Introduction
Dysbarism is defined as any harmful medical disease brought on by variations in the surrounding pressure. These pressure shifts must occur either more frequently or for longer than the body can safely adjust. Decompression sickness (DCS), nitrogen narcosis (NN), high-pressure neurological syndrome (HPNS), barotrauma, and arterial gas emboli (AGE) are all included under the broad term dysbarism.
What Are the Causes of Dysbarism?
Although diving underwater is the most prevalent cause of dysbarism, any setting with significant pressure changes can result in dysbaric damage. High altitude, decompression of airplane cabins, explosions or blasts, space travel, caissons, and tunnel-boring operations are just a few examples.
What Are the Types and Pathophysiology of Dysbarism?
Since the majority of the human body is made up of water, which is only slightly compressible, pressure changes rarely have an immediate impact on these parts of the body. The structures impacted by barotrauma (injury to the body due to change in the air or water pressure) are those that are air-filled, such as the lungs, sinuses, middle ear, gas in the bowels, and cavities in the teeth. When these structures are blocked, high-pressure air will push on the tissues around the low-pressure area, which can result in tissue damage when the pressure gradient exceeds the tensile strength of the tissues involved. Normally, these structures are connected to the outside to allow for free air exchange.
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Squeeze Injuries: When a diver has sinus or nasal congestion or a nasal polyp that restricts the openings to the sinuses or the eustachian tubes, they may get sinus or middle ear barotrauma, often known as squeeze injuries. As a result, pressure is not equalized. Teeth are also susceptible to this condition. The condition is then referred to as barodontalgia. When flying, it can happen during descent but happens more frequently during ascent. There are numerous etiologic theories. If a loose crown, gas pockets following dental surgery, or bacterial decay are present, it can harm the tympanic membrane and cause transudation or bleeding into the middle ear. When there is a rapid pressure difference between the inner ear and the middle ear, which causes the round or oval window to burst, middle-ear barotrauma may occasionally be linked with inner-ear barotrauma. Labyrinthine fistulas (abnormal communication between the inner ear and surrounding structures) or perilymph leaks (a hole or tear in the membrane separating the middle ear and inner ear) could occur from this. The Valsalva maneuver (breathing technique) is most frequently used when the eustachian tube is obstructed in a patient. Due to the blockage, this 'block and lock' scenario results in no change in middle ear pressure, but it raises the perilymph pressure in the cochlea and causes the round or oval window to rupture.
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Decompression Sickness (DCS): DCS (commonly known as 'the bends') occurs when divers ascend too quickly and do not make the appropriate decompression stops. The blood and tissues (most frequently the spine, nerves, joints, and skin) contain bubbles made of dissolved inert gas (nitrogen) that have broken free from the solution. According to Henry's Law, the amount of gas that dissolves into liquid is precisely proportional to the partial pressure of that gas if the temperature is constant. When diving, the higher partial pressure leads to a gradual rise in the amount of nitrogen that dissolves in tissue, and the elevated undersea pressure maintains the gas in the solution. If a diver emerges too rapidly, their nitrogen escapes the solution and generates bubbles, much like when a person quickly opens a carbonated drinks bottle, and the rapid fall in pressure results in bubble production.
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Nitrogen Narcosis: When the partial pressure of nitrogen is greater than what is experienced when inhaling compressed air at 100 feet of seawater (FSW), nitrogen narcosis (also known as the 'rapture of the deep') develops. Anesthesia, disorientation, poor vision, changes in behavior or attitude, and other signs and symptoms similar to intoxication are caused by the elevated nitrogen partial pressure in neural tissue. When divers descend deeper than 300 FSW, the symptoms typically worsen with depth and frequently result in hallucinations and loss of consciousness. Divers who have recently consumed alcohol, are hypercarbic, hypothermic, or exhausted are particularly vulnerable. On ascension to a shallower depth, symptoms resolve quickly. Divers who are exposed repeatedly can develop a tolerance.
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Helium Tremors: HPNS (high-pressure neurological syndrome, sometimes called helium tremors) is a dysbarism that happens while a diver is breathing a helium-oxygen mixture and occurs below 500 FSW. It is characterized by neurological, psychological, and EEG problems such as tremors, somnolence, myoclonic jerks, motion sickness, vertigo, and reduced mental function. Although the precise process is not yet obvious, it seems to be connected to the compression effect of pressure on the lipid component of CNS (central nervous system) cell membranes and its effects on transmembrane proteins, membrane surface receptors, and ion channels. Neurotransmitters (including dopamine, serotonin, and acetylcholine), anesthetic gasses, neuronal calcium ions, and genetics all seem to play a part in the pathophysiology of the HPNS.
What Are the Clinical Manifestations of Dysbarism?
It is crucial to keep in mind that how the results of the physical examination and history are presented is frequently unclear and subject to change. Focus on the dive and symptom history during the interview after taking a history. Asking about a diver's diving history involves finding out about their frequency, depth, history of quick ascent or other issues during a dive, level of experience, equipment quality, and history of decompression diseases.
Inquire about the patient's history of symptoms, focusing on the time that the symptoms initially appeared. Barotrauma can be distinguished from gas toxicity and decompression syndrome based on the stage of the dive at which symptoms start to appear. Gas toxicity will be most pronounced at depth, barotrauma is more likely to happen on descent, and decompression illness (DCI) typically happens during or right after ascent. While DCS symptoms typically take hours to manifest, AGE (arterial gas embolism) signs show up within a few minutes of emergence. The kind of symptoms can also be used to distinguish between AGE and DCS. AGE typically manifests as pulmonary and brain issues. DCS more frequently manifests as spinal cord and joint involvement.
Past medical history and risk factors for dysbarisms, such as dehydration, URI (upper respiratory infections), allergies, a high workload, poor fitness, and advancing age, are additional issues to address. An ear, lung, skin, joint, and neurological evaluation should be included in a physical examination. Numerous people with minimal DCS will have normal vitals, an examination, and a mental state. Significant neurological abnormalities, such as paralysis, may be present in more severe cases. Look for otic (ear) or pulmonary barotrauma during the ear and pulmonary exam. It is necessary to perform a thorough neurologic examination in order to detect any hidden signs of harm to the cranial nerves, motor, sensory, reflexes, vestibular, cerebellar, and mental status.
How Is Dysbarism Evaluated?
In general, diagnostic tests like blood work and imaging are not very helpful in making a diagnosis, although they can help rule out alternative possibilities. A chest X-ray could reveal barotrauma or signs of near-drowning. When thinking about recompression therapy, it is crucial to rule out pneumothorax. Typically normal, CT (computed tomography) and MRI (magnetic resonance imaging) scans may be useful in identifying additional reasons for the patient's symptoms. Rarely, air concentrations in artery branches may be visible on a brain CT or MRI. Hemoconcentration or increased CPK - creatine phosphokinase (in the presence of AGE) may be found in laboratory tests.
How Is Dysbarism Treated?
These dysbarisms typically show delayed and hazy signs. It is crucial to have a low threshold for treatment as a result. The precise diagnosis of DCI is frequently not made until a therapeutic response is observed.
In the emergency context, the first step in treating DCI is to evaluate and stabilize the airway, breathing, and circulation. Early 100 percent oxygen administration should begin, and the nearest hyperbaric facility should be contacted. In-water recompression is risky and needs a lot of sophisticated preparation and equipment; it should always be done in a hyperbaric chamber. These treatments will lessen bubble size, stop tissue ischemia (reduced blood flow), and lessen ischemia-reperfusion harm (tissue damage when the blood supply returns).
Management of tympanic membrane rupture includes enabling drainage and maintaining a dry ear canal. Except in cases where an infection manifests, ear drops are not advised. The patient has to see an otolaryngologist (ENT doctor) again. Since the holes normally heal within six weeks, no additional treatments are frequently required. Membrane grafting is rarely required.
Treatment for middle ear barotrauma and inner ear barotrauma are identical. The patient must refrain from blowing their nose throughout treatment. Both rest and anti-vertiginous drugs are beneficial. Hyperbaric oxygen (HBO) recompression and oxygen are not indicated for middle ear barotrauma or inner ear barotrauma unless the patient additionally exhibits symptoms of DCS or AGE.
Conclusion
A small fraction of people experience dysbarism, yet it is a widespread issue that a few doctors are prepared to identify and treat. Even while its symptoms are frequently moderate, the most severe forms of it can nevertheless result in lifelong harm, especially if it is not identified or treated properly. On the basis of the patient's clinical and medical history, the emergency physician must be trained to suspect dysbarism and treat these diseases.
