The Bends: How Long Should You Wait Before Diving After DCS?

ANSWER: With the information you have provided, my answer has to be “it depends”. There are different levels of seriousness to “getting bent.” One end of the spectrum includes simple joint pain that resolves completely with treatment or even symptoms that are vague and may or may not truly be decompression sickness (DCS). At the other end are serious cases of decompression sickness that include neurological symptoms like numbness or even paralysis. You also need to take into account whether the hit is explained by the dive profile.

What It’s Like To Get An Unexplained Hit

The treatment for decompression sickness, while somewhat time and labor intensive, is relatively benign enough that all diving medical officers are certain that we have occasionally treated people who did not really have decompression sickness. There is no blood test or alternate method of making the diagnosis other than having an individual who recently completed a diver presenting with the right symptoms.

The U.S. Navy policy is for a return to diving after 30 days for severe decompression sickness or air embolism (AGE) that completely resolves with treatment. The time period is shorter for pain only DCS. Of course this recommendation is for professional divers who are paid extra to dive and are typically in excellent physical condition. The time period should be doubled for most recreational divers and a thorough medical evaluation prior to a return to diving is recommended. Diving more conservative profiles is a valid recommendation for the future and in cases of serious DCS or AGE without a provocative dive profile, the diver should consider being evaluated for a patent foramen ovale.

Traditionally decompression sickness (DCS) has been divided into two categories, Type I or mild DCS and Type II or severe DCS. Type I DCS has also been known as “pain only” DCS and, as the name implies, there is typically joint pain and/or muscle soreness and possibly even some perceived numbness/tingling but otherwise no neurological deficits. More severe DCS includes cases with significant neurological deficits such as bowel and bladder control issues, neurological issues that appear to have spinal cord involvement, and in extreme cases cardiovascular collapse (also known as “the chokes”).

While very minor symptoms of DCS may go away with just rest and over the counter pain medications, it is thought that treatment with recompression and oxygen is ideal to prevent any possible long term effects from the injury. For cases of severe DCS, recompression therapy using hyperbaric oxygen is critical and should not be delayed. Many clinical studies have demonstrated that a delay prior to treatment results in the need for more aggressive therapy and increases the chances of having incomplete resolution of symptoms.

Treatment of decompression sickness with hyperbaric oxygen (HBO) has few associated risks but is both time and labor intensive. Because of this, physicians who treat divers have a low threshold for initiating treatment. Distinguishing between pain due to trauma during the dive and pain from mild DCS can be very difficult. There is even a phenomenon that occurs when the weight belt presses on some nerves in the hips, giving the diver numbness down the thighs. The treating physician should take a very detailed history regarding the dive if time allows. Divers who present with symptoms of decompression sickness shortly after completing a dive will likely receive treatment as there is more concern for under-treatment than over-treatment.

If there is incomplete resolution of symptoms after treatment has been completed, a return to diving should be discouraged. Returning to diving after complete resolution of mild DCS is appropriate after a brief recovery period of a few weeks. With complete resolution of symptoms of severe DCS, a longer interval is recommended. It is highly recommended that a diver who suffers a severe “hit” discuss the dive profile and initial symptoms with an expert who can offer some insight on the incident. It should be mentioned however that decompression sickness can occur despite a dive profile that is well within table or computer no decompression limits. In cases where a diver suffers severe decompression symptoms after a seemingly very benign dive, further evaluation and possibly an echocardiogram to check out the heart anatomy would be worthwhile.

Decompression Sickness and Scuba Diving • Scuba Diver Life

What is decompression sickness?

When we breathe underwater, approximately 79 percent of the air (depending on the gas blend) we’re breathing is nitrogen. As we descend deeper, the pressure around our bodies increases, causing our body tissue to absorb nitrogen.

Doctors use the term decompression sickness, or “the bends” to describe the illness and effects that result from a reduction in the ambient pressure surrounding the human body.

As long as the diver remains at pressure, the gas presents no problem. If the pressure is reduced too quickly, however, the nitrogen comes out of solution and forms bubbles in the tissues and bloodstream. This commonly occurs as a result of violating or approaching too closely the dive-table limits, but it can also occur even when accepted guidelines have been followed. (Like in the video above)

Bubbles forming in or near joints are the presumed cause of the joint pain of a classical “bend.” When high levels of bubbles occur, complex reactions can take place in the body, usually in the spinal cord or brain. Numbness, paralysis and disorders of higher cerebral function may result. If great amounts of decompression are missed and large numbers of bubbles enter the venous bloodstream, congestive symptoms in the lung and circulatory shock can then occur.

Doctors diagnose DCS on the basis of signs and/or symptoms after a dive or altitude exposure.

Two Types of DCS

Type 1: Type 1 DCS is the least serious form of DCS. It usually involves pain in the body and is usually not life threatening. It is important to understand that type 1 DCS can be part of the warning signs for type 2 DCS.

• Cutaneous Decompression Sickness
  This occurs when nitrogen bubbles come out of solution in skin capillaries, resulting in a rash, often near the chest and shoulders.
• Joint and Limb Pain Decompression Sickness
  Aching and/or pain in the joints characterize type 1 DCS. The pain can be in one place or it can move around the joint.

Type 2: Type 2 DSC is more serious and can be life threatening, usually affecting the nervous system.

• Neurological Decompression Sickness
  When nitrogen bubbles affect the nervous system they can cause problems throughout the body. This type of decompression sickness normally shows as tingling, numbness, respiratory problems and unconsciousness. Symptoms can spread quickly and, if left untreated, can lead to paralysis or even death.
• Pulmonary Decompression Sickness
  This is a rare form of decompression sickness that occurs when bubbles form in lung capillaries. Fortunately, the bubbles dissolve naturally through the lungs most of the time. However, it is possible for them to interrupt blood flow to the lungs which can lead to serious and life-threatening respiratory and heart problems.
• Cerebral Decompression Sickness
  It is possible for bubbles that make their way into the arterial blood stream, move to the brain, and cause an arterial gas embolism. This is extremely dangerous and can be identified by symptoms such as blurred vision, headaches, confusion and unconsciousness.

Symptoms of DCS

• Extreme fatigue
• Joint and limb pain
• Tingling
• Numbness
• Red rash on skin
• Respiratory problems
• Heart problems
• Dizziness
• Blurred vision
• Headaches
• Confusion
• Unconsciousness
• Ringing of the ears
• Vertigo
• Stomach sickness

Signs of DCS

• Skin may show a blotchy rash
• Paralysis, muscle weakness
• Difficulty urinating
• Confusion, personality changes, bizarre behavior
• Amnesia, tremors
• Staggering
• Coughing up bloody, frothy sputum
• Collapse or unconsciousness

**Symptoms and signs usually appear within 15 minutes to 12 hours after surfacing. In severe cases, symptoms may appear before surfacing or immediately afterwards. Delayed occurrence of symptoms is rare, but it does occur, especially if air travel follows diving.

Preventing Decompression Sickness

You can help minimize the risk of DSC by using a dive planner or a dive computer properly. You also need to follow other dive-safety practices that you should have learned in your scuba training.

Factors to consider when diving

• Never dive to the limits. Always have a margin before you hit your dive/table limit.
• Fat: Nitrogen dissolves easily into fat tissue. People with a larger ration of fat to body weight may absorb more nitrogen when diving.
• Age: As you get older, your circulatory system becomes less efficient, affecting nitrogen elimination.
• Alcohol: Any type of alcohol before or right after a dive can accelerate and alert your circulation.
• Cold Water: Diving in cold water can cause your extremities to receive less circulation as they cool, which effects nitrogen elimination.
• Hot shower/bath: Hot showers and baths after a dive cause capillaries to dilate, which will draw blood away from other areas. These areas will then eliminate nitrogen more slowly.

Molecular Changes in White Blood Cells May Help Diagnose ‘the Bends’ in Scuba Divers

A new study headed by researchers at the University of Malta claims to be the first to investigate gene expression changes in scuba divers with decompression sickness (DCS), a potentially deadly condition that is also known as “the bends.” The study results point to the upregulation of genes involved in inflammation and white blood cell activity in DCS, and could lead to the identification of biomarkers that will help doctors to diagnose the condition more precisely.

“We showed that decompression sickness activates genes involved in white blood cell activity, inflammation, and the generation of inflammatory proteins called cytokines,” explained Nikolai Pace, PhD, who is the corresponding author of the team’s published paper in Frontiers in Physiology. “Basically, decompression sickness activates some of the most primitive body defense mechanisms that are carried out by certain white blood cells.” Pace and colleagues described their findings in a report titled, “Acute effects on the human peripheral blood transcriptome of decompression sickness secondary to scuba diving.”

Decompression sickness is a potentially lethal condition that can affect divers. Symptoms include joint pain, a skin rash, and visual disturbances, and in some individuals, the condition can be so severe that it leads to paralysis and death. Researchers have known about “the bends” for more than 100 years—a paper published in 1908 correctly hypothesized the involvement of gas bubbles forming in blood and tissue because of a decrease in pressure—but we still understand relatively little about its physiological basis. Animal studies have suggested that inflammatory processes may have a role in decompression sickness, but no one had previously studied this in humans.

Divers have developed methods, such as controlled ascents, to reduce the risk of DCS, but for suspected cases, there is no definitive diagnostic test, and clinicians instead rely on observing symptoms and seeing whether patients respond to hyperbaric oxygen (HBO) therapy, which involves breathing oxygen at high pressures. While HBO resolves the symptoms in 80–90% of cases, the authors also noted that the effects may be long-lasting, and “ … victims may suffer from long-term sequelae.” DCS involving the spinal cord is particularly challenging to treat, they pointed out, and may result in permanent paraplegia or paraparesis, bladder dysfunction and incontinence, and sexual dysfunction. However, they continued, “The search for new treatments for DCS as adjuncts to HBO and fluid resuscitation has so far been largely unsuccessful.”

Studying the transcriptome of divers could feasibly provide new insights into gene expression changes and pathophysiologic pathways and mechanisms that drive DSC. “Potentially, this can serve as a stepping stone towards the identification of novel biomarkers or druggable targets,” the investigators suggested. Animal models have already demonstrated upregulation of proinflammatory signaling molecules in DCS. But, while uneventful diving and DCS can both trigger changes in the peripheral blood transcriptome, distinguishing physiological responses from pathological changes in humans remains “a major challenge.” And as the scientists continued, “To the best of our knowledge, no study has evaluated a DCS-induced transcriptomic signature in humans.”

To investigate transcriptomic changes associated with decompression sickness, the researchers took blood samples from seven divers who had been diagnosed with DCS after a deep dive, and from another six divers who had completed a dive without developing any signs of DCS. Blood samples were taken from each of the divers at two distinct times, first within 8 hours of their emerging from the water, and again 48 hours afterward, when the divers with decompression sickness had undergone hyperbaric oxygen treatment. The team performed RNA sequencing analysis to measure gene expression changes in white blood cells, and relate their functions to biological pathways. The results showed that in DCS cases there was an enrichment of transcripts involved in acute inflammation, activation of innate immunity and free radical scavenging pathways, “… with specific upregulation of transcripts related to neutrophil function and degranulation,” the team wrote. “We show that cutaneous DCS elicits the differential expression of several transcripts involved in leukocyte activity, inflammation, and cytokine production, with prominent perturbation of genes in the PI3K-AKT and TLR pathway. In fresh DCS cases within 8 hours of surfacing from diving, upregulated transcripts are characteristic of the leukocyte myeloid lineage—specifically granulocytes.”

Interestingly, the DCS-induced transcriptomic changes were reversed at the second time-point, after the individuals had received hyperbaric oxygen therapy. The team said the findings provide a first step towards potentially developing a diagnostic test for decompression sickness, and may also point to new treatment targets. “To the best of our knowledge, this is the first study that evaluates DCS-induced transcriptomic alterations in man,” they commented. “This study sheds light on the inflammatory pathophysiology of DCS and the associated immune response. Such data may potentially be valuable in the search for novel treatments targeting this disease.”

“We hope that our findings can aid the development of a blood-based biomarker test for human decompression sickness that can facilitate diagnosis or monitoring of treatment response,” said co-author Ingrid Eftedal, PhD, of the Norwegian University of Science and Technology. “This will require further evaluation and replication in larger groups of patients.”

Neurological Complications of Scuba Diving

HERBERT B. NEWTON, M.D., Ohio State University Hospitals, Columbus, Ohio

Am Fam Physician. 2001 Jun 1;63(11):2211-2218.

 
See patient information handout on complications of scuba diving, written by the author of this article.

Recreational scuba diving has become a popular sport in the United States, with almost 9 million certified divers. When severe diving injury occurs, the nervous system is frequently involved. In dive-related barotrauma, compressed or expanding gas within the ears, sinuses and lungs causes various forms of neurologic injury. Otic barotrauma often induces pain, vertigo and hearing loss. In pulmonary barotrauma of ascent, lung damage can precipitate arterial gas embolism, causing blockage of cerebral blood vessels and alterations of consciousness, seizures and focal neurologic deficits. In patients with decompression sickness, the vestibular system, spinal cord and brain are affected by the formation of nitrogen bubbles. Common signs and symptoms include vertigo, thoracic myelopathy with leg weakness, confusion, headache and hemiparesis. Other diving-related neurologic complications include headache and oxygen toxicity.

Recreational scuba diving, which is defined as pleasure diving without mandatory decompression to a maximum depth of 130 ft, has become a popular activity in the past 20 years. In the United States alone, there are almost 9 million certified divers.1 Although divers are concentrated along coastal regions, many others dive in inland lakes, streams, quarries and reservoirs, or fly to distant dive sites. Physicians practicing almost anywhere in the United States may see a patient with a dive-related injury or complaint.

In general, severe injury and death are uncommon in recreational diving accidents.1–5 The Divers Alert Network1 reports an average rate of 90 fatalities per year since 1980. Each year, between 900 and 1,000 divers are treated with recompression therapy for severe dive-related complications. In many of these patients, one or more of the major symptoms are neurologic in origin. The nervous system is frequently involved in dive-related complications and fatalities.5 Physicians need to be aware of the broad spectrum of neurologic injuries that can occur during dive accidents to ensure early recognition, accurate diagnosis and appropriate therapy.

Dive-Related Barotrauma

During descent and ascent in the water, the diver is constantly exposed to alterations of ambient pressure. Barotrauma refers to tissue damage that occurs when a gas-filled body space (e.g., lungs, middle ear) fails to equalize its internal pressure to accommodate changes in ambient pressure.2–4 The behavior of gasses at depth is governed by Boyle’s law: the volume of a gas varies inversely with pressure.6 During descent, as ambient pressure increases, the volume of gas-filled spaces decreases unless internal pressure is equalized. If the pressure is not equalized by a larger volume of gas, the space will be filled by tissue engorged with fluid and blood. This process underlies the common “squeezes” of descent that affect the middle ear, external auditory canal, mask, sinuses and teeth.

OTIC AND SINUS BAROTRAUMA

Barotrauma to the middle or inner ear can occur during the descent or ascent phases of the dive and may cause vertigo and other neurologic symptoms.2–5,7 Middle ear barotrauma of descent is the most common type of diving injury and may involve hemorrhage and rupture of the tympanic membrane. Symptoms include the acute onset of pain, vertigo and conductive hearing loss that lateralizes to the affected side during the Weber’s test. In severe cases (usually during ascent), increased pressure in the middle ear can cause reversible weakness of the facial nerve and Bell’s palsy (facial baroparesis).8

Vertigo can also be induced if barotrauma differentially affects the two vestibular organs (alternobaric vertigo). The vertigo resolves after pressure equalization occurs. Treatment of middle ear barotrauma involves decongestants (e.g., intranasal oxymetazoline, oral pseudoephedrine), antihistamines, analgesics and antibiotics (amoxicillin-clavulanate [Augmentin] in a dosage of 500/125 mg three times per day or clindamycin [Cleocin] in a dosage of 300 mg three times per day for 10 to 14 days) in patients with otorrhea and perforation.2,4,7

Inner ear barotrauma also can develop in patients with middle ear barotrauma.2–5,7 A pressure gradient between the perilymph of the inner ear and the middle ear cavity can occur, causing rupture of the labyrinthine windows (round and oval) and leakage of perilymph into the middle ear (i.e., fistula). Symptoms include the acute onset of vertigo, sensorineural hearing loss, tinnitus, nausea and emesis. The Weber’s test will lateralize to the unaffected side in this group of patients. Reducing intracranial and perilymphatic pressures through bed rest, head elevation and with stool softeners can help. Surgical exploration may be necessary for repair of the fistula if conservative treatment is ineffective within five to 10 days (i.e., the symptoms persist or worsen).

PULMONARY BAROTRAUMA

Pulmonary barotrauma is the most severe form of barotrauma and occurs during ascent.2–4,9 In accordance with Boyle’s law, as the ambient pressure is reduced during ascent, gas inside the lungs will expand in volume.6 If the expanding gas is not allowed to escape by exhalation, the alveoli and surrounding tissues will tear. The most common cause of pulmonary barotrauma among recreational divers is breath holding. Other causes are related to pulmonary obstructive diseases, such as asthma or bronchitis, which can lead to the trapping of gas. Several forms of pulmonary barotrauma can develop, including mediastinal emphysema, subcutaneous emphysema, pneumothorax and arterial gas embolism. Arterial gas embolism is the most dangerous form of pulmonary barotrauma and accounts for nearly one fourth of fatalities per year among recreational divers.3 In addition, it is the only form in which neurologic symptoms predominate over pulmonary symptoms.9

Arterial gas embolism develops when free air enters the pulmonary vasculature and is carried to the heart and arterial circulation.9,10  A large proportion of air bubbles can reach the brain, occlude blood vessels and cause stroke-like events. The most common signs and symptoms of arterial gas embolism are neurologic (Table 12,4,6,7), although pulmonary symptoms may also be present. In more than 80 percent of patients, symptoms develop within five minutes of reaching the surface, but they also can occur during ascent or after a longer surface interval.

View/Print Table

TABLE 1

Presenting Signs and Symptoms in Patients with Arterial Gas Embolism

TABLE 1

Presenting Signs and Symptoms in Patients with Arterial Gas Embolism

Almost two thirds of patients with arterial gas embolism have alterations of consciousness (i.e., coma or obtundation). Seizures, focal motor deficits, visual disturbances, vertigo and sensory changes are also common. Spinal cord lesions occur less frequently. Many patients show initial improvement within minutes to hours, secondary to partial clearance of air emboli. Magnetic resonance imaging (MRI) may demonstrate focal lesions in the brain after arterial gas embolism.10  Arterial gas embolism can mimic decompression sickness, and the presentation of the two syndromes may be clinically indistinguishable (Table 21–5,7–10).2,4,6 Arterial gas embolism and decompression sickness can develop simultaneously in some patients. In fact, the air emboli of arterial gas embolism may act as a nidus, or “seed,” to precipitate decompression sickness. Therefore, the two syndromes are often described and treated together using the more global term, decompression illness.4

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TABLE 2

Clinical Features, Dive Profile and Treatment of the Neurologic Complications of Scuba Diving

TABLE 2

Clinical Features, Dive Profile and Treatment of the Neurologic Complications of Scuba Diving

Treatment of arterial gas embolism consists of basic or advanced cardiac life support, 100 percent oxygen, rehydration and transport to a recompression facility.2,4,9,10

Oxygen reduces ischemia in affected tissues and accelerates the dissolution of air emboli. Seizures, arrhythmias, shock, hyperglycemia and pulmonary dysfunction should be treated, if present. Recompression therapy should be initiated immediately, using the United States Navy (USN) Table 6 algorithm.2–5,10,11 Recompression therapy reduces the size of air bubbles by increasing ambient pressure, expedites passage of emboli through the vasculature and re-establishes blood flow to ischemic tissues.

Decompression Sickness

Decompression sickness is caused by the release of inert gas bubbles (usually nitrogen) into the bloodstream and tissues after ambient pressure is reduced.2–5,10 At depth, the partial pressures of gasses in the breathing mixture increase in proportion to the ambient pressure, according to Dalton’s law.6 Although oxygen is actively metabolized, nitrogen is inert and becomes dissolved in body tissues until saturation, proportional to the ambient pressure as defined by Henry’s law.6 The propensity for the formation of nitrogen bubbles depends on the depth of the dive, the length of time at depth and the rate of ascent. If ambient pressure is released too quickly, the dissolved nitrogen gas that cannot remain in solution will form air bubbles within the blood, interstitial fluids and organs (Figure 1).

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FIGURE 1.

Experimental preparation of decompression illness (i.e., cerebral decompression sickness and arterial gas embolism) demonstrating the presence of bubbles passing within vasculature of the cortical subarachnoid space (arrow). Note the regions of surface hemorrhage (upper right) on surrounding gyri.

FIGURE 1.

Experimental preparation of decompression illness (i.e., cerebral decompression sickness and arterial gas embolism) demonstrating the presence of bubbles passing within vasculature of the cortical subarachnoid space (arrow). Note the regions of surface hemorrhage (upper right) on surrounding gyri.

Decompression sickness is traditionally classified into type I and type II. In type I decompression sickness, symptoms are usually mild and may manifest as fatigue or malaise (i.e., constitutional decompression sickness) or may be more specific, involving the muscles, joints and skin.10 Type II decompression sickness is more severe and can affect the lungs, vestibular apparatus and the nervous system.

In inner ear and neurologic decompression sickness, the formation of bubbles affects the brain, spinal cord, cranial and peripheral nerves, and the neural vasculature. Nitrogen bubbles can injure neural tissues by mechanical disruption, compression, vascular stenosis or obstruction, and activation of inflammatory pathways (e.g., cytokines, complement).4,10 Cerebral decompression sickness (30 to 40 percent of cases) usually involves arterial circulation, while spinal cord decompression sickness (50 to 60 percent of cases) involves obstruction of venous drainage and the formation of bubbles within the cord parenchyma.12

The incidence of decompression sickness among recreational scuba divers is estimated to be one case per 5,000 to 10,000 dives.1 Diving within the limits of dive tables is no guarantee against decompression sickness, because more than 50 percent of cases of decompression sickness occur after no-decompression dives. In addition to the dive profile and rate of ascent, other factors may influence the risk of decompression sickness, including hypothermia, fatigue, increased age, dehydration, alcohol intake, female gender, obesity and patent foramen ovale.2–5,13

In type II neurologic decompression sickness, more than 50 percent of patients develop symptoms within one hour of ascent; within six hours, 90 percent of divers are symptomatic.1,4,14  Inner ear decompression sickness presents with acute vertigo, nausea, emesis, nystagmus and tinnitus. The pathophysiology remains unclear; one mechanism is bubble rupture of the intraosseous membranes in the semicircular canals. In many cases, inner ear decompression sickness is clinically indistinguishable from otic barotrauma, although the dive profile and timing of symptoms may help to clarify the diagnosis (Table 2).2–5,7,10

Neurologic decompression sickness can present with a wide spectrum of symptoms (Table 3). The most severe presentation is partial myelopathy referable to the thoracic spinal cord.10,15 Patients complain of paresthesias and sensory loss in the trunk and extremities, a tingling or constricting sensation around the thorax, ascending leg weakness ranging from mild to severe, pain in the lower back or pelvis and loss of bowel and/or bladder control. The neurologic examination will often reveal monoparesis or paraparesis, a sensory level and sphincter disturbances. However, neurologic examination also may be normal.

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TABLE 3

Presenting Signs and Symptoms in Patients with Decompression Sickness

TABLE 3

Presenting Signs and Symptoms in Patients with Decompression Sickness

Pathologic features within the spinal cord include hemorrhagic infarctions, edema, bubble defects, axonal degeneration and demyelination (Figure 2).12,15 Cerebral decompression sickness can occur alone or in combination with spinal decompression sickness and manifests as an alteration of mentation or confusion, weakness, headache, gait disturbance, fatigue, diplopia or visual loss. The neurologic examination may show hemiparesis, dysphasia, gait ataxia, hemianopsia and other focal signs. Behavioral and cognitive aspects of cerebral decompression sickness may be persistent or slow to improve.10,16 The pathologic features are similar to those of spinal decompression sickness, although not as pronounced.10,17

The rightsholder did not grant rights to reproduce this item in electronic media. For the missing item, see the original print version of this publication.

FIGURE 2.

The diagnosis of neurologic decompression sickness is clinical and should be suspected in any patient with a recent history of diving who has a consistent presentation. Neuroimaging studies may further clarify the diagnosis but should not delay treatment. MRI demonstrates high-signal lesions of the brain and spinal cord in 30 to 55 percent of cases (Figure 3), which suggests ischemia, edema and swelling. The lesions do not enhance with contrast. However, images on MRI are often normal.5,10,16

The rightsholder did not grant rights to reproduce this item in electronic media. For the missing item, see the original print version of this publication.

FIGURE 3.

The initial management of neurologic decompression sickness is similar to that of arterial gas embolism and decompression illness, and requires transport to a recompression facility.2–5,10,16 If transport by helicopter is necessary, the patient should be flown at an altitude of less than 1,000 ft to minimize exacerbation of symptoms. The definitive treatment is recompression therapy using the USN Table 6 algorithm.11 USN Table 6 consists of initial recompression to 60 ft of salt water with 100 percent oxygen for 60 minutes. The patient is then decompressed to 30 ft of salt water for two additional periods each of breathing pure oxygen and air. Recompression therapy reduces the size of bubbles, allowing easier reabsorption and dissipation, and increases the nitrogen gradient to expedite off-gassing. The majority of recreational divers with neurologic decompression sickness have an excellent recovery after prompt recompression therapy.

The Divers Alert Network (DAN) at Duke University Medical Center, Durham, N.C., is available 24 hours a day to discuss arterial gas embolism or decompression sickness and provide divers a referral to the nearest recompression facility, if necessary. The emergency hotline number is 919-684-8111. For nonemergency medical questions, call DAN at 919-684-2948.

Headache

Headache is a common symptom in divers. There are numerous benign causes, including exacerbation of tension or migraine headaches, exposure to cold, mask or sinus barotrauma, sinusitis and a tight face mask. Migraines are not often precipitated by diving, but can be severe when they occur. If a migraine develops, the dive should be terminated because of the potential for nausea, emesis and alteration of consciousness. Dangerous causes of headache include cerebral decompression sickness, contamination of the breathing gas with carbon monoxide, arterial gas embolism, severe otic or sinus barotrauma with rupture, and oxygen toxicity.2–5,10 If headache occurs in a patient with potential arterial gas embolism or decompression sickness, it should be considered an emergency, because it suggests the presence of intracerebral bubbles. This type of headache usually develops within minutes of ascent. Immediate use of 100 percent oxygen and of recompression therapy is indicated.

Oxygen Toxicity

In the recreational diver, the most likely cause of oxygen toxicity is diving with oxygen enriched air (i.e., Nitrox). Nitrox is a breathing mixture that contains more than 21 percent oxygen (usually 32 to 36 percent), and allows extended bottom time. When diving with Nitrox, the diver is at risk of oxygen toxicity if the maximum oxygen depth limit and/or the oxygen time limit is exceeded. In general, the higher the oxygen content in the Nitrox mixture, the shallower the dive to minimize the potential for oxygen toxicity. Symptoms develop at depth without warning and consist of focal seizures (e.g., facial or lip twitching occurs in 50 to 60 percent of patients), vertigo, nausea and emesis, paresthesias, visual constriction and respiratory changes.18 Generalized seizures or syncope can also occur in 5 to 10 percent of patients. Although uncommon, generalized seizures at depth are often fatal, because divers may drown or arterial gas embolism may be precipitated during rescue to the surface.4 The cause of oxygen toxicity to the nervous system mainly involves oxygen-free radical formation, as well as reduction of the inhibitory neurotransmitter, gamma-aminobutyric acid. Treatment consists of reducing oxygen exposure and dive depth and, if necessary, managing seizures.

Decompression sickness | Britannica

Decompression sickness, also called bends or caisson disease, physiological effects of the formation of gas bubbles in the body because of rapid transition from a high-pressure environment to one of lower pressure. Pilots of unpressurized aircraft, underwater divers, and caisson workers are highly susceptible to the sickness because their activities subject them to pressures different from the normal atmospheric pressure experienced on land.

At atmospheric pressure the body tissues contain, in solution, small amounts of the gases that are present in the air. When a pilot ascends to a higher altitude, the external pressures upon his body decrease, and these dissolved gases come out of solution. If the ascent is slow enough, the gases have time to diffuse from the tissues into the bloodstream; the gases then pass to the respiratory tract and are exhaled from the body.

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Underwater divers breathing compressed air are also faced with the possibility of a form of decompression sickness known as the bends. As they descend into the water, the external pressure increases proportionally to the depth. The compressed air that is breathed is equal in pressure to that of the surrounding water. The longer a diver stays down and the deeper the dive, the more compressed gas that is absorbed by the body. When the diver ascends, time must be allowed for the additional gases to be expelled slowly or they will form bubbles in the tissues.

The major component of air that causes decompression maladies is nitrogen. The oxygen breathed is used up by the cells of the body and the waste product carbon dioxide is continuously exhaled. Nitrogen, on the other hand, merely accumulates in the body until the tissue becomes saturated at the ambient pressure. When the pressure decreases, the excess nitrogen is released.

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Nitrogen is much more soluble in fatty tissue than in other types; therefore, tissues with a high fat content (lipids) tend to absorb more nitrogen than do other tissues. The nervous system is composed of about 60 percent lipids. Bubbles forming in the brain, spinal cord, or peripheral nerves can cause paralysis and convulsions (divers’ palsy), difficulties with muscle coordination and sensory abnormalities (divers’ staggers), numbness, nausea, speech defects, and personality changes. When bubbles accumulate in the joints, pain is usually severe and mobility is restricted. The term bends is derived from this affliction, as the affected person commonly is unable to straighten joints.

Small nitrogen bubbles trapped under the skin may cause a red rash and an itching sensation known as divers’ itches. Usually these symptoms pass in 10 to 20 minutes. Excessive coughing and difficulty in breathing, known as the chokes, indicate nitrogen bubbles in the respiratory system. Other symptoms include chest pain, a burning sensation while breathing, and severe shock.

Relief from decompression sickness usually can be achieved only by recompression in a hyperbaric chamber followed by gradual decompression, but this process is not always able to reverse damage to tissues.

hyperbaric chamber

Hyperbaric chamber used to treat divers suffering from decompression sickness.

Mark Murphy

Veteran Scuba Diver Regains Ability to Walk After “the Bends”

Memorial Hermann
August 13, 2018

For Katie Sorrentino, her Mother’s Day scuba dive started off as normal as the hundreds of dives she had completed over the last 35 years. The veteran, licensed diver was on vacation with her family in the Bahamas when she experienced symptoms of decompression sickness or “the bends.”

Decompression sickness occurs when there is a rapid decrease in the pressure that surrounds someone underwater. The body attempts to eliminate excess inert gas and – if unsuccessful – develops bubbles in its veins and tissues. When the body has more bubbles than tissue to bear the load, a person can develop decompression sickness.

For Sorrentino, those bubbles were present in her spine, which resulted in a spinal cord injury.

According to Sorrentino, the Mother’s Day dive was a beautiful dive with her family. “Nothing out of the ordinary happened. We did all of our safety stops, including my 78-year-old mother who came with us and was in great shape,” said Sorrentino. “We got back on the boat and about 10 minutes later I began to feel excruciating pain in my upper right abdomen.”

Sorrentino’s brother, a dive master, got her on oxygen quickly and the group rushed her back to her brother’s home where shortly after she began to feel tingling in both legs. Sorrentino was soon airlifted from the Bahamas to a local Miami hospital to quickly undergo hyperbaric chamber treatment, the only form of treatment for decompression sickness. During her time there, doctors told her she would likely be unable to walk again. “I had no feeling or movement from my navel down,” added Sorrentino. “It was terrifying as my mind went through all of the ‘what if’s’ of not being able to walk again.”

After a month of treatment and regaining some sensation in her legs, she was airlifted to Texas and admitted into TIRR Memorial Hermann-The Woodlands, where she would begin intensive physical and occupational therapy to improve her weakness.

According to doctors, each year 1,000 people in the world develop decompression sickness and 2.5 percent experience the injury in their spine.

Under the care of Dr. Mary E. Russell, Medical Director at TIRR Memorial Hermann-The Woodlands,  Sorrentino underwent three weeks of physical and occupational therapy. For Russell, treating decompression sickness was a first. “Decompression sickness isn’t something we normally see at TIRR Memorial Hermann, but our team was dedicated to helping Katie in her recovery,” said Dr. Russell. “Our therapists spent time researching and approached her treatment similar to many spinal cord injuries.”

Sorrentino’s therapy consisted of a lot of weight bearing exercises to increase her lower body strength.

After three weeks of intense therapy, Sorrentino woke up one morning in excruciating pain due to a reoccurrence of the bubbles she initially felt after getting on the boat in May. She was taken by Memorial Hermann Life Flight® to Memorial Hermann-Texas Medical Center due to concerns she was experiencing a severe neurological issue. “It’s common for individuals who experience decompression sickness to have reoccurrence of pain out of nowhere,” said Dr. Russell.

After 10 days of unexplainable pain, Sorrentino woke up pain free. She returned to TIRR Memorial Hermann-The Woodlands. “I marveled when I returned because I could move my legs even more than before I left,” said Sorrentino. “I felt like I was back home when I returned. I cried when I saw my care team, and from there it felt like an accelerated path to walking on my own.”

She continued her intense occupational and physical therapy, and went from standing with assistance to walking on her own.

“Katie was an extremely hard worker her entire time with us and that played a huge role in her recovery,” said Dr. Russell. “She was always ready for the next thing and next challenge.”

After spending 76 days in the hospital, Sorrentino walked out on her own. “I’m forever grateful to Dr. Russell, my therapists Mithu and Ashley, and everyone on my care team,” said Sorrentino. Although doctors do not recommend she  scuba dive again, Sorrentino affirms that snorkeling is just as beautiful. “It makes me sad and I’m going to miss it. We’re a scuba diving family and I don’t think that will change; I’ll just be up on the boat.”

To learn more about rehabilitation services, visit TIRR Memorial Hermann-The Woodlands. Watch Sorrentino’s amazing recovery below.

How Do Marine Mammals Avoid the Bends? – Woods Hole Oceanographic Institution

April 25, 2018

Deep-diving whales and other marine mammals can get the bends—the same painful and potentially life-threatening decompression sickness that strikes scuba divers who surface too quickly. A new study offers a hypothesis of how marine mammals generally avoid getting the bends and how they can succumb under stressful conditions.

The key is the unusual lung architecture of whales, dolphins and porpoises (and possibly other breath-holding diving vertebrates), which creates two different pulmonary regions under deep-sea pressure, say researchers at the Woods Hole Oceanographic Institution (WHOI) and the Fundacion Oceanografic in Spain. Their study was published April 25, 2018, in the journal Proceedings of the Royal Society B.

“How some marine mammals and turtles can repeatedly dive as deep and as long as they do has perplexed scientists for a very long time,” says Michael Moore, director of the Marine Mammal Center at WHOI and co-author of the study. “This paper opens a window through which we can take a new perspective on the question.”

When air-breathing mammals dive to high-pressure depths, their lungs compress. That collapses their alveoli—the tiny sacs at the end of the airways where gas exchange occurs. Nitrogen bubbles build up in the animals’ bloodstream and tissue. If they ascend slowly, the nitrogen can return to the lungs and be exhaled. But if they ascend too fast, the nitrogen bubbles don’t have time to diffuse back into the lungs. Under less pressure at shallower depths, the nitrogen bubbles expand in the bloodstream and tissue, causing pain and damage.

Marine mammals’ chest structure allows their lungs to compress. Scientists have assumed that this passive compression was marine mammals’ main adaptation to avoid taking up excessive nitrogen at depth and getting the bends.

In their study, the researchers took CT images of a deceased dolphin, seal, and a domestic pig pressurized in a hyperbaric chamber. The team was able to see how the marine mammals’ lung architecture creates two pulmonary regions: one air-filled and the other collapsed. The researchers believe that blood flows mainly through the collapsed region of the lungs. That causes what is called a ventilation-perfusion mismatch, which allows some oxygen and carbon dioxide to be absorbed by the animal’s bloodstream, while minimizing or preventing the exchange of nitrogen. This is possible because each gas has a different solubility in the blood. The terrestrial pig did not show that structural adaptation.

This mechanism would protect cetaceans from taking up excessive amounts of nitrogen and thus minimize risk of the bends, says lead author Daniel García-Parraga of the Fundacion Oceanografic.

However, he said, “Excessive stress, as may occur during exposure to human-made sound, may cause the system to fail and increase blood to flow to the air-filled regions. This would enhance gas exchange, and nitrogen would increase in the blood and tissues as the pressure decreases during ascent.”

Scientists once thought that diving marine mammals were immune from decompression sickness, but a 2002 stranding event linked to navy sonar exercises revealed that 14 whales that died after beaching off the Canary Islands had gas bubbles in their tissues—a sign of the bends. The researchers say the paper’s findings could support previous implications of decompression sickness in some cetacean mass strandings associated with navy sonar exercises.

The team says further research will require the development of tools to analyze how lung blood flow and ventilation patterns change with various stressors during diving.

This work was supported by funding from the Fundacion Oceanografic and the Office of Naval Research.

The Woods Hole Oceanographic Institution is a private, non-profit organization on Cape Cod, Mass., dedicated to marine research, engineering, and higher education. Established in 1930 on a recommendation from the National Academy of Sciences, its primary mission is to understand the ocean and its interaction with the Earth as a whole, and to communicate a basic understanding of the ocean’s role in the changing global environment. For more information, please visit www.whoi.edu.

Scuba diving, swimming training

Recommendations

Can I swim without fins? Undoubtedly. You can dive with a mask and without fins, enjoying the beauty of the underwater world. But everything changes when we put on scuba gear. The weight of the cylinders under water is small, but the mass, i.e. the inertial force remains the same as on land – about 20 kg. In addition, rigid cylinders impede freedom of movement. The use of fins compensates for the difficulties encountered.Correctly selected, comfortable and effective fins largely determine the comfort of a scuba diver under water. The choice of the most suitable fins model depends on your tasks and your individual characteristics.

To assess the suitability of fins, we will highlight two parameters:

• ease of attachment to the leg;
• swimming efficiency.

The first is determined by the design of the overshoes, the second – by the design of the blade and the general shape of the fin.

The variety of designs for galoshes comes down to two principal options: fins with closed and open heels.

The first ones are very comfortable when putting on bare feet and provide the most tight connection between the fin and the foot.

For putting on the boots of a wetsuit, it is more convenient to use fins with an open heel, equipped with a strap. They are also called regulated. Modern models of adjustable fins allow you to tighten and loosen the strap directly on your foot.

The variety of fin blade designs is very large. For fins, as for any engine, the efficiency is extremely important, i.e. the ratio of useful work to expended energy.

Under water, everything is measured by air: the more energetic physical work, the greater its consumption. The more efficient the fins are, the less air is needed to cover a certain distance.

All other things being equal, the efficiency of the fins and their suitability for your individual characteristics can change the air flow rate by 20 – 30%.Accordingly, the time spent under water will change by the same amount.

Long fins with blades made of thin, resilient and fairly rigid plastic and rubber overshoes have excellent hydrodynamic properties.

In terms of speed qualities, such fins surpass the vast majority of other models and are optimal for swimming without scuba gear. It is no coincidence that underwater hunters all over the world prefer fins of this design.

Scuba divers, on the other hand, rarely use them, as they are inferior to smaller fins in maneuverability. For swimming with the apparatus, fins with shorter blades of a similar material are produced.

Another way to increase efficiency is with window fins. What is their meaning?

During the stroke, a zone of increased pressure is created on one side of the paddling surface, and on the other – a zone of reduced pressure. The resulting eddy currents along the edges of the fin create additional drag.

Slots in the base of the blade allow water to pass through, reduce the pressure difference and thereby weaken the vortex flows.

This design does not increase the speed imparted by the fins, but reduces the force during the stroke.

The efficiency of the fins is significantly increased when using the tunnel effect.

During the stroke, a certain amount of water inevitably rolls to the sides, not participating in the creation of the forward movement of the diver.

If the inner part of the fin blade is made of a softer material than the side parts, then during the stroke of the fin it bends, forming a groove that directs the water flow in the desired direction, thereby reducing the amount of water rolling down idle.

Another way to create a tunnel effect is to split the plastic blade with 2 to 4 longitudinal rubber grooves that allow lateral bending.

A variation of the tunnel effect is the spoon or bucket effect, achieved by a wedge-shaped insert of softer material or rubber grooves of different lengths.

Today, tunnel effect fins are the most popular among scuba divers.

When choosing fins for scuba diving, you must take into account that water is a denser medium than air, and as a result, scuba diving will add additional resistance to you, and it will be quite difficult to swim underwater without fins. There are two main types of fins – closed heel and open heel. Fins can also vary in stiffness, material used, length, shape.

The choice of the right ones, just for you, is a purely individual matter. In order to make the right choice of fins, it is necessary to determine for what purpose the fins are needed. Whether it’s scuba diving, freediving, spearfishing, snorkelling or just swimming in the pool. Will it be swimming in calm water or swimming in current conditions, or generally diving to great depths while holding your breath.

A very wide range of fins is currently being produced.The time spent by the scuba diver on the correct and careful selection of fins will be rewarded with the comfort and ease with which he can move in the water.

Fins can be divided into several types:

1. Adjustable open heel fins.

Adjustable open heel fins are most comfortable for scuba diving. The use of such fins is determined by the fact that the scuba diver must wear wet suit boots in cold water.The rigid articulation of the blade and shoe gives the necessary power to the stroke underwater. This is a valuable trait when you need to overcome the additional drag created by scuba gear and bulky protective suits, or when you need to swim against strong currents. In addition, scuba diving fins are slightly wider and longer than their snorkeling counterparts. When swimming on the surface, the adjustable fins are not very effective.

This is due to the rigidity of the structure and the fact that they tend to break the surface of the water in the upper part of the swimmer’s leg movement.Also, the design of fins with an open heel often implies the use of a boat, which is not always advisable when swimming on the surface.

2. Closed heel fins.

Closed heel fins are mainly used for snorkeling. Such fins are sufficient to pull a swimmer in minimal equipment with a mask and snorkel, as well as in such fins it is possible to dive to shallow depths without scuba gear. In some cases, if the diving takes place in a closed reservoir, without currents and without a strong load, for a short time, it is possible to use this type of fins when diving with scuba diving.But it should be borne in mind that fins do not provide protection from the cold and in some cases it is advisable to use them with a neoprene toe.

3. Long plastic fins with a closed heel.

Long plastic fins are characterized by extremely long blades. They are designed for special diving, such as sports speed diving or simple speed diving, as they allow you to reach very high speeds. It is also suitable for diving to depths without scuba gear, as well as for deep-sea hunting.But for ordinary scuba diving, we do not need such a speed, such fins cannot always provide the maneuverability necessary for a scuba diver.

This type of fins can often be made of hard plastic, fiberglass, carbon. That provides them with the dynamics necessary for diving and high-speed swimming. These fins can be described as highly specialized.

4. Short, hard rubber or plastic fins.

Short rigid rubber or plastic fins are convenient when maneuverability is required (underwater photography, various courses by instructors).During normal swimming in such fins, the leg gets very tired, and when swimming in the current conditions it makes it impossible. Fins of this type are more often used by amateurs of swimming on the board and body surfers, as well as swimmers. These closed heel fins are commonly used for striking swimmers.

Materials

Most modern fins are made from a variety of materials.

“Galoshes” for feet and heel straps are usually made of rubber or other similar material, and the blade is made of materials that are classified as “thermoplastics”.Fins are very common, the blade of which is made of composite or several different materials, to give the fins optimal dynamic properties. The basic requirement for all fins is a soft overshoe and a relatively stiff blade.

The most common fins are composite or thermoplastic fins, they have a number of advantages over rubber ones: they weigh less, provide more traction due to greater rigidity and are made in a variety of colors.Structurally, the fins’ blades have: ribs that increase rigidity and work as vertical stabilizers, channels – increase efficiency by directing water, and can have holes – which reduce drag during movement and increase efficiency.

When choosing fins for scuba diving, you must take into account that water is a denser medium than air, and as a result, scuba diving will add additional resistance to you, and it will be quite difficult to swim underwater without fins.There are two main types of fins – closed heel and open heel. Fins can also vary in stiffness, material used, length, shape.

based on the book

D. Orlova and M. Safonova “Scuba diving and scuba diving

How diving and snorkeling affect human health

A person spends the first nine months of his life, but only intrauterine, in water. Therefore, it is not surprising that this element has such a beneficial effect on his body.Its influence is widely used for the development of physical capabilities in children and adults, for hardening, for strengthening the immune system, as well as for treatment – swimming and other similar procedures are prescribed as therapeutic measures for many diseases.

Underwater swimming (diving) occupies a special place among water sports. It can be called quite difficult, but very interesting, exciting and healthy (but only with the right approach).What happens in the human body when he dives under the water with a scuba diving?

Circulatory system

The first thing that feels the influence of new conditions is the circulatory system. Under water, the heart has to work with greater stress, since the vessels in the periphery are narrowed due to the action of water pressure . In addition, adrenaline, which is released from the fear that arises during diving, especially among beginners, also has an effect on the circulatory system.But if a person is healthy, such training for his heart and blood vessels is even beneficial .

Effect on respiratory organs

Respiratory organs can also withstand severe stress under water. To breathe in such conditions, a person needs to make great efforts , therefore regular diving exercises well the respiratory muscles. Well, the exhalation, on the contrary, turns out to be lighter and deeper. Thus the mobility of the chest is well developed, the diver begins to breathe to his full chest even on land.He has a significant increase in the vital capacity of the lungs.

General changes

Under water, a person feels weightless, all muscles relax, the static load on the spine disappears, which occurs on land when the body is fixed in a certain position. This has a positive effect on the entire human musculoskeletal system . Immersion under water is a sharp change in temperature conditions, forcing the body to actively use all the mechanisms of thermoregulation.Such exercises are a good tempering procedure. The aquatic environment also trains the nervous system. After a dive, a person feels relaxation and euphoria, but at the same time the swimmer must be able to quickly concentrate his attention and make decisions .

Contraindications to diving

It should be borne in mind that diving is useful only for a healthy body. Underwater swimming can cause serious health problems in people with circulatory and respiratory diseases, as well as in the elderly.In addition, a person who wants to become a diver must strictly follow the instructions given by a swimming coach instructor. Self-discipline and rejection of bad habits are also prerequisites for successful training in this type of water sports.

If you made the right decision – call us at +7 (812) 939-66-00 and sign up for a trial lesson.

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