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CE Credit Article Clinical & Refractive Optometry is pleased to present this continuing education (CE) article by Dr. Timothy B. White and Dr. Nathan A. Whitaker entitled Ocular and Systemic Manifestations of Decompression Illness: A Case Report and Review. In order to obtain 1-hour of COPE-approved CE credit, please refer to page 110 for complete instructions. Ocular and Systemic Manifestations of His best corrected visual acuity measured 5/500 Decompression Illness: A Case Report and Review (20/2000) in each eye with normal pupil and muscle Timothy B. White, OD; Nathan A. Whitaker, OD, FAAO functions OU. Because of the profound vision loss, he was unable to perform visual fields or any other form of subjective testing. Anterior segment findings were ABSTRACT unremarkable OU and intraocular pressure measured Pressure changes affect compressible structures 20 mmHg OU. Dilated fundus examination revealed within the body. The gases of hollow spaces and clear media OU, healthy optic nerves, maculae and organs, as well as gases dissolved in the blood, are all peripheral retinae. subject to variations in pressure. As an individual Review of our patient’s medical records revealed that descends, the total pressure of the air he/she breathes imaging had been performed and magnetic resonance increases and in turn, the partial pressures of the imaging (MRI) demonstrated bilateral occipital lobe individual components of air increase proportionally. infarction secondary to occlusion of the basilar artery A reduction in pressure, such as occurs while (Figs. 1, 2). He was treated with hyperbaric therapy soon ascending from a dive, releases dissolved gases after the episode, but experienced no visual recovery. (primarily nitrogen) from solution in the tissues Subsequent to our examination, we referred him to a and blood, into various sites throughout the body. regional blind rehabilitation center. These bubble formations present the potential for complications that range from mild joint pain to unconsciousness or death. DISCUSSION Herein, we report the case of a 41-year-old male The air we breathe is primarily composed of nitrogen who went scuba diving while on vacation. He failed to (78%) and oxygen (21%). Since nitrogen is not observe proper decompression procedures and a gas metabolized by the body, most of what we breathe in is embolus occluded his basilar artery resulting in expelled when we exhale. At sea level only small amounts infarction of each occipital lobe and profound vision of nitrogen dissolve into the blood and tissues. loss in each eye. During a dive the pressure of compressed air increases in proportion to the surrounding water pressure. Since the body continuously uses oxygen, excess oxygen CASE REPORT molecules that accumulate under higher pressure are of no A 41-year-old white male presented for his initial consequence. However, when nitrogen in compressed air examination indicating that two months prior he had been is inhaled at a higher pressure it dissolves into the tissues scuba diving and after ascending too quickly, experienced and stays there until the diver begins to surface. The bilateral vision loss. There were no other associated amount of excess nitrogen entering the tissues during a neurological symptoms. He had no history of ocular dive is variable and depends on the depth and duration of surgery or trauma and reported no family history of the dive. Tables are readily available that specify how long ocular disease. divers can remain at certain depths, and when these limits are exceeded, the diver must pause at specified intervals during their ascent (known as decompression stops) to allow for diffusion of nitrogen out of the tissue into the T.B. White, N.A. Whitaker — Tuscaloosa Veterans Affairs Medical Center, bloodstream so that it can be safely expelled through the Tuscaloosa, AL pulmonary capillary bed.1 If a diver surfaces too quickly Correspondence to: Dr. Nathan A. Whitaker, 3701 Loop Road, Tuscaloosa and the rate of ascent exceeds that at which nitrogen can Veterans Affairs Medical Center, Tuscaloosa, Alabama 35404; safely be cleared, potentially dangerous nitrogen bubbles E-mail: Nathan.Whitaker@med.va.gov form in the tissues and bloodstream (in a manner similar 104 Clinical & Refractive Optometry 17:3, 2006 Fig. 1 Major arterial supply to the brain. The internal carotid artery divides into the anterior cerebral artery (ACA) and middle cerebral artery (MCA), with the ACA responsible for perfusion of the medial aspect of the cerebral hemisphere and the MCA supplying the lateral aspect. The posterior circulation, or the vertebrobasilar system, supplies blood to the brainstem, cerebellum, and occipital lobes via paired vertebral arteries. The vertebral arteries converge at the base of the pons to form the Fig. 2 Anatomy: circle of Willis. (1) posterior cerebral artery, (2) superior basilar artery. Cerebellar and pontiene arteries branch from the basilar cerebellar artery, (3) basilar artery, (4) anterior inferior cerebellar artery, artery before it bifurcates to form the paired posterior cerebral arteries. (5) vertebral artery, (6) posterior inferior cerebellar artery. The site of The posterior cerebral artery (PCA) perfuses areas of the cortex below the occlusion in our patient occurred at the junction of the basilar artery bold black line including the visual cortex. (3) and posterior cerebral arteries (1). to opening a bottle of soda too quickly) resulting in the occurs when nitrogen is unable to be exhaled efficiently complications associated with decompression illness during ascent and bubbles form in the blood and tissue. (DCI). Approximately 50% of cases of DCI will occur With inadequate decompression, the bubbles increase in despite claims of compliance with these ascension size as the diver surfaces and injures tissues through intervals.2 Other factors that increase a diver’s risk for compressive mechanisms, ischemia, or by the initiation of developing DCI are included in Table I. a local inflammatory response that produces swelling in An estimated 9 million dives occur in the United the muscles, joints, or tendons. Pain is the most common States annually.3 According to the Divers Alert Network symptom among divers that experience type 1 DCS and (DAN), a non-profit medical and research group occurs in 70% to 85% of affected patients.7 The pain is dedicated to the safety of divers, less than 1% of divers typically described as deep, dull, or throbbing and is will experience DCI. Seventy-two percent of those who usually located in the vicinity of a joint or tendon. The experience DCI are males, most of whom are between the most commonly affected sites include the shoulder, ages of 30 and 59.4 elbow, hip, and knee joints.8-10 Divers with cutaneous involvement, also know as “skin bends”, frequently Decompression Sickness (DCS) manifest symptoms that include pruritis and a burning Decompression illness (DCI) is a term that encompasses sensation in their skin. A mottled, papular, plaque-like, two conditions which includes decompression sickness violaceous rash, known as “cutis marmorata”, is also (DCS) and arterial gas embolization (AGE).5 characteristic of type 1 DCS. Lymphedema and pain in Decompression sickness, often referred to as “the bends” the regional lymph nodes is known to occur if nitrogen or “caissons disease”, is categorized as either type 1 or bubbles affect the lymphatic system.6 type 2 sickness. Type 1 DCS represents the mildest form Patients who experience type 2 DCS will often of disease and exists when i) the illness is limited to the manifest components of type 1 sickness in addition to musculoskeletal, cutaneous, and/or lymphatic tissues, ii) complications that arise secondary to the effects of there is a normal neurological examination before the nitrogen bubbles on the spinal cord, heart, and lungs.11 initiation of treatment, and iii) symptom resolution occurs Neurological deficits of type 2 sickness are varied, but within 10 minutes of the initiation of oxygen at 2.8 ATA often include sensory deficits, hemiplegia, paraplegia, (atmosphere of absolute pressure).6 Type 1 sickness paresthesia, dizziness, and neuropathies.12 Hypovolemic Ocular and Systemic Manifestations of Decompression Illness — White, Whitaker 105 Table I Factors that increase the risk of decompression illness6,26-30 Cold water dive Gases dissolve better in cool liquids than warm. If a diver is cold, nitrogen uptake into tissues is greater. A working dive Working dives require greater physical exertion and greater intake of air. Increased levels of oxygen and nitrogen are inhaled under these circumstances. Obesity Nitrogen dissolves 5 times better in fat than in water. Skip breathing Skip breathing (holding your breath for short periods of time) is a technique employed by some divers to make air last longer while submerged. This results in an accumulation of CO2 which, in turn, causes vasodilation and increased nitrogen uptake. Multi-day diving If making multiple dives during a week, it is recommended that divers take a day off in the middle and diving to the of the week to allow all tissues to return to normal atmospheric pressure. limit of dive tables Older age It is estimated that 60-year-old divers have 30% more “silent” bubbles than divers half their age. Silent bubbles are nitrogen bubbles that form after a “safe” dive, and generally cause no obvious symptoms. Smoking Heavy smokers who develop DCI are at approximately twice the risk of experiencing severe symptoms as non-smokers. Patent Foramen Thirty percent of adults have a patent foramen ovale. This congenital opening in the heart generally closes at birth. Ovale When it fails to close, there is a direct route for gas emboli to enter the circulatory system and bypass the normal filtering that occurs in the capillary bed of the lungs. Pregnancy Diving is not recommended for those who are pregnant as the fetus absorbs nitrogen from the mother through the umbilical cord. A fetus doesn’t clear nitrogen as quickly as the mother and if nitrogen bubbles form, the bubbles may bypass the lungs through the foramen ovale and an embolus travel directly to the brain. Fetal blindness has been reported as a consequence of hyperbaric therapy for pregnant divers who developed DCI. Flying after a dive In an attempt to save fuel costs, commercial airlines set cabin pressure much lower than the pressure at sea level. This means that for those who have just completed a dive, further decompression continues as the plane ascends to cruising altitudes. Recommendations are to wait 12 hours before flying after a no-decompression dive, at least 24 hours after a decompression dive and 72 hours after hyperbaric therapy. Dehydration In a review of patients requiring hyperbaric therapy, 90% were dehydrated. Pushing fluids during diving periods is essential. Alcohol consumption Impairs judgment and can predispose to dehydration, vasodilation, and heat loss. Physical injury Scarring and alterations in local tissue may increase a divers risk. shock, pulmonary emboli and myocardial infarction from a dive.13 Presentations may include unconsciousness, represent potentially fatal cardiopulmonary complications. hemispheric deficits (motor and/or sensory), convulsions, Pain is reported in only about 30% of cases of type 2 and confusion.14 Peripheral neuropathy and pain, which DCS, and occurs most often in the abdominal and thoracic are commonly encountered in DCS, are not typically regions.7 experienced by patients suffering from AGE. Common signs and symptoms of DCS and AGE are included Arterial Gas Embolization in Table II. The most severe form of decompression illness, known as arterial gas embolization (AGE), results from pulmonary Temporal Profile of Decompression Illness barotrauma. If a diver surfaces too quickly and/or fails to The temporal profile, in relation to the most recent dive, exhale appropriately, air trapped in the lungs expands is imperative as most clinicians define DCS as the during ascent and ruptures the alveoli introducing gas emergence of signs and symptoms 10 minutes after a emboli directly into the pulmonary venous system where diver has surfaced. Symptoms of DCS develop more they are carried to the heart and then into the systemic slowly than those associated with AGE. Approximately circulation. Emboli can travel throughout the body and 50% of individuals diagnosed with DCS will develop occlude vessels, inducing damage through ischemic symptoms within 1 hour after surfacing and 90% of mechanisms and infarction.6 patients will have symptoms within 6 hours of surfacing.6 Complications from AGE are generally localized In less than 2% of cases will problems develop beyond to the cerebral circulation but, on occasion, cardiac the 24-hour, post-dive interval and it is extremely rare involvement may occur if emboli occlude coronary for symptoms of DCS to develop 48 hours after the vessels. Classically, symptoms of AGE are sudden in completion of a dive.15 Symptoms of AGE typically onset, occurring within seconds to minutes after surfacing manifest suddenly and within minutes after surfacing. 106 Clinical & Refractive Optometry 17:3, 2006 Table II Common signs and symptoms of decompression illness31 Decompression Sickness (DCS) Arterial Gas Embolization (AGE) Symptoms Symptoms Fatigue Dizziness Pruritis (skin itching) Blurred vision, loss of vision Pain in joints (shoulders, elbows, hips and knees) Sensory deficits Dizziness, vertigo, tinnitus Chest pain Numbness, paresthesias Disorientaion Shortness of breath Signs Signs Bloody froth from mouth or nose Skin rash Paralysis, weakness Paralysis, weakness Seizures Difficulty with urination Unconsciousness Personality changes, confusion Shortness of breath Amnesia Death Tremor Staggering Cough with bloody, frothy sputum Collapse or unconsciousnes Table III Ophthalmic manifestations of decompression illness27 Table IV Crucial elements of a dive history in cases of suspect DCI31 Diplopia 1. What is the dive history for the previous 48 hours? Describe Nystagmus dive times, depths, intervals between dives, symptoms before Visual field deficits or after the dive, and breathing gases. Orbicularis pain 2. Determine symptoms onset and progression after the diver Cortical blindness surfaced. Central retinal artery occlusion Optic neuropathy 3. Describe any previous medical interventions, such as oxygen Convergence Insufficiency delivery since the dive. 4. Determine extent of neurological involvement if possible. Currently, AGE is responsible for approximately 10% of 5. Describe location of all pain. cases of DCI annually. Various dive series suggest that 6. Describe and record distribution of skin rashes. recreational divers are more likely to experience more 7. Describe any traumatic injuries suffered before, during severe forms of DCI, specifically type 2 DCS and AGE, or after the dive. while the majority of DCI among professional divers tends to be type 1 DCS.16 epithelial abnormalities indistinguishable from those seen in eyes with choroidal ischemia, with these changes Ophthalmic Manifestations being attributed to decompression-induced intravascular Eye care providers rarely encounter decompression gaseous micro-emboli.21 In general, estimates of the illness in an acute setting as divers are generally well- incidence of ocular findings associated with DCS ranges educated about the signs and symptoms that warrant their from 7% to 12%.22, 23 seeking recompression therapy. However, we may see residual ocular sequelae, such as field loss or cortical Management blindness, in those cases where therapy is unsuccessful. Common sense and careful observation of dive tables are In one series, visual disturbances were identified 30% of critical in creating a safe diving environment and reducing the time in patients who developed type 2 DCS.17 The the risk of DCI. If symptoms occur within 24 hours of etiology of visual disturbances while diving are varied, surfacing, DCI should be suspected and an accurate and frequently include ultraviolet keratopathy, corneal diving history (Table IV) and a neurological assessment edema secondary to bubbles being trapped under a rigid should be obtained. Table V summarizes U.S. Naval lens, and other contact-lens related issues such as lens recommendations for determining the order and urgency of displacement and lens adherence syndrome.18-20 Other actions that need to be taken for divers experiencing DCI. ocular complications, directly associated with In cases of DCS, the initial treatment should include decompression sickness, and specifically arterial gas the administration of 100% pure oxygen. This will cause embolization, are included in Table III. Angiography oxygen levels in the body to increase significantly and in studies of divers have also documented retinal pigment those areas where nitrogen bubbles impede blood flow, Ocular and Systemic Manifestations of Decompression Illness — White, Whitaker 107 Table V Recommended protocols of care for those suspected of DCI31 Category A – Emergency Cases Symptoms: Onset typically sudden and progressively worsening. Generally occurs within an hour of surfacing from dive. Intervention: If unconscious, begin CPR and arrange for immediate evacuation. If available and the patient regains consciousness, 100% oxygen should be administered and continued until arriving at medical facility. If trained medical personnel are available intravenous fluids should be pushed. Contact DAN for advice about nearest hyperbaric chamber location. Category B – Urgent Cases Symptoms: Primary symptom is pain that is either unchanged or has only slowly progressed over several hours. Intervention: Immediately place injured diver on 100% oxygen and arrange medical transport. Continue oxygen until arriving at medical center. Push fluids by mouth. Do not administer analgesics for pain. Get detailed history and attempt to determine extent of neurological involvement. Contact DAN for advice about nearest hyperbaric chamber location. Category C – Timely Cases Symptoms: Symptoms are not obvious or have progressed slowly over a period of days. 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