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Most of the previous literature concerning otologic problems in compressed gas environments has emphasized middle ear barotrauma. With recent increases in commercial, military, and sport diving to deeper depths, inner ear disturbances during these exposures have been noted more frequently. Studies of inner ear physiology and pathology during diving indicate that the causes and treatment of these problems differ depending upon the phase and type of diving. Humans exposed to simulated depths of up to 305 meters without barotrauma or decompression sickness develop transient, conductive hearing losses with no audiometric evidence of cochlear dysfunction. Transient vertigo and nystagmus during diving have been noted with caloric stimulation, resulting from the unequal entry of cold water into the external auditory canals, and with asymmetric middle ear pressure equilibration during ascent and descent (alternobaric vertigo). Equilibrium disturbances noted with nitrogen narcosis, oxygen toxicity, hypercarbia, or hypoxia appear primarily related to the effects of these conditions upon the central nervous system and not to specific vestibular end-organ dysfunction. Compression of humans in helium-oxygen at depths greater than 152.4 meters results in transient symptoms of tremor, dizziness, and nausea plus decrements in postural equilibrium and psychomotor performance, the high pressure nervous syndrome. Vestibular function studies during these conditions indicate that these problems are due to central dysfunction and not to vestibular end-organ dysfunction. Persistent inner ear injuries have been noted during several phases of diving: 1) Such injuries during compression (inner ear barotrauma) have been related to round window ruptures occurring with straining, or a Valsalva's maneuver during inadequate middle ear pressure equilibration. Divers who develop cochlear and/or vestibular symptoms during shallow diving in which decompression sickness is unlikely or during compression in deeper diving, should be placed on bed rest with head elevation and avoidance of maneuvers which result in increased cerebrospinal fluid and intralabyrinthine pressure. With no improvement in symptoms after 48 hours, exploratory tympanotomy and repair of a possible labyrinthine window fistula should be considered. Recompression therapy is contraindicated in these cases...
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PMID:Diving injuries to the inner ear. 40 82

The U.S. Navy diving accident records of 2,500 cases for the years 1933 to 1970 were analyzed and sorted into Type I and Type II decompression sickness. Type II was further sorted into "vestibular" and "other" categories. It was concluded that Type II symptoms accounted for 30% of the decompression accidents and it was estimated that the overall incidence of vestibular symptomatology was between 10 and 20%. Nearly 30% of the Type II cases were diagnosed as having vestibular involvement, although almost 60% of the cases contained a report of a symptom typically associated with the vestibular system complex, e.g., dizziness and nausea.
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PMID:Incidence of vestibular symptomatology in 2,500 U.S. Navy diving accidents (1933-1970). 108 48

Decompression sickness (DCS) is a well-known hazard of exposure to significant variations in ambient pressure. The diagnosis and management of DCS is frequently a source of confusion. Although the majority of cases are manifested by joint or limb pains (Type I DCS), patients may present with a wide array of symptoms, such as neurologic deficits, headache, fatigue, nausea, and respiratory difficulty. A thorough knowledge of the differential diagnosis and a strong index of suspicion are crucial to the proper management of DCS. Presented herein are two cases of altitude-related DCS which were confused initially with a viral syndrome. A discussion of the symptoms of DCS is included.
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PMID:Decompression sickness presenting as a viral syndrome. 199 34

Eighteen professional divers (age range 24-33 yr, mean 28.3) participated in one simulated dive to 360 meters of seawater (msw) in a helium-oxygen (heliox) atmosphere with equal compression and decompression profiles. All divers were given an extensive neurologic examination before diving. Clinical neurologic symptoms observed during the dives were equilibrium disorder, sleep disturbances, fatigue, nausea, loose stools, stomach pain, tremor, mental disturbances, reduced appetite, and headache. Symptoms were scored individually by each diver. The symptoms were analyzed statistically by factor analysis, which grouped them into four factors. These symptoms are presumably related to functional disturbances in the brain stem and the cerebellum. Factor 3 symptoms (tremor, mental disturbances, reduced appetite) correlated significantly to a history of predive decompression sickness (P = 0.006) and to cerebral concussion (P = 0.023). Three divers were periodically unable to work at bottom due to equilibrium disorder, diarrhea, or nausea. One diver with mild polyneuropathy and slight cerebral atrophy as seen by computerized tomography and another diver with abnormal electroencephalography were periodically unable to work due to equilibrium disorder and nausea, respectively. We advocate that divers with signs of central or peripheral nervous system dysfunction should not be selected for deep diving.
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PMID:Analysis of neurologic symptoms in deep diving: implications for selection of divers. 232 22

Inner Ear Decompression Sickness (IEDCS)--manifested by tinnitus, vertigo, nausea, vomiting, and hearing loss--is usually associated with deep air or mixed gas dives, and accompanied by other CNS symptoms of decompression sickness (DCS). Early recompression treatment is required in order to avoid permanent inner ear damage. We present an unusual case of a scuba diver suffering from IEDCS as the only manifestation of DCS following a short shallow scuba dive, successfully treated by U.S. Navy treatment table 6 and tranquilizers. This case suggests that diving medical personnel should be more aware of the possible occurrence of IEDCS among the wide population of sport scuba divers.
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PMID:Inner ear decompression sickness following a shallow scuba dive. 236 97

This study concerns four cases of sinus pericranii observed at the Neurological Department of Nancy. Sinus pericranii is a direct communication between the outer surface of the skull and the intracranial venous sinuses. It may be congenital, acquired or traumatic. This abnormality, usually located in the midline and often in the frontal region, is usually symptomless, but some patients complain of headache, nausea and vertigo. Sinus pericranii shows as a fluctuating non pulsatile mass of reddish or bluish colour, expanding when the patient bends his head down. Radiography usually shows one or several bone defects opposite the lesion found at CT bone window. On soft tissue window the mass is not calcified and usually enhanced by contrast injection. It is sometimes possible to visualize the vascular communication between the extracranial region and the underlying dural sinus. When visualization is blurred, or CT shows intracerebral abnormalities, MRI examination is required. Angiography with subtraction in venous phase (40 to 60 seconds after the injection), sometimes aided by films taken in head down position. It is of interest only in cases where CT and MRI have shown associated vascular abnormalities. Otherwise, direct injection of contrast medium into the malformation makes it possible to assert the diagnosis of sinus pericranii and to determine the flow rate within the malformation, which to some extent commands the the therapeutic technique. In patients with small and asymptomatic sinus pericranii absention is the rule. When the sinus is of moderate size, and the flow rate not rapid and when there is no significant communication with the cerebral veins, endovascular sclerosis may be advocated. In all other cases, surgical removal is recommended and is usually easy.
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PMID:[Pericranial sinus]. 919 Mar 68

Although diving with compressed air is generally safe, neurological problems resulting from infarction in SCUBA diving are well known, including arterial gas embolism and decompression sickness (caisson's disease, bends) involving the brain and spinal cord. While air gas embolism forms the overwhelming majority of causes for stroke in divers, internal carotid artery (ICA) dissection is another potential mechanism for central nervous system infarction in the setting of SCUBA diving. A 38 year-old female, who presented with complaints of headache, nausea, vomiting, and left sided hemiparesis after rapid ascent to the surface from a depth of 120 feet of seawater was initially treated for decompression illness in a hyperbaric chamber. Further neurological workup revealed a right ICA dissection. This case demonstrates the dangers of ICA dissection following rapid ascent to the surface from underwater and emphasizes an interesting presentation of stroke associated with SCUBA diving.
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PMID:Internal carotid artery dissection in stroke from SCUBA diving: a case report. 1267 Jan 19

A 27-year-old flight instructor experienced 5 to 10 minutes after a scuba-dive to 29 m, which lasted totally 50 minutes, dizziness, nausea and severe vertigo. The symptoms lasted about an hour. The patient vomited several times and noted sudden onset headache and vertigo lasting the following three days. Hyperbaric oxygen therapy was started 30 hours after the event because decompression sickness was suspected. Transthoracic echocardiographic evaluation showed a patent foramen ovale. Diving accidents may be caused by decompression sickness, the formation of a free intravascular gas phase (bubbles) may result in transatrial shunting in the presence of a patent foramen ovale and may lead to neurological signs and symptoms. In this context the diver was advised to undergo closure of the atrial septal defect. Five months after the incident the patient underwent successful transcatheter occlusion of the PFO.
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PMID:[Severe vertigo after a scuba-dive to 29 meters]. 1517 13

We describe the first case of Weber's Syndrome to present as a manifestation of decompression illness in a recreational scuba diver. Weber's Syndrome is characterized by the presence of an oculomotor nerve palsy and contralateral hemiparesis. The patient was a 55 year-old male with a past medical history of a pulmonary cyst, in whom symptoms developed after a multilevel drift dive to a depth of 89 feet for 53 minutes, exceeding no-decompression limits. Symptom onset was within 30 minutes of surfacing and included the Weber's Syndrome, a sixth nerve palsy, dizziness, nausea, sensory loss, and ataxia. The patient received four U.S. Navy Treatment Tables with complete resolution of all neurological signs and symptoms. The mechanism of injury remains unclear, but may involve aspects of both air gas embolism and decompression sickness. Individuals with pre-existing pulmonary cysts may be at increased risk for dive-related complications.
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PMID:Weber's syndrome and sixth nerve palsy secondary to decompression illness: a case report. 1592 1

Ischemic colitis (IC) secondary to air embolism from decompression sickness or barotrauma during diving is an extremely rare condition. After extensive review of the available literature, we found that there has been only one reported case of IC secondary to air embolism from diving. Although air embolization from diving and the various medical complications that follow have been well documented, the clinical manifestation of IC from an air embolism during diving is very rare and thus far unstudied. Common symptoms of IC include abdominal pain, bloody or non-bloody diarrhea or nausea or vomiting or any combination. Emergency physicians and Critical Care specialists should consider IC as a potential diagnosis for a patient with the above-mentioned symptoms and a history of recent diving. We report a case of IC from air embolism after a routine dive to 75 feet below sea level in a 53-year-old White female who presented to a community Emergency Department complaining of a 2-day history of diffuse abdominal pain and nausea. She was diagnosed by colonoscopy with biopsies and treated conservatively with antibiotics, bowel rest, and a slow advancement in diet.
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PMID:Acute ischemic colitis secondary to air embolism after diving. 2209 77


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