Decompression sickness followed by diabetic ketoacidosis and sepsis shock: an unusual case report.

Decompression sickness (DCS) is caused by abrupt changes in extracorporeal pressure with varying severity. Symptoms range from mild musculoskeletal pain to severe organ dysfunction and death, especially among patients with chronic underlying disease. Here, we report an unusual case of a 49-year-old man who experienced DCS after a dive to a depth of 38 meters. The patient's symptoms progressed, starting with mild physical discomfort that progressed to disturbance of consciousness on the second morning. During hospitalization, we identified that in addition to DCS, he had also developed diabetic ketoacidosis, septic shock, and rhabdomyolysis. After carefully balancing the benefits and risks, we decided to provide supportive treatment to sustain vital signs, including ventilation support, sugar-reducing therapy, fluid replacement, and anti-infection medications. We then administered delayed hyperbaric oxygen (HBO2) when his condition was stable. Ultimately, the patient recovered without any sequelae. This is the first case report of a diver suffering from DCS followed by diabetic ketoacidosis and septic shock. We have learned that when DCS and other critical illnesses are highly suspected, it is essential to assess the condition comprehensively and focus on the principal contradiction.

Decompression illness: a comprehensive overview.

Decompression illness is a collective term for two maladies (decompression sickness [DCS] and arterial gas embolism [AGE]) that may arise during or after surfacing from compressed gas diving. Bubbles are the presumed primary vector of injury in both disorders, but the respective sources of bubbles are distinct. In DCS bubbles form primarily from inert gas that becomes dissolved in tissues over the course of a compressed gas dive. During and after ascent ('decompression'), if the pressure of this dissolved gas exceeds ambient pressure small bubbles may form in the extravascular space or in tissue blood vessels, thereafter passing into the venous circulation. In AGE, if compressed gas is trapped in the lungs during ascent, pulmonary barotrauma may introduce bubbles directly into the pulmonary veins and thence to the systemic arterial circulation. In both settings, bubbles may provoke ischaemic, inflammatory, and mechanical injury to tissues and their associated microcirculation. While AGE typically presents with stroke-like manifestations referrable to cerebral involvement, DCS can affect many organs including the brain, spinal cord, inner ear, musculoskeletal tissue, cardiopulmonary system and skin, and potential symptoms are protean in both nature and severity. This comprehensive overview addresses the pathophysiology, manifestations, prevention and treatment of both disorders.

S2k guideline for diving accidents.

For the purposes of this guideline, a diving accident is defined as an event that is either potentially life-threatening or hazardous to health as a result of a reduction in ambient pressure while diving or in other hyperbaric atmospheres with and without diving equipment. This national consensus-based guideline (development grade S2k) presents the current state of knowledge and recommendations on the diagnosis and treatment of diving accident victims. The treatment of a breath-hold diver as well as children and adolescents does not differ in principle. In this regard only unusual tiredness and itching without visible skin changes are mild symptoms. The key action statements: on-site 100% oxygen first aid treatment, immobilization/no unnecessary movement, fluid administration and telephone consultation with a diving medicine specialist are recommended. Hyperbaric oxygen therapy (HBOT) remains unchanged as the established treatment in severe cases, as there are no therapeutic alternatives. The basic treatment scheme recommended for diving accidents is hyperbaric oxygenation at 280 kPa.

Pulsatile gas-liquid flow resembling Decompression Sickness: Computational Fluid Dynamics simulation and experimental validation.

BACKGROUND: This work performs two-dimensional Computational Fluid Dynamics (CFD) simulations of pulsatile bubbly flow in a column resembling the flow inside human vena cava during Decompression Sickness (DCS), aiming to illustrate the effect of certain parameters in bubbly blood flow and so facilitate the design of the: a) corresponding in-vitro bubbly flow experiments under pulsatile flow conditions inside a flow loop and b) in-vivo trials on swines for assessing a novel electrical impedance spectroscopy technique on the detection of bubbles (as those found during DCS) in their bloodstream. MATERIALS AND METHODS: The commercially available ANSYS 2019-R3 CFD code was employed to simulate the pulsatile bubbly flow that resembled DCS. Simulations were validated against experiments conducted in a vertical co-current upward pulsatile bubbly flow provided by a flow loop equipped with electrical, optical and pressure diagnostics. RESULTS: CFD simulations under pulsatile conditions were initially validated by oscillatory in-vitro bubbly flow experiments. Then, the influence of pulsation parameters on void fraction, α, and flow velocity, U, profiles was computationally investigated. Intense periodic fluctuations of void fraction were observed along the column and their intensity increases with pulsation amplitude. Moreover, U and α radial profiles were uniform for bubbles 30 µm but showed a core-peaking profile for bubbles 300 µm. CONCLUSIONS: CFD simulations of pulsatile bubbly flow resembling DCS provided unconventional information about the influence of different-sized sub-millimetre bubbles on the flow velocity and void fraction profiles, which are expected to improve the design of in-vitro and in-vivo trials for the detection of bubbles such as those found in DCS.

Delayed treatment for decompression illness: factors associated with long treatment delays and treatment outcome.

INTRODUCTION: Effectiveness of delayed hyperbaric oxygen treatment (HBOT) for decompression illness (DCI) and factors affecting treatment delays have not been studied in large groups of patients. METHODS: This 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. RESULTS: 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. CONCLUSIONS: 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.

Hysteria as a Trigger for Epidemic Decompression Sickness Following Hypobaric Hypoxia Training.

INTRODUCTION: Although hypobaric hypoxia training (HHT) is an essential component of aviation physiology training, it poses a risk of decompression sickness (DCS). DCS can sometimes be observed as a cluster of cases, which is referred to as epidemic DCS. In this report, we aim to evaluate an epidemic DCS episode that occurred following two consecutive HHT sessions.METHODS: A total of 16 trainees, all of whom were medical doctors, attended the aviation medicine training course in the aeromedical research and training center. They went through HHT in two sessions, each with eight trainees.RESULTS: Following two HHT sessions, five Type 1 DCS cases occurred among 18 personnel (16 trainees and 2 inside observers). DCS incidence rate was found to be 27.77%. They were successfully treated with hyperbaric oxygen therapy (HBOT).DISCUSSION: Since the DCS incidence rate was found to be higher than the average in such a short period of time, this cluster of cases was labeled as epidemic DCS. We carried out a thorough investigation into all possible causes by following some templates that were developed to conduct comprehensive investigations into epidemic DCS episodes. According to the psychological arguments discussed here, we placed a special emphasis on hysterical and psychosocial components, among other probable factors. In cases where the possibility of hysteria and placebo-nocebo responses exist, it is appropriate to conduct the training and treatment processes with these factors in mind. No matter what the triggering factor is and how the symptoms manifest, HBOT remains crucial in the treatment of DCS.Demir AE, Ata N. Hysteria as a trigger for epidemic decompression sickness following hypobaric hypoxia training. Aerosp Med Hum Perform. 2022; 93(10):712-716.

Decompression Illness Treated with the Hart-Kindwall Protocol in a Monoplace Chamber.

BACKGROUND Hyperbaric oxygen (HBO2) therapy in a multiplace chamber is the standard treatment for severe altitude decompression illness (DCI). However, some hospitals may only have a monoplace chamber. Herein, we present the case of a patient with severe altitude DCI caused by rapid decompression during an actual flight operation that was successfully treated through emergency HBO2 therapy with the Hart-Kindwall protocol, a no-air-break tables with the minimal-pressure oxygen approach in a monoplace chamber due to unavailability of rapid access to a multiplace chamber. CASE REPORT A 34-year-old male aviator presented with chest pain, paresthesia, and mild cognitive impairment following rapid decompression 20 minutes after take-off, which comprised 10 minutes of reaching a height of 10 058 m (33 000 feet) and 10 minutes of cruising at that altitude. He then initiated flight descent and landing. He visited a primary clinic, and severe DCI was suggested clinically. However, since the closest hospital with a multiplace chamber was a 3-hour drive away, we provided emergency HBO2 therapy with the Hart-Kindwall protocol in a monoplace chamber at a nearby hospital 4 hours after the initial decompression. He recovered fully and returned to flight duty 2 weeks later. CONCLUSIONS Emergency HBO2 therapy with the Hart-Kindwall protocol in a monoplace chamber may be a suitable option for severe DCI, especially in remote locations with no access to facilities with a multiplace chamber. However, prior logistical coordination must be established to transfer patients to hospitals with multiplace chambers if their symptoms do not resolve.

Exceptional survival of an airplane stowaway, treated successfully with hyperbaric oxygen.

Survival of airplane stowaways is rare. Here we report an exceptional case of successful treatment and full recovery. After a transcontinental flight an unconscious stowaway was discovered in a wheel well of a Boeing 747-400F. Airport paramedics confirmed regular respiration and achieved 100% oxygen saturation (pulse oximetry) by high-flow oxygen. Rectal body temperature was 35.5 °C. On arrival at the emergency department, the patient's vital signs were stable. He did not respond to verbal stimuli. He localized to painful stimuli with both arms, however, there was no reaction to stimuli to both legs. We suspected his neurological deficits were caused by posthypoxic encephalopathy or altitude decompression sickness (DCS), the latter amenable to hyperbaric oxygen therapy (HBOT). HBOT was performed for 5 h (US Navy Treatment Table 6) and afterwards, full neurological recovery was documented. About 24 h after admission a new proximal paresis of the left leg was noted. Assuming recurrence of DCS, daily HBOT was scheduled for three days, after which motor function had again returned to normal. Stowaways travelling in airplane wheel wells experience extreme environmental circumstances. The presented patient survived an eight-hour exposure to calculated barometric pressures as low as 190 mmHg and ambient PO2 of 40 mmHg. Apart from creating awareness of this rare patient category, we want to stress the risk of altitude DCS in unpressurized flights. When DCS is suspected, immediate high-flow oxygen therapy should be initiated, followed by HBOT at the earliest opportunity.

A prospective single-blind randomised clinical trial comparing two treatment tables for the initial management of mild decompression sickness.

INTRODUCTION: Limited evidence suggests that shorter recompression schedules may be as efficacious as the US Navy Treatment Table 6 (USN TT6) for treatment of milder presentations of decompression sickness (DCS). This study aimed to determine if divers with mild DCS could be effectively treated with a shorter chamber treatment table. METHODS: All patients presenting to the Fremantle Hospital Hyperbaric Medicine Unit with suspected DCS were assessed for inclusion. Participants with mild DCS were randomly allocated to receive recompression in a monoplace chamber via either a modified USN TT6 (TT6m) or a shorter, custom treatment table (FH01). The primary outcome was the number of treatments required until resolution or no further improvement (plateau). RESULTS: Forty-one DCS cases were included, 21 TT6m and 20 FH01. Two patients allocated to FH01 were moved to TT6m mid-treatment due to failure to significantly improve (as per protocol), and two TT6m required extensions. The median total number of treatments till symptom resolution was 1 (IQR 1-1) for FH01 and 2 (IQR 1-2) for TT6m (P = 0.01). More patients in the FH01 arm (17/20, 85%) showed complete symptom resolution after the initial treatment, versus 8/21 (38%) for TT6m (P = 0.003). Both FH01 and TT6m had similar overall outcomes, with 19/20 and 20/21 respectively asymptomatic at the completion of their final treatment (P = 0.97). In all cases where two-week follow-up contact was made, (n = 14 FH01 and n = 12 TT6m), patients reported maintaining full symptom resolution. CONCLUSIONS: The median total number of treatments till symptom resolution was meaningfully fewer with FH01 and the shorter treatment more frequently resulted in complete symptom resolution after the initial treatment. There were similar patient outcomes at treatment completion, and at follow-up. We conclude that FH01 appears superior to TT6m for the treatment of mild decompression sickness.

Delayed recognition of Type II decompression sickness in a diver with chronic atrial fibrillation.

Introduction: This case report describes an initially overlooked Type II decompression sickness (DCS) occurrence that was confused with a cerebral vascular accident in a patient with chronic atrial fibrillation (AF). The purpose of this case report is to reinforce the maxim that DCS needs to be suspected anytime a scuba diver experiences signs or symptoms compatible with DCS after completing a scuba dive. Methods: A 71-year-old scuba diver with a history of AF and who was taking warfarin made four dives, all with maximum depths less than 60 fsw (20 msw) over a 10-hour interval. Shoulder pain developed before entering the water on the fourth dive and was worse after exiting from the fourth dive. Twenty minutes later the diver collapsed while standing and was unable to make a grip using his left hand. A literature review failed to locate any case reports of divers with AF presenting with strokelike symptoms only to find the cause was Type II DCS.. Findings: Initially the patient's findings were reviewed with a diving medicine team. The recommendation was for the patient to be managed for a stroke. The patient was transferred to a hospital for a computed tomography scan, but no recommendation was made for a hyperbaric oxygen recompression treatment. The scan showed no brain bleed or infarct. The attending neurologist (not diving medicine-trained) was concerned that the patient's findings were diving-related and arranged for transferring the patient to a hyperbaric medicine facility 25 hours later. With hyperbaric oxygen (HBO2) therapy the patient's symptoms remitted over several weeks. Conclusion: The presence of symptoms attributed to a stroke immediately after a scuba dive should not deter a trial of HBO2 therapy. The delay in starting HBO2 therapy is concerning and perhaps the reason recovery was delayed and the need for repetitive HBO2 therapies.

Severe acute kidney injury caused by decompression sickness syndrome.

Decompression sickness (DCS) occurs when divers are exposed to reduced barometric pressure during their ascent from depth. We report a case of DCS causing severe acute kidney injury (AKI) after an uneventful dive in which all decompression stops were made as instructed by a dive computer. A 26-year-old man presented with abdominal and bilateral flank pain ~ 24 hours after scuba diving to a depth of 23 m. Vitals and physical exam were unremarkable. Lab results revealed elevated serum creatinine at 2.3 mg/dL from a normal baseline and elevated blood urea nitrogen at 23 mg/dL. The patient was non-oliguric. Other biochemical parameters were unremarkable. Dipstick urinalysis showed presence of blood and 100 mg/dL proteinuria. Urine microscopy revealed hyaline casts and red blood cells ~ 16 - 30/HPF but no acanthocytes. Urine protein-to-creatinine ratio was 340 mg/g. Renal ultrasound showed normal sized kidneys with increased cortical echogenicity, and computed tomography of the abdomen/pelvis showed bilateral striated nephrogram with delayed excretion, both radiographic signs of acute tubular necrosis. The patient received isotonic IV fluids and 5 sessions of hyperbaric oxygen therapy. Symptomatic improvement was observed by day 3 of hospitalization with full recovery of kidney function after discharge. Due to a wide range of associated symptomology, a thorough and prompt evaluation is warranted in suspected cases of DCS, particularly if presentation is more than 24 hours following ascent.

Dysbarism: An Overview of an Unusual Medical Emergency.

Dysbarism is a general term which includes the signs and symptoms that can manifest when the body is subject to an increase or a decrease in the atmospheric pressure which occurs either at a rate or duration exceeding the capacity of the body to adapt safely. In the following review, we take dysbarisms into account for our analysis. Starting from the underlying physical laws, we will deal with the pathologies that can develop in the most frequently affected areas of the body, as the atmospheric pressure varies when acclimatization fails. Manifestations of dysbarism range from itching and minor pain to neurological symptoms, cardiac collapse, and death. Overall, four clinical pictures can occur: decompression illness, barotrauma, inert gas narcosis, and oxygen toxicity. We will then review the clinical manifestations and illustrate some hints of therapy. We will first introduce the two forms of decompression sickness. In the next part, we will review the barotrauma, compression, and decompression. The last three parts will be dedicated to gas embolism, inert gas narcosis, and oxygen toxicity. Such an approach is critical for the effective treatment of patients in a hostile environment, or treatment in the emergency room after exposure to extreme physical or environmental factors.

Patent Foramen Ovale Closure and Decompression Sickness Among Divers.

BACKGROUND: Decompression sickness is a diving-related disease that results in various clinical manifestations, ranging from joint pain to severe pulmonary and CNS affection. Complications of this disease may sometimes persist even after treatment with hyperbaric oxygen therapy. In addition, it may hamper the quality of life by forcing divers to restrict their recreational practice. The presence of a patent foramen ovale (PFO) increases the risk of decompression sickness by facilitating air embolization. Therefore, PFO closure may play a role in reducing such complications. However, PFO closure remains associated with its own set of risks and complications. We sought to assess the benefit and harm of PFO closure for the prevention of decompression sickness in divers. METHODS: We conducted a comprehensive search of MEDLINE, Embase, CENTRAL, and Web of Science. Two-armed studies comparing the incidence of decompression sickness with or without PFO closure were included. We used a random-effects model to compute risk ratios comparing groups undergoing PFO closure to those not undergoing PFO closure. RESULTS: Four observational studies with a total of 309 divers (PFO closure: 141 and no closure: 168) met inclusion criteria. PFO closure was associated with a significantly lower incidence of decompression sickness (PFO-closure: 2.84%; no closure: 11.3%; RR: 0.29; 95% CI: 0.10 to 0.89; NNTB = 11), with low heterogeneity (I2 = 0%). The mean follow-up was 6.12 years (Standard deviation 0.70). Adverse events occurred in 7.63% of PFO closures, including tachyarrhythmias and bleeding. CONCLUSION: PFO closure may potentially reduce the risk of decompression sickness among divers; however, it is not free of potential downsides, with nearly one in thirteen patients in our analysis experiencing an adverse event.

Inner ear barotrauma and inner ear decompression sickness: a systematic review on differential diagnostics.

INTRODUCTION: Inner ear barotrauma (IEBt) and inner ear decompression sickness (IEDCS) are the two dysbaric inner ear injuries associated with diving. Both conditions manifest as cochleovestibular symptoms, causing difficulties in differential diagnosis and possibly delaying (or leading to inappropriate) treatment. METHODS: This was a systematic review of IEBt and IEDCS cases aiming to define diving and clinical variables that help differentiate these conditions. The search strategy consisted of a preliminary search, followed by a systematic search covering three databases (PubMed, Medline, Scopus). Studies were included when published in English and adequately reporting one or more IEBt or IEDCS patients in diving. Concerns regarding missing and duplicate data were minimised by contacting original authors when necessary. RESULTS: In total, 25 studies with IEBt patients (n = 183) and 18 studies with IEDCS patients (n = 397) were included. Variables most useful in differentiating between IEBt and IEDCS were dive type (free diving versus scuba diving), dive gas (compressed air versus mixed gas), dive profile (mean depth 13 versus 43 metres of seawater), symptom onset (when descending versus when ascending or surfacing), distribution of cochleovestibular symptoms (vestibular versus cochlear) and absence or presence of other DCS symptoms. Symptoms of difficult middle ear equalisation or findings consistent with middle ear barotrauma could not be reliably assessed in this context, being insufficiently reported in the IEDCS literature. CONCLUSIONS: There are multiple useful variables to help distinguish IEBt from IEDCS. Symptoms of difficult middle ear equalisation or findings consistent with middle ear barotrauma require further study as means of distinguishing IEBt and IEDCS.

Estimating Inert Gas Bubbling from Simple SCUBA Diving Parameters.

Inert gas bubbles frequently occur in SCUBA divers' vascular systems, eventually leading to decompression accidents. Only in professional settings, dive profiles can be adjusted on individual basis depending on bubble grades detected through ultrasonography. A total of 342 open-circuit air dives following sports diving profiles were assessed using echocardiography. Subsequently, (Eftedal-Brubakk) bubble grades were correlated with dive and individual parameters. Post-dive cardiac bubbles were observed in 47% of all dives and bubble grades were significantly correlated with depth (r=0.46), air consumption (r=0.41), age (r=0.25), dive time (r=0.23), decompression diving (r=0.19), surface time (r=- 0.12). Eftedal-Brubakk categorical bubble grades for sports diving with compressed air can be approximated by bubble grade = (age*50-1 - surface time*150-1+maximum depth*45-1+air consumption*4500-1)2 (units in years, hours, meter, and bar*liter; R2=0.31). Thus, simple dive and individual parameters allow reasonable estimation of especially relevant medium to higher bubble grades for information on relevant decompression stress after ascent. Echo bubble grade 0 is overestimated by the formula derived. However, echo might fail to detect minor bubbling only. The categorical prediction of individual decompression stress with simple bio and dive data should be evaluated further to be developed towards dive computer included automatic ex-post information for decision-making on individual safety measures.

European position paper on the management of patients with patent foramen ovale. Part II - Decompression sickness, migraine, arterial deoxygenation syndromes and select high-risk clinical conditions.

Patent foramen ovale (PFO) is implicated in the pathogenesis of a number of medical conditions but to date only one official position paper related to left circulation thromboembolism has been published. This interdisciplinary paper, prepared with the involvement of eight European scientific societies, reviews the available evidence and proposes a rationale for decision making for other PFO-related clinical conditions. In order to guarantee a strict evidence-based process, we used a modified grading of recommendations, assessment, development, and evaluation (GRADE) methodology. A critical qualitative and quantitative evaluation of diagnostic and therapeutic procedures was performed, including assessment of the risk/benefit ratio. The level of evidence and the strength of the position statements were weighed and graded according to predefined scales. Despite being based on limited and observational or low-certainty randomised data, a number of position statements were made to frame PFO management in different clinical settings, along with suggestions for new research avenues. This interdisciplinary position paper, recognising the low or very low certainty of existing evidence, provides the first approach to several PFO-related clinical scenarios beyond left circulation thromboembolism and strongly stresses the need for fresh high-quality evidence on these topics.

Retroperitoneal extensive free air bubbles due to decompression illness.

Decompression illness (DCI) is a rare condition caused by air bubbles that arise because of a rapid decrease in ambient pressure. These air bubbles exert both physical and chemical effects associated with a range of findings from asymptomatic clinical presentation to death. In the literature, changes in consciousness, severe musculoskeletal and abdominal pain, respiratory distress, and skin changes have been described. The diagnosis of DCI is difficult, but anamnesis and physical examination are helpful. Radiologic evaluation is useful for determining possible complications in patients with severe disease and excluding other acute pathologies. In computed tomography (CT) images of patients diagnosed with DCI, air bubbles in the portal venous system, iliac and mesenteric veins, the vena cava inferior (VCI), and the cerebral and spinal arteries have been described before. Herein, we present the clinical and CT findings of two cases of DCI with extensive intra-abdominal free bubbles evident on abdominal CT.