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PubMed1980

Amelioration of decompression sickness in mice by pretreatment with cyproheptadine.

Substances that stimulate smooth muscle have been previously implicated in the pathogenesis of decompression sickness. This concept was strongly supported by the demonstration that compounds that combine activities against histamine, bradykinin, and serotonin prevent or ameliorate decompression sickness. This communication deals with the prophylactic effect of cyproheptadine (Periactin), a drug exhibiting such pharmacologic properties. More than 500 obese mice were used. Experimental groups, subcutaneously injected with cyproheptadine (0.5-40 mg/kg) prior to compression, and corresponding control animals were simultaneously subjected to 75 psig air pressure for 6 h and then rapidly decompressed. Most control animals exhibited signs of decompression sickness (chokes, scratching, twitching, convulsions, paralysis) and died. Gross and histologic examination revealed gas bubbles in vessels and tissues, perivascular edema, and other changes. In cyproheptadine-treated animals the incidence and severity of clinical manifestations and pathologic alterations were reduced, and mortality was marked decreased. Statistically significant results were obtained with doses of 2.5-10.0 mg/kg. The 5-mg/kg does lowered mortality by 45.9%. These results support the proposed pathogenetic concept and suggest a potential preventive treatment for human subjects.

Animals↗
PubMed2000

Management of decompression sickness in Jordan.

This study, conducted at Princes Haya Hussein Hospital Hyperbaric Department, examined 23 cases (22 males, 1 female), diagnosed with decompression sickness (types I and II) and treated with hyperbaric therapy. The results showed 61% of dive accidents were decompression sickness type II; 26% of treated patients had residual symptoms after the first session of recompression treatment and 74% made a full recovery. There were no deaths and no complications were observed. The study concludes that decompression sickness type II is the most common type, found mainly in sports divers. Early recognition of symptoms and commencement of treatment lead to a much better outcome.

Adolescent↗
PubMed1994

Visual manifestations of neurologic decompression sickness.

Although visual changes are considered a common finding in Type II altitude-related decompression sickness (DCS), the specific symptoms have not been described. To better understand the visual symptomatology of neurologic DCS, 38 cases of neurologic DCS that identified visual changes (on file at the Davis Hyperbaric Medicine Laboratory, Brooks AFB, TX) were reviewed. Information obtained from each record included date of treatment, patient age and sex, exposure environment, maximum altitude, onset time of symptoms, clinical manifestations, treatment table type and results of therapy. Most cases (87%) resulted from altitude chamber exposure. Visual changes were reported as the initial symptom in 24% of cases, with blurred vision the most common manifestation. Hyperbaric oxygen treatment produced completely successful results in 97% of the cases. A better understanding of visual changes that occur in neurologic DCS will, we hope, lead to early diagnosis and treatment, reducing the potential for severe secondary effects and residual deficits.

Adolescent↗
PubMed2000

The effect of staged decompression while breathing 100% oxygen on altitude decompression sickness.

INTRODUCTION: Space Shuttle extravehicular activity (EVA) requires decompression from sea level pressure (14.7 psia) to a 4.3 psia (30,300 ft) pressure suit. The transition currently involves altering the shuttle atmosphere to allow shirt-sleeve denitrogenation to occur during a 12 to 36-h staged decompression (SD) at 10.2 psia (9,800 ft) with an oxygen-enriched breathing gas (26.5% oxygen, 73.5% nitrogen). The denitrogenation provides protection from decompression sickness (DCS) during EVA in a 4.3 psia pressure suit. Our goal was to determine the highest altitude at which SD while breathing 100% oxygen (SD100) could provide effective protection from development of DCS symptoms after further decompression to 29,500 ft (4.5 psia). METHODS: There were 30 male subjects exposed to at least 6 of 11 conditions in random order on successive months to 29,500 ft for 4 h while performing mild exercise and being monitored for venous gas emboli (VGE) with an echo-imaging system. The subjects received 15 min of ground-level (GL) preoxygenation and an additional 60 or 120 min of SD100 at one of four altitudes between 8,000 ft (10.9 psia) and 18,000 ft (7.3 psia). Control exposures followed a 75- or 135-min ground-level preoxygenation. RESULTS: During SD100, one case of DCS occurred at 18,000 ft, but not at lower staging altitudes. Higher levels of VGE were observed during SD100 at 18,000 ft than during SD100 at any lower altitude. CONCLUSION: Staged decompression at 16,000 ft and below results in decompression risk during subsequent decompression to 29,500 ft similar to that following equivalent periods of ground-level preoxygenation.

Altitude Sickness↗
PubMed2003

Inner ear decompression sickness and inner ear barotrauma in recreational divers: a long-term follow-up.

OBJECTIVES/HYPOTHESIS: The objectives were to report the authors' experience with the long-term follow-up of patients with diving-related inner ear decompression sickness and inner ear barotrauma and to discuss residual cochlear and vestibular damage in relation to the question of fitness to dive. STUDY DESIGN: Retrospective consecutive case series. METHODS: Eleven recreational divers with inner ear decompression sickness and nine with inner ear barotrauma (IEB) were followed. A complete otoneurological physical examination and laboratory evaluation were carried out. The latter included audiometry, electronystagmography, a rotatory chair test using the sinusoidal harmonic acceleration protocol, and computerized dynamic posturography. RESULTS: Residual cochleovestibular deficits were found in 10 (91%) of the patients with inner ear decompression sickness and 3 (33%) of those with IEB (P <.02, Fisher's Exact test; odds ratio, 20). A significantly shorter follow-up period was required for the inner ear barotrauma group (P <.05, simple t test) because three patients (33%) recovered completely within 1 month of the diving accident. Eight patients had residual vestibular deficits on follow-up, but only one (12.5%) was symptomatic. However, five (56%) of the nine patients who had a cochlear insult, as documented by follow-up audiometry, complained of significant hearing loss and tinnitus. CONCLUSION: Inner ear decompression sickness carries a high risk for residual inner ear damage despite hyperbaric oxygen recompression therapy. A favorable prognosis might be anticipated for inner ear barotrauma. The finding that most patients with residual vestibular deficits were asymptomatic at the time of follow-up emphasizes the need for a complete vestibular evaluation, including specific bedside testing and laboratory examinations, before a return to diving activity may be considered.

Adult↗
PubMed2005

[A study on etiology and pathogenic mechanism of decompression sickness].

OBJECTIVE: To explain the etiology of decompression sickness (DCS) and to elucidate its pathogenic mechanism. METHOD: Tunica conjunctiva was examined by microscopy and blood pressure was measured at the exposed femoral arteries in inadequately decompressed animals after hyperbaric exposure. Then pathological examinations were done. RESULT: Animals with vascular spasm and dysfunction after decompression showed DCS symptoms. Severe DCS was found in the period of increasing of blood pressure swelling. Appeared in endothelial cells, fracted, hemorrhages were also formed in the body of DCS animals. CONCLUSION: DCS is a disease with vascular spasm and dysfunction caused by decompression. It's resulted from anoxia or pathological change caused by vascular spasm, dysfunction or even failure of blood vessels due to the gas tension (etiology) provoked by supersaturated gas in the blood during descending of ambient pressure. Vascular spasm and dysfunction impede the elimination of gas from the blood, and once the gas amount is sufficient to cause severe ischemia of the circulation system, the state of disease would be severe.

Animals↗
PubMed1987

Twenty years of treating decompression sickness.

Twenty years of treatment records were searched for cases of serious decompression sickness (DCS). Spinal cord DCS was the most common presentation. The efficacy of various treatment tables were compared. Oxygen tables were found to be as effective as long air tables in treating cases presenting within 12 h of the onset of symptoms and were superior for cases presenting later. Using RN 61 (USN 5) to treat serious decompression sickness resulted in a high post-treatment relapse rate. Other inappropriate practices such as in-water air treatment and nontreatment of spontaneously recovering cases resulted in a high incidence of deterioration or relapse.

Air↗
PubMed1998

Presumed venous infarction in spinal decompression sickness.

We describe the serial MR imaging findings in a patient with spinal decompression sickness. In the acute phase, the spinal cord was swollen, with increased T2 signal in the posterior part of the column; 1 month later, marked contrast enhancement was noted in the same location; and 2 months later, the swelling and T2 signal had decreased. MR imaging may facilitate the early diagnosis of spinal decompression sickness.

Decompression Sickness↗
PubMed2000

[Classification of altitude decompression sickness].

The article is devoted to the discussion of principles of and approaches to classification of altitude decompression sickness (DCS), one of the most methodically formidable aspects of the problem. Based on his own multiyear experience in altitude DCS investigations and critical review of literature, the author reasons his concept of clinical classification of altitude DCS. The author's concept places emphasis on obligatory consideration of three stages in DCS development: A--pre-disease (the premorbid syndrome), B--uncomplicated (light) and C--complicated (severe) forms. The objective sign of the premorbid state is "silent" gas bubbles in organism detectable by ultrasonic devices. Signs of uncomplicated altitude DCS are musculoarticular pains, local edema and skin itching. Complicated altitude DCS is diagnosed by systemic (respiratory, neurological and cardiovascular) disorders.

Altitude Sickness↗
PubMed1986

Decompression sickness incidence over 63 months of hypobaric chamber operation.

U.S. Army hypobaric chamber operations over a 63-month period were retrospectively reviewed, and incidence rates for decompression sickness were calculated. The overall incidence rate was 1.38/1000 exposures. The rate for interior technicians monitoring chamber operations was 6.16/1000 exposures. The rate for students was 0.64/1000 exposures. The increased incidence of decompression sickness for technicians was especially pronounced for the 10,668-m and 13,106-m flight profiles. Rapid decompression after the 7,620-m flight profile did not appear to increase the incidence of decompression sickness.

Altitude↗
PubMed2003

MR imaging of subclinical cerebral decompression sickness. A case report.

Diving accidents related to barotrauma constitute a unique subset of ischemic insults to the central nervous system. Victims may demonstrate components of arterial gas embolism, which has a propensity for cerebral involvement, and/or decompression sickness, with primarily spinal cord involvement. Decompression sickness-related radiology literature is very limited. We present our MR findings including FLAIR images in a decompression sickness patient with atypical presentation and review the related literature. We believe MR can be useful in follow-up studies and in early diagnosis of decompression sickness when symptoms do not fit the classic picture or loss of consciousness in surfacing.

Brain↗
PubMed1995

Decompression sickness in a private pilot.

Although safe, civil aviation can result in some unique medical problems. Most physicians are not familiar with aviation-related medical problems. One such problem, decompression sickness, is not mentioned in most medical texts, and is not included in most medical school instruction. If not promptly recognized and treated, decompression sickness can result in permanent disability or death. I report a case of altitude-induced decompression sickness after a flight in an unpressurized aircraft.

Aerospace Medicine↗
PubMed1983

Bubbles and hematologic alterations in intracranial veins during experimental decompression sickness.

Rats were exposed to 6.1 bar (abs.) air for 90 min and subsequently decompressed to the ambient pressure. After a decompression rate of 6.8 bar/min pial veins and superior sagittal sinuses were found to contain gas bubbles; no intravascular bubbles were observed subsequent to a decompression rate of 1.5 bar/min. Under the electron microscope platelet aggregates were observed at both the electron-dense layer of the blood-bubble interface and in pial veins with no bubbles. It is concluded that during decompression sickness bubbles and both activation and aggregation of platelets occur in intracranial veins. Subsequent venous congestion may contribute to the neuronal lesions and symptoms of acute decompression sickness.

Animals↗
PubMed1985

Additional pressurisation for treating nonresponding cases of serious air decompression sickness.

In this study, 20 years of decompression sickness (DCS) treatment records were reviewed to establish whether or not compression to 50m (165 fsw) was a useful response to serious DCS cases which failed to respond satisfactorily at 18m (60 fsw) breathing oxygen. It was concluded from 14 cases that further compression rarely altered the recovery of cases which were not already recovering at 18m or were of a relatively mild nature. The only case with motor deficits to recover at 50m later relapsed. In general, cases without motor deficits were more likely to be cured, and then only slowly. The only real justification for compression to 50m is rapid deterioration at 18m. This does not guarantee to stop or prevent deterioration as four cases of deterioration at 50m are reported. Nine cases of compression beyond 50m to as deep as 76m (250 fsw) on air are reported with the conclusion that it provides little or no benefit.

Atmospheric Pressure↗
PubMed1985

Delayed treatment of serious decompression sickness.

We report the cases of three patients with residual symptoms from diving decompression sickness, each of whom presented to a recompression chamber three to seven days following original exposure. All three had complete resolution of symptomatology despite the delayed treatment. The late resolution of symptoms is evidence both of residual bubble effect and of distal tissue hypoxia responding to oxygen therapy with the recompression. We recommend that decompression sickness symptoms be treated whenever they are seen, even ten to 14 days postinjury.

Adult↗
PubMed1979

Pathophysiology of bends and decompression sickness. An overview with emphasis on treatment.

Current concepts in the pathophysiology of decompression sickness are reviewed. Mild, moderate, and severe forms of this syndrome resulting from gaseous and lipid emboli are described. Therapy is aimed at restoring or specifically treating each alteration. Plasma volume deficit is restored by colloidal re-expansion. Decompression sickness is partially treated when recompression alone is used. Blood lipid alterations are managed by use of antilipemic agents. Dextran is mentioned. Divers at depths of 61 m display changes in hematocrit, platelet, and blood lipid profiles. Cord paralysis may occur from bubbles in the vena cava. Retrograde migration blocks the venous circulation of the spinal cord. Ultrasonic devices can detect "silent" bubbles during decompression. Recompression, when available, is a lifesaving treatment for diving accidents involving saturation diving. Air embolism is discussed. Monitoring emboli by EEG and fundoscopy are reported.

Blood Coagulation Factors↗
PubMed1998

An abrupt zero-preoxygenation altitude threshold for decompression sickness symptoms.

INTRODUCTION: The altitude threshold for decompression sickness (DCS) symptoms has been variously described as being 18,000 ft (5,487 m) to above 25,000 ft (7,620 m). Safety and efficiency of aerospace operations require more precise determination of the DCS threshold. METHODS: Subjects were 124 males who were exposed to simulated altitudes (11 at 11,500 ft; 10 at 15,000 ft; 8 at 16,500 ft; 10 at 18,100 ft; 10 at 19,800 ft; 20 at 21,200 ft; 20 at 22,500 ft; 10 at 23,800 ft, and 25 at 25,000 ft) for 4 to 8 h. All breathed 100% oxygen beginning with ascent. Subjects were monitored for precordial venous gas emboli (VGE) and DCS symptoms. Probit curves representing altitude vs. incidence of DCS symptoms and VGE allowed estimation of respective risk. RESULTS: VGE were first observed at 15,000 ft with increasing incidence at higher altitudes; over 50% at 21,200 ft and 70% or higher at 22,500 ft and above. The lowest altitude occurrence of DCS was a 5% incidence at 21,200 ft. At 22,500 ft, the DCS incidence abruptly climbed to 55%. CONCLUSION: A 5% threshold for DCS symptoms was concluded to be 20,500 ft under the conditions of this study. The abrupt increase in DCS symptoms, with zero-preoxygenation exposure above 21,200 ft implies a need for reconsideration of current USAF and FAA altitude exposure guidance.

Aerospace Medicine↗