmospheric pressure. While typically associated with underwater excursions or deep-sea dive encounters, this process can also occur during sudden changes in high altitude or unpressurized air travel. Sudden shifts in atmospheric pressure trigger the formation of nitrogen gas bubbles in the bloodstream that fail to clear from the blood and instead accumulate, leading to an obstruction in circulation. Symptoms of DCS may range from joint and musculoskeletal pain to headaches and even stroke-like symptoms, including visual impairment and altered sensorium. The optimal treatment approach for DCS involves hyperbaric oxygen therapy (HBOT) to allow for the dissolution of nitrogen. However, despite the benefits of HBOT, it is not always readily accessible due to the limited availability of hyperbaric chambers. We present the case of a 50-year-old man diagnosed with acute DCS successfully treated using only high-flow oxygen supplementation.

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Received 08/25/2024
Review began 09/08/2024
Review ended 09/29/2024
Published 10/06/2024
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DOI: 10.7759/cureus.70939
Under Pressure: A Case Report of a Diver's Close
Encounter With the Bends
Shelby Remmel , Neha Chintapally , Juan Enciso
1. Internal Medicine, University of South Florida Morsani College of Medicine, Tampa, USA 2. Internal Medicine,
University of South Florida (USF) Health, Tampa, USA 3. Cardiology, Medical University of South Carolina, Charleston,
USA
Corresponding author: Juan Enciso, jenciso@usf.edu
Abstract
Generalized barotrauma, also referred to as decompression sickness (DCS), is a condition that occurs when
there is a sudden shift in atmospheric pressure. While typically associated with underwater excursions or
deep-sea dive encounters, this process can also occur during sudden changes in high altitude or
unpressurized air travel. Sudden shifts in atmospheric pressure trigger the formation of nitrogen gas bubbles
in the bloodstream that fail to clear from the blood and instead accumulate, leading to an obstruction in
circulation. Symptoms of DCS may range from joint and musculoskeletal pain to headaches and even stroke-
like symptoms, including visual impairment and altered sensorium. The optimal treatment approach for DCS
involves hyperbaric oxygen therapy (HBOT) to allow for the dissolution of nitrogen. However, despite the
benefits of HBOT, it is not always readily accessible due to the limited availability of hyperbaric chambers.
We present the case of a 50-year-old man diagnosed with acute DCS successfully treated using only high-
flow oxygen supplementation.
Categories: Internal Medicine, Medical Physics, Pulmonology
Keywords: barotrauma, decompression sickness, generalized barotrauma, hyperbaric oxygen, hyperbaric oxygen
thetapy, the bends, underwater diving
Introduction
Decompression sickness (DCS), colloquially referred to as "the bends," is a rare but potentially life-
threatening condition that affects countless divers. With an estimated incidence of 0.4 to one case per
10,000 dives, it remains a clinically relevant outcome and concern for diving medicine. DCS occurs when the
atmospheric pressure drops below the cumulative partial pressures of oxygen, carbon dioxide, nitrogen,
helium, and water vapor in the vascular system [1]. When this happens, gas bubbles can form in the
circulation during decompression, leading to mechanical disruption of tissues. The resultant vascular
obstruction and ischemia can cause edema and pain, which can mimic symptoms of cerebrovascular
accidents [1]. We present the case of a 50-year-old man who exhibited symptoms of underwater barotrauma
and was later diagnosed with DCS.
Case Presentation
A 50-year-old military veteran with over 20 years of combined recreational and military service experience
and no prior history of DCS arrived at the Emergency Department (ED) with severe pain and noticeable
swelling in his right shoulder. He had been engaged in a spearfishing dive, reaching a depth of 70 feet
(approximately 21.3 meters). While underwater and handling his spearfishing gun, he experienced a sharp,
intense pain in his right shoulder. Despite ascending appropriately, he noticed increasing swelling and
worsening pain in the shoulder, which extended to the right anterior chest. The patient had severe
limitations in his range of motion without any associated focal numbness or paresthesia. Before this dive
and the subsequent retropulsion trauma from the kickback of his weapon, the patient reported a recent
history of a mechanical ground-level fall to the right shoulder. Mild musculoskeletal tenderness was
reported, but the patient denied any limitations to his strength, range of motion, or activities of daily living.
Following a thorough assessment in the ED, the patient exhibited stable vital signs, and laboratory tests
showed acute kidney injury (AKI) related to a previously treated case of nephrolithiasis. An X-ray of the
shoulder revealed minor degenerative changes in the acromioclavicular joint. A CT scan simultaneously
revealed the presence of gas within the proximal humeral diaphysis (Figure 1) and extensive edema medial
to the base of the coracoid process and nearby soft tissues (Figure 2).
1 1 2, 3
Open Access Case Report Published via University of South Florida
How to cite this article
Remmel S, Chintapally N, Enciso J (October 06, 2024) Under Pressure: A Case Report of a Diver's Close Encounter With the Bends. Cureus
16(10): e70939. DOI 10.7759/cureus.70939

FIGURE 1: Multiple small hypodense foci in the medullary cavity of the
proximal humeral diaphysis.
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FIGURE 2: Punctate foci of air in the soft tissues just medial to the base
of the coracoid process and punctate focus of air further proximally
near the lateral base of the neck.
Based on the patient's clinical presentation and imaging results, our initial diagnostic considerations
included a potentially worrisome indication of DCS, necrotizing fasciitis in the context of underwater
barotrauma, or other subcutaneous gas-forming organisms or conditions pertinent to the underwater nature
of the injury. To refine our diagnostic approach, we considered our patient's presentation and recent diving
history with a meticulous clinical and physical examination to scrutinize potential cutaneous/subcutaneous
trauma in conjunction with his clinical presentation and imaging findings. Upon admission, the patient was
started on maximum allotted oxygen supplementation via nasal cannula at a rate of 6 L; additionally, due to
concerns regarding necrotizing fasciitis, empirical antibiotic therapy was initiated, consisting of
vancomycin, piperacillin-tazobactam, and clindamycin (for its antitoxin effects against beta-hemolytic
strep). In the absence of an operational hyperbaric oxygen delivery facility in close proximity, the decision
was made to manage the patient medically using high-flow oxygen therapy, administering 15 L of 100% O2
via a non-rebreather mask as an alternative treatment. While not standard for DCS, this approach has
effectively treated mild cases in prior studies and reports [2].
Further testing and imaging, including CT imaging, revealed that the patient had developed blood clots in
the right axillary and brachial veins. Although this occurrence is uncommon in cases of DCS, it is scarcely
documented in the literature. Some case reports have mentioned instances of portal and mesenteric vein
thromboses being discovered after diving [2,3]. Based on these findings, the patient started anticoagulation
therapy with therapeutic heparin. Upon reassessment of the patient's clinical presentation, which did not
meet the qualifying criteria for systemic inflammatory response syndrome (SIRS) due to the absence of
leukocytosis and fever, alongside a comprehensive imaging review in collaboration with our surgical
colleagues, it was concluded that the patient was presented with an acute manifestation of DCS, as
evidenced by cutaneous and musculoskeletal symptoms.
Consequently, empiric antibiotic coverage was discontinued. The patient remained on high-flow oxygen
therapy with subsequent taper decrement based on continuous clinical and functional assessments,
improvement in pain tolerance and symptomatic control, and return of baseline functional status.
Remarkably, this treatment strategy effectively mitigated the nitrogenous gas burden within the patient's
vascular system without the sequelae commonly associated with DCS, such as neurological impairment,
peripheral neuropathy, or cerebrovascular events. The patient was discharged four days after admission,
showing a restored range of motion and no signs of neurovascular compromise in the right upper extremity.
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Discussion
DCS arises from the departure of depressurized gas, typically nitrogen, from tissues, forming obstructive
bubbles and impeding circulation. This condition is commonly triggered by rapid tissue decompression
during swift ascent from deep-sea diving, unpressurized aircraft flight, and extravehicular activities in space
[2]. Experts have classified the manifestations of this disorder into three types: type I DCS presents with
skin, musculoskeletal, or lymphatic involvement; type II DCS manifests with symptoms of brain or spinal
injury; and type III DCS presents with potentially fatal pulmonary complications [2].
Various factors, including dehydration, patent foramen ovale, prior injury, cold ambient temperature, high
body fat composition, and recent alcohol consumption, can influence the risk of DCS in individuals. DCS can
be subdivided into different variants based on their clinical presentation and systemic effects. Type I DCS
presents symptoms related to the skin, lymphatic system, or musculoskeletal system and represents the most
prevalent form of this condition. On the other hand, type II DCS affects the nervous system and is linked to
the presence of venous bubbles with right-to-left shunting [4,5].
Approximately 75% of individuals with DCS exhibit symptoms within one hour following the triggering
event. Healthcare providers must conduct a prompt, targeted assessment and initiate immediate measures
for stabilization. Even in cases where oxygen saturation levels are normal, it is advisable to administer high-
flow oxygen to suspected DCS patients, as it can aid in the elimination of nitrogen gas pockets in the tissues
[2].
The clinical history of DCS typically includes rapid decompression, followed by manifestations in the skin,
muscles, bones, joints, inner ear, brain, spine, and, rarely, the lungs. These symptoms may arise within
minutes to several hours. Type I DCS commonly affects the shoulder joint, although any joint can be
involved. Cutis marmorata, which can be localized or widespread, may also be present. Additionally, patients
may exhibit lymph node swelling and pain. Type II DCS may present with the symptoms mentioned above,
as well as headache, visual and hearing impairment, nausea, tinnitus, poor coordination, and, in some cases,
altered sensorium [6,7]. Our patient's presentation, consisting of severe musculoskeletal and joint pain with
swelling and without neurological compromise, aligns with the symptoms of type I DCS. However, the rare
adjunctive presentation of coagulopathy in the axillary and brachial veins is an uncommon finding not
typically seen in type I DCS [3-5]. Although our patient properly ascended from his dive, his prior injury to
the right arm likely was a predisposing factor for his development of DCS. One could hypothesize that a
disruption in the soft tissues from the fall on the right shoulder served as a nidus for gas bubbles to escape.
Indeed, DCS in recreational scuba divers is low, approximately 0.4 to one case per 10,000 dives, primarily
due to increased awareness and education about prevention in recent years [6]. The most common
presenting symptom of DCS is musculoskeletal pain, much like our patient experienced, followed by patchy
paresthesia, motor weakness, and constitutional symptoms such as headache and fatigue. Ischemia and
inflammation typically cause widespread tissue damage [6]. Cutis marmorata, characterized by pruritic,
netlike, red lesions, can develop in the skin. Patients may also experience pain in areas affected by bone and
joint necrosis. Additionally, swollen and painful lymph nodes may be observed [7,8]. Symptoms are often
vague and non-discrete. However, practitioners should maintain a healthy level of suspicion in patients who
present with the above symptoms following a recent dive. Compliance with recommended dive tables, or
ascension rates dependent on maximum dive depth, is the most effective way to reduce the risk of DCS, but
this does not eliminate the risk [9,10]. This could explain why our patient suffered from DCS despite
ascending correctly, according to the recommended guidelines. Other risk factors for DCS include dives
deeper than 21 meters, dives conducted in cold water, dives in which divers physically exert themselves more
than typical, and a history of DCS [9,10]. For our patient, age, recent illness, including recent hospitalization
for nephrolithiasis, and immersion in cold fall-winter waters at depths above 21 meters were proponents for
his development of DCS.
The diagnosis of DCS remains clinical mainly, as there are no specific lab values that definitively point
towards the diagnosis. Imaging may suggest the diagnosis, but often, these measures do not meaningfully
contribute to decisions about treatment and may even delay the diagnosis further [7,8]. Type I DCS may even
be confused with systemic viral illness, systemic lupus erythematosus, presentations indicative of acute
bacterial diseases such as gonorrhea and syphilis, new presentations of leukemia or lymphoma, and
dehydration [11,12]. Type II DCS may be confused on initial clinical presentation to disease processes
involving thermal stress, nitrogen narcosis, meningococcemia, multiple sclerosis, hypoglycemia, acute
stroke, or inner ear barotrauma [11,12].
Treatment for DCS is often based on the severity of the patient's presentation, but standard measures
include oxygen supplementation with the highest possible fraction of inspired oxygen available [2,13]. A
definitive treatment for DCS is recompression in a hyperbaric chamber to reduce bubble volume by
enhancing the diffusion gradient for inert gas from bubbles to dissolution in blood [2,13,14]. A consensus
has emerged that patients with "mild" DCS, primarily defined as musculoskeletal, cutaneous, or
constitutional symptoms, can be effectively treated with oxygen supplementations without simultaneous
recompression [2,14]. Our patient's clinical course adds evidence to this claim, as the patient presented with
symptoms consistent with mild DCS and was effectively treated with 100% oxygen supplementation.
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However, it is strongly recommended that patients with any signs of focal neurologic deficits undergo
recompression therapy as urgently as possible, and this is often complicated by the fact that divers do not
present with symptoms until one to two days following their dive [2,14,15]. Additionally, there are
contraindications to hyperbaric oxygen therapy, namely, ear injury, pneumothorax, and any condition in
which lung collapse may be possible [8]. These conditions may concurrently manifest in divers as DCS, which
presents a clinical fork in the road.
Traditional, definitive management for DCS involves immediate administration of 100% oxygen, with
subsequent transfer to a hyperbaric oxygen chamber facility if patients show signs of neurologic or
respiratory symptoms [14-16]. Our patient exhibited solely musculoskeletal symptoms, so he was properly
and adequately managed with 15 L/minute of high-flow oxygen supplementation. Significantly, our patient
did not suffer lasting sequelae of DCS or develop new or worsening symptoms.
Conclusions
Our case highlights the necessity of maintaining a heightened level of clinical suspicion for DCS in
individuals who have recently participated in dives or air travel. Compression sickness ensued despite the
patient's extensive diving experience, adherence to proper ascending procedures, and preventive measures
taken to prevent the condition. This was likely attributed to a predisposing shoulder trauma sustained days
before the dive. Although the differential diagnosis was diligently broadened to incorporate the possibility
of necrotizing fasciitis, the most probable clinical scenario pointed toward DCS. Owing to a high level of
suspicion for this diagnosis, the patient received suitable treatment through high-flow oxygen
supplementation, thereby avoiding enduring or long-term sequelae associated with gas embolism.
The treatment protocol for DCS is contingent upon the severity of the patient's condition. The established
standard involves the administration of oxygen, aiming for the highest possible fraction of inspired oxygen.
Recompression in a hyperbaric oxygen chamber is the definitive therapy for DCS, facilitating the elimination
of nitrogenous gas bubbles from the circulatory system and assisting in the dissolution of blood. The current
consensus generally agrees that patients with "mild" DCS, characterized by musculoskeletal, cutaneous, or
constitutional symptoms, can be effectively managed with oxygen supplementation alone, provided there is
no clinical progression or development of new symptoms. However, if such progression or development
occurs despite adequate oxygen supplementation, transfer to a facility capable of recompression therapies is
warranted. This case underscores three crucial considerations for clinicians managing DCS: (1) It is
necessary to consider DCS even when adhering to proper diving protocols; (2) the potential efficacy of high-
flow oxygen therapy in the absence of hyperbaric chambers; and (3) the imperative need for a high index of
suspicion for DCS in divers presenting with musculoskeletal symptoms in the absence of neurological and
infectious causes.
Additional Information
Author Contributions
All authors have reviewed the final version to be published and agreed to be accountable for all aspects of the
work.
Concept and design: Juan Enciso, Shelby Remmel, Neha Chintapally
Acquisition, analysis, or interpretation of data: Juan Enciso, Shelby Remmel, Neha Chintapally
Critical review of the manuscript for important intellectual content: Juan Enciso
Supervision: Juan Enciso
Drafting of the manuscript: Shelby Remmel, Neha Chintapally
Disclosures
Human subjects: Consent was obtained or waived by all participants in this study. Conflicts of interest: In
compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services
info: All authors have declared that no financial support was received from any organization for the
submitted work. Financial relationships: All authors have declared that they have no financial
relationships at present or within the previous three years with any organizations that might have an
interest in the submitted work. Other relationships: All authors have declared that there are no other
relationships or activities that could appear to have influenced the submitted work.
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