Barotrauma 

Updated: Jun 16, 2017
Author: Joseph Kaplan, MD, MS, FACEP; Chief Editor: Joe Alcock, MD, MS 

Overview

Background

Barotrauma is an injury caused by a difference in pressure between a gas inside, in contact with, or outside the body and the pressure of the surrounding gas or fluid. Damage results from overtension or sheer forces from expansion of the gas within, or by pressure hydrostatically transmitted through, the tissues. Complications include local infiltration of gas into the damaged tissue or local circulation interfering with organ function or resulting in circulatory compromise.

This article is overview of the various types of barotrauma, such as decompression sickness, altitude sickness, medically induced barotrauma, primary blast injury, and self-inflicted barotrauma. The latter is new category and is seen in individuals using nitrous oxide as a recreational drug.

Diving as a profession can be traced back more than 5000 years, yet diving-related disease was not described until Paul Bert wrote about caisson disease in 1878. Symptoms of caisson disease were noted among bridge workers after finishing their shifts underwater and coming back to the surface. These symptoms included dizzy spells, difficulty breathing, and sharp pain in the joints or abdomen. The caisson workers often noted that they felt better while working. This was usually attributed to their being rested at the beginning of the shift as opposed to being tired when the workday was through. The workers would often have severe back pain that left them bent over, which is how caisson disease earned the nickname "the bends."

Diving barotrauma can present with various manifestations, from ear, face or mouth pain and headaches to major joint pain, paralysis, coma, and death. As a result of the wide variety of presentations, these disorders must be considered in any patient who has recently been exposed to a significant change in barometric pressure. The three major manifestations of barotrauma include (1) sinus or middle ear effects, (2) decompression sickness (DCS), and (3) arterial gas emboli. There have also been minor sequelae to include isolated nerve involvement and facial baroparesis.[1] Most commonly, the sinuses and middle ear are affected, and this can occur from relatively shallow dives, from deep dives, and in diver’s training.

Barotrauma has also reportedly been caused by an airbag rupturing during deployment, forcing high-pressure gas into a person's lungs.[2] It has also reportedly been associated with rapid ascent in military aircraft and with pressure changes associated with space exploration. Barotrauma has also been reported with both tracheal intubation and fiberoptic endotracheal intubation. Fiberoptic endotracheal intubation requires insufflated oxygen, which increases airway pressure. This leads to alveolar rupture with pneumothorax and subcutaneous emphysema.[3]

The most current research in barotrauma has been dealing with ventilator-associated barotrauma and barotrauma prevention.

 

Pathophysiology

Injuries caused by pressure changes are generally governed by the Boyle and Henry laws of physics.

The Boyle law states, "For any gas at a constant temperature, the volume of the gas will vary inversely with the pressure," or P1 X V1 = P2 X V2. Pressure rises by 1 atmosphere for every 33 ft (10 m) of seawater depth. This means that a balloon (or lungs) containing a volume of 1 cubic foot of gas at 33 ft of seawater depth will have a volume of gas of 2 cubic feet at the surface. If this air is trapped, as occurs when a person holds his or her breath during rapid ascent, it expands with great force against the walls of that space (reverse squeeze). During rapid ascent, incidents of pneumothorax and pneumomediastinum as well as sinus squeeze and inner ear injuries can occur. Sinus squeeze occurs with eustachian tube dysfunction, which may result in inner ear hemorrhage, tearing of the labyrinthine membrane, or perilymphatic fistula.

The Henry law states that the solubility of a gas in a liquid is directly proportional to the pressure exerted upon the gas and liquid. Thus, when the cap is removed from a bottle of soda pop, the soda begins to bubble as gas is released from the liquid. In addition, when nitrogen in a diver's air tank dissolves in the diver's fatty tissues or synovial fluids at depth, nitrogen will be released from those tissues as the diver ascends to a lower pressure environment. This occurs slowly and gradually if the diver ascends slowly and gradually, and the nitrogen enters the bloodstream to the lungs and is exhaled. However, should the diver ascend rapidly, nitrogen exits tissues rapidly and forms gas bubbles.

Once bubbles are formed, they can affect tissues in many ways. They can simply obstruct blood vessels leading to ischemic injury. This can be devastating when occurring in critical areas in the brain. The bubbles can also form a surface to which proteins in the bloodstream can cling, unravel, and begin a clotting/inflammatory cascade. This cascade can lead to endothelial breakdown and permanent tissue damage.

Decompression sickness

Decompression sickness (DCS) usually results from the formation of gas bubbles, which can travel to any part of the body, accounting for many disorders. A gas bubble forming in the back or joints can cause localized pain (the bends). In the spinal cord or peripheral nerve tissues, a bubble may cause paresthesias, neurapraxia, or paralysis. A bubble forming in the circulatory system can lead to pulmonary or cerebral gas emboli.[4]

Some gases are more soluble in fats. Nitrogen, for example, is 5 times more soluble in fat than in water. Approximately 40-50% of serious DCS injuries involve the central nervous system (CNS). Women may be at an increased risk of DCS because they have more fat in their bodies. DCS also may occur at high altitudes. Those who dive in mountain lakes or combine diving with subsequent flying are at increased risk as well.

DCS is classified into two types. Type I is milder, is not life threatening, and is characterized by pain in the joints and muscles and swelling in the lymph nodes. The most common symptom of DCS is joint pain, which begins mildly and worsens over time and with movement. DCS type II is serious and life threatening. Manifestations may include respiratory, circulatory, and, most commonly, peripheral nerve and/or CNS compromise.[5]

Arterial gas embolism (AGE) is the most dangerous manifestation of DCS type II. AGE occurs after a rapid ascent, when a gas bubble forms in the arterial blood supply and travels to the brain, heart, or lungs. This is immediately life threatening and can occur even after ascent from relatively shallow depths. However, AGE can also occur from iatrogenic causes.

Patients with a patent foramen ovale (up to 30% of the population) are at higher risk of gas passing from a right-to-left shunt and causing CNS injuries.[6, 7]

Medically induced barotrauma

Medically induced barotrauma most often occurs in patients receiving respiratory support via positive-pressure ventilation (PPV).[8] The age of the patient, comorbidities such as COPD, malignancy of the upper or lower airway, trauma to the airways, or surgical procedures to the thoracic cavity or upper airway increase the risk for barotrauma due to PPV.[9]

Complications of barotrauma due to PPV include the following:

  • Systemic air embolism: This is uncommon, but it can result in life-threatening complications such as cardiac arrest [9] or cerebrovascular accident. [10]
  • Air cardiac tamponade: This is another uncommon but serious complication of barotrauma. Golota et al, [11] document a case study of air cardiac tamponade in a patient presenting with respiratory distress due to pneumothorax. The pneumothorax was treated with a chest tube, without relief of symptoms. CT scan revealed air in the pericardium.
  • Pneumothorax: This is the most common barotrauma as the result of PPV. Chang et al [12] present a comparison study that suggests pressure-regulated volume control PPV reduces the incidence of pneumothorax versus synchronized intermittent mandatory ventilation in elderly COPD patients.
  • Pneumomediastinum: This is less serious than the above conditions. It may present with chest pain, mild dyspnea, dysphagia, and vocal changes. It is usually treated supportively and resolves without intervention. [13] Ocakcioglu et al [14] report a case of pneumomediastinum after tooth extraction using high-pressure air dental drills. The patient was 1 week post procedure when he presented to the local emergency department with chest pain and a sore throat.
  • Otic barotrauma: This usually involves injury to the middle ear with tympanic rupture, hemotympanum, transient hearing lost, and otalgia. McCormick et al [15] report a case of otic barotrauma as a result of continuous positive airway pressure (CPAP) therapy for obstructive sleep apnea.
  • Self-inflicted barotrauma: Jeddy et al [16] present a case study of pneumomediastinum and subcutaneous emphysema of the neck and upper chest self-induced by the patient’s use of nitrous oxide as a recreational drug. The abusers use balloons or canisters used for pressurizing commercial whip cream containers (known as whip-its) filled with nitrous oxide as an inhalant.
  • Insufflation: Procedures requiring insufflation of carbon dioxide or other medical gases have resulted in barotrauma to the surrounding tissues. Tracheal, esophageal, and bowel perforation have occurred. [17]

Blast injury

This barotrauma occurs from an external explosive force causing atmospheric overpressure. This is primary blast injury (PBI). Blast injuries are further delineated into secondary, tertiary, and quaternary. Secondary is impact with flying debris, tertiary deals with the person being thrown by the force of the blast or injuries from structural collapse, and quaternary is all other injuries.[18, 19] PBI involves the respiratory, digestive, auditory, and nervous systems.

Respiratory PBI is the most likely to produce immediate fatal injury. Pulmonary contusion, systemic air embolism, disseminated intravascular coagulation, and acute respiratory distress syndrome frequently follow PBI of the lungs. PBI of the thorax may also cause decreased heart rate, stroke volume, and cardiac index with resulting hypotension without compensation from the systemic vascular resistance reflex.[18]

PBI affecting the gastrointestinal system produces organ contusion and/or rupture. Hemorrhage, peritonitis, mesenteric emboli, and organ dysfunction or failure can occur. These injuries can be occult on initial examination, prompting the clinician to reevaluate any patient with exposure to significant explosive force often and with a high degree of suspicion for developing gastrointestinal injury.[18]

Auditory PBI includes tympanic rupture, ossicle fracture, or dislocation and hemotympanum.[18]

Neurological PBI produces injuries ranging from mild postconcussion syndrome to cerebral edema, hematoma, and intracranial hemorrhage.[18, 19] Reports from military observations suggest that cerebral swelling occurs much faster with PBI than with other traumatic closed head injury.[20] Aggressive treatment with early decompressive craniotomy has been shown to decrease mortality.[18, 19]

 

Patient Education

For patient education resources, visit the First Aid and Injuries Center. Also, see the patient education articles Scuba Diving: Barotrauma/Decompression Sickness, Scuba Diving: Ear Pain, and The Bends - Decompression Syndromes.

 

Presentation

History

Patients with decompression sickness (DCS) present with a history of diving, generally within 24 hours of the onset of symptoms. Patients may also have a recent history of occupational pressurization or depressurization. For example, this occurs with aircraft mechanics who must test aircraft windows by working in pressurized aircraft. Air emboli have also occurred in mechanics who maintain training altitude chambers. Recently, military operations involving troops traveling from ground level to high-altitude environments in a relatively short time and operations involving soldiers doing strenuous activities at higher altitudes have resulted in many cases of DCS. Recent studies have indicated that aerobic exercise either prior to a dive or during decompression stops may decrease the post dive gas bubble formation.[21, 22]

Sinus squeeze

Patients usually present with complaints of facial or oral pain, nausea, vertigo, or headache.

Other important information to gather includes any history of recent upper respiratory infections, allergic rhinitis, sinus polyps, and sinus surgeries and whether the pain worsened during descent or ascent.

Middle ear squeeze

Patients often have a history of sudden vertigo, nausea, tinnitus, ear pain, deafness, or headache.

They may have a history of previous diving ear injury or a history of previous or current ear infection.

Decompression sickness type I

Patients often have a history of recent diving followed by a flight home. They may complain of slowly progressing pain or numbness in their limbs or back.

Patients present with joint, muscle, or back pain that worsens over time. The pain worsens with motion but is always present. The pain may range from mild (tickles) to severe (the bends).

Patients may have a history of previous decompression illness and multiple dives in the same day and frequently have not followed the dive tables closely. New dive computers that offer more "bottom time" do so by modifying the US Navy dive tables and possibly place divers at an increased risk for DCS injuries. Divers should be questioned as to the method of computing bottom and ascent times with safety stops. This information should be recorded as part of the medical record.

Decompression sickness type II

DCS type II usually presents sooner than DCS type I.

Patients may present with shortness of breath (the chokes), chest pain, severe headache, altered mental status, and shock. They also may complain of dizziness or weakness. Patients may rapidly deteriorate without emergent intervention.

Essential history to ascertain includes time since dive ended, the dive profile (see images below), when the symptoms began, and prior medical history. The dive profile consists of prior dives that day, depth of dive, bottom time, decompression stop depth, and length of stop.

Basic US Navy dive table used to compare the patie Basic US Navy dive table used to compare the patient's dive profile to the standard dive profile. Reprinted with permission of the US Navy.
US Navy dive table for altitude diving used to com US Navy dive table for altitude diving used to compare the patient's dive profile with the standard dive profile at altitude. Reprinted with permission of the US Navy.

Diver should be asked about his or her prior dive category.

Inquiry should be made specifically about previous decompression injuries, pulmonary blebs, Marfan syndrome, asthma, congenital pulmonary illnesses, HIV status, chronic obstructive pulmonary disease (COPD), lung tumors, histiocytosis X, cystic fibrosis, pregnancy,[23] and any prior pulmonary injuries or surgeries.

Arterial gas embolism

AGE usually occurs shortly after ascending very rapidly, often from fairly shallow depths. People may be described to scream suddenly and lose consciousness. Onset of AGE often occurs within a few minutes of surfacing. Patients who experience AGE often die before reaching a medical facility. Air emboli have also recently been noted to occur iatrogenically in association with central venous monitoring during surgical procedures. Case reports have shown AGE occurring secondary to occupational rapid decompression in both aircraft maintenance and altitude-chamber maintenance personnel.[24]

Obtaining a history from these patients can be difficult because they often present with altered mental status or are in shock.

Witnesses often report that divers experience a sudden or immediate loss of consciousness or collapse, usually within minutes of surfacing.

Ask the patient or dive partner about a history of patent foramen ovale.

Abdominal compartment syndrome[25]

Divers can develop large amounts of intraperitoneal extraluminal gas, which can compress the intraperitoneal organs. This can lead to venous compression of these organs and secondary compartment syndrome.

Physical Examination

The physical examination should be tailored to the patient's history.

Perform a general physical examination on all patients, with initial emphasis on ears, sinuses, and neck as well as on the pulmonary, cardiovascular, and neurologic systems. AGE often presents with signs and symptoms of acute stroke.

Inspect and palpate the extremities, and test range of motion in all joints.

Sinus squeeze

Inspect nasal mucosa for polyps, hemorrhage, or lesions.

Palpate and transilluminate sinuses to inspect for hemorrhage.

Percuss upper teeth with a tongue blade to inspect for severe sinus tenderness.

Ear squeeze

Carefully inspect the tympanic membrane (TM), looking in particular for the following signs:

  • Amount of congestion around the umbo

  • Percent of TM involvement

  • Amount of hemorrhage noted behind eardrum

  • Evidence of TM rupture

Palpate the eustachian tube for tenderness.

Test the patient's balance and hearing.

Evaluate the TM on the Teed scale, as follows:

  • Teed 0 - No visible damage, normal ear

  • Teed 1 - Congestion around the umbo, occurs with a pressure differential of 2 pounds per square inch (PSI)

  • Teed 2 - Congestion of entire TM, occurs with a pressure differential of 2-3 PSI

  • Teed 3 - Hemorrhage into the middle ear

  • Teed 4 - Extensive middle ear hemorrhage with blood bubbles visible behind TM; TM may rupture

  • Teed 5 - Entire middle ear filled with dark (deoxygenated) blood

Decompression sickness type I

Inspect for swelling or effusion in the affected joint.

Test for range of motion both actively and passively.

Palpate the affected area for crepitus and compartment tightness.

Evaluate neurovascular status by performing a complete neurologic examination. The examination should include testing motor and sensory functions, cerebellar function, and mental status. The findings from this examination must be recorded and used as a baseline to determine improvement in postdive chamber treatment.

Decompression sickness type II

Evaluate cardiovascular and pulmonary systems.

Note neck vein distention or petechiae on the head or neck.

Palpate the skin for crepitus.

Auscultate the lungs and heart for decreased breath sounds, muffled heart tones, or heart murmurs.

Evaluate neurologic status, including gross motor, sensory, and cerebellar examinations. Tandem walking (heel to toe, with eyes closed) is an excellent method of evaluation.

Document Glasgow Coma Scale and Mini Mental State Examination.

Arterial gas embolism

Use the same examination used for decompression sickness type II.

Causes

The causes of DCS are related to predisposing medical or genetic factors, as listed above, and to diver error. Diver error includes the following practices:

  • Multiple daily dives

  • Poor adherence to the dive tables

  • Breath holding (most common scenario for pulmonary barotrauma)

  • Rapid ascent: This can occur from relatively shallow depths. For example, pilots undergoing rapid ascent while performing underwater escape training after flight may experience DCS.

  • Flying or traveling to high altitudes within 24 hours after diving

  • Occupational causes: These causes include rapid depressurization by maintenance workers and mechanics after working in pressurized aircraft cabins. Reports of altitude chamber mechanics who have depressurized too quickly while working on the altitude chambers have also been documented. Pilots and crewmembers performing high-altitude air drops on military missions and special-operations soldiers involved in such missions have also reported instances of DCS.

 

DDx

 

Workup

Laboratory Studies

Do not delay treatment while waiting for laboratory studies. Laboratory studies helpful in treating patients with DCS include a complete blood cell  (CBC) count and arterial blood gas (ABG) determination.

Complete blood cell count

In one study, patients who had a hematocrit of 48% or higher had persistent neurologic sequelae 1 month after the injury.

White blood cell (WBC) count with differential may help to determine infectious causes.

ABG determination

Determine the alveolar-arterial gradient in patients suspected of having an embolism.

Serum creatine phosphokinase level

Increases in creatine phosphokinase (CPK) levels indicate tissue damage associated with barotrauma. Rising CPK levels indicate increasing tissue damage due to microemboli.

Imaging Studies

Chest radiography

Obtain a chest radiograph if the patient complains of chest discomfort or difficulty breathing.

Obtain inspiratory and expiratory views if a pneumothorax is suspected clinically.

Radiographs of joints or extremities

When indicated clinically, obtain these to evaluate for the presence of a fracture or dislocation.

Computed tomography (CT) scans and magnetic resonance imaging (MRI)

Patients who may benefit the most from these diagnostic modalities are often the most unstable, making their transport to the radiology suite potentially dangerous.

Any patient who presents with a severe headache or severe back pain after a dive, subcutaneous emphysema, change in level of consciousness, difficulty breathing, or unexplained chest pain is a potential candidate for these imaging studies.[26]

Spiral CT is the most sensitive method to evaluate for pneumothorax.[27] It should be performed in all patients suspected of having a barotrauma-related pneumothorax when chest radiograph findings are negative for pneumothorax. One study, using the porcine model, indicates that CT done within 6 hours can show a significant amounts of gas in both the arterial and venous systems. This information could be used for prognostic or pathologic evaluation.[28]

Echocardiography and ultrasonography

Echocardiography and ultrasonography can be used to detect the number and size of gas bubbles in the right side of the heart, gas in the subcutaneous tissues, the presence of abscess in swelling of the face and neck, and air in the peritoneum.[29] This can be used both for diagnosis and prognosis.

Other Tests

ECG is useful for determining potential cardiac causes of the altered mental status, chest pain, dyspnea, or shock.

 

Treatment

Prehospital Care

Prehospital care should consist of assessing the ABCs and correcting any immediate life-threatening conditions while maintaining adequate oxygenation and perfusion. Patients should be placed on high-flow oxygen and have large-bore venous access with isotonic fluid infusion to maintain blood pressure and pulse. Although research is being done on the use of surfactants being given prior to high-risk activities such as deep dives or space missions, it is still in the bench research stage of development.[30] Several in vitro studies have been promising, and there is hope that surfactant use will someday greatly decrease the frequency of barotrauma.

Emergency Department Care

Stabilize the airway, breathing, and circulation.

Intubation

Perform endotracheal intubation on a patient who has an unstable airway or has persistent hypoxia despite breathing 100% oxygen.

Perform tube thoracostomy to evacuate a pneumothorax or hemothorax.

Perform nasotracheal or orotracheal intubation when appropriate.

Needle decompression

Needle decompression of the chest is indicated for suspected tension pneumothorax. A large-bore needle is inserted over the rib in the second intercostal space, midclavicular line.

Foley catheterization

Place a Foley catheter in patients who present with shock to assist in assessing volume and hydration status. Normal urine output is 1 mL/kg of body weight per hour.

Place a Foley catheter in patients with spinal cord manifestations of DCS who are unable to void due to a neurogenic bladder.

Hydration

Continue intravenous hydration to maintain adequate blood pressure.

Recompression therapy

Recompression therapy should be performed at a dive chamber by a dive medical officer or personnel certified in hyperbaric medicine. Indications include spinal cord injury and neurologic impairment.

Sinus squeeze

Symptomatic therapy with decongestants, both oral and nasal, is indicated.

Pain control should be instituted with nonsteroidal anti-inflammatory drugs (NSAIDs) or narcotic analgesic medications.

Middle ear squeeze

Severity and treatment are based on the Teed scale, as follows:

  • Mild (Teed 0-2): Decongestants, both nasal (0.05% oxymetazoline hydrochloride spray bid for 3 d) and oral (pseudoephedrine 60-120 mg bid/qid) are administered.

  • Moderate (Teed 3-4): Treatment is same as above, but a short course of oral steroids, such as prednisone 60 mg/d for 6 days then tapering over 7-10 days, may be needed. If TM has ruptured or water is contaminated, consider antibiotics that treat acute otitis media.

  • Severe (Teed 5): Treatment is same as above. Consider myringotomy if the above have failed. Control pain with Tylenol with codeine (acetaminophen 300 mg with codeine phosphate 30 mg) 1-2 tablets every 4-6 hours.

Decompression sickness type I

These patients should receive high-flow oxygen via a nonrebreather mask.

After establishing intravenous access, administer isotonic fluids (isotonic sodium chloride solution or lactated Ringer solution) to maintain urine output at 1-2 mL/kg/h.

These patients should also receive aspirin 325-650 mg for antiplatelet effects as well as pain control.

Obtain appropriate radiographs to evaluate for fractures or dislocations.

If a patient's medical condition continues to deteriorate, he or she is then classified as having DCS type II.

Currently, the United States Air Force is developing a new, shorter Treatment Table 8 (TT8) that allows for dives of shorter duration (lasting 30 min with air breaks between each 2 atmospheric absolute [ATA] dive). This is done with 4 dives each for 30 minutes with 10-minute air breaks. The TT8 should only be used to treat DCS type I when symptoms occur within 2 hours of altitude chamber or flight and when partial response on oxygen after 10 minutes has occurred. Treatment Table 6 (TT6) should be used immediately if symptoms persist after the first 30-minute interval or recur within 24 hours.

Decompression sickness type II

All of the interventions for DCS type I are appropriate for DCS type II.

These patients need recompression therapy to resolve their symptoms.

The most appropriate management is to transfer the patient to the nearest hyperbaric chamber.

Arterial gas embolism

Patients with AGE can have mild symptoms from a small embolism that may improve with therapy for DCS type I, including intravenous hydration, high-flow oxygen, and aspirin.

Patients with severe AGE (ie, unstable blood pressure, respirations, neurologic status) require immediate recompression therapy in a hyperbaric chamber.

Medical Care

Further inpatient care

Patients may require multiple recompression "dives" in a hyperbaric oxygen chamber to reverse neurologic impairment or to treat air emboli.

Patients with continued pain despite appropriate treatment at sea level require recompression.

Patients who are seriously ill or do not respond to initial treatment may require higher pressure recompressions at 4-5 atm of absolute pressure and may need breathing gas of 50% helium/50% oxygen mixture (heliox).

No definitive studies have proven that other modalities provide increased long-term benefit.

Transfer

Patients with DCS type II or severe AGE should be transferred to a recompression chamber. The chamber specialist must be contacted prior to any transfer to determine availability. When presenting the case, the dive medical officer needs to know the following signs and symptoms:

  • Vital signs

  • Pertinent medical symptoms (especially neurologic)

  • Time last dive finished

  • Onset of symptoms

  • Length of dive

  • Depth of dive

  • Decompression stops (length of time and depth)

  • Any flight or change in altitude after dive

    If the patient is to be transferred by air, the aircraft must stay below 1000 ft if possible, depending on the terrain, or be transported in a pressurized aircraft. Flight crew must be aware of the patient's condition to assist the pilot in keeping the aircraft fully pressurized before attaining altitude.

Consultations

Consult a specialist at a recompression chamber for any patient with DCS type II or an unstable AGE. The recompression chamber specialist must be contacted prior to transfer to determine chamber availability. A complete list of recompression chambers is available from the Divers' Alert Network and is only provided by calling (919) 684-8111 or (919) 684-4326.

Prevention

Any patient who sustains pulmonary barotrauma should not dive again.

Patients with asthma, Marfan syndrome, or COPD are at very high risk of pneumothorax and should be warned against diving.

Avid divers should be warned against multiple daily dives, diving and flying on the same day, and trying to "shave" their dive profile.[31]

Long-Term Monitoring

Outpatient care is based on the type of dysbaric injury. Adequate hydration and pain control are the hallmarks of outpatient care.

Recommendations for recovery time vary depending on the individual and amount of barotrauma.

Consult a dive medical officer (hyperbaric specialist) prior to giving recommendations to patients.

 

Aspirin (Anacin, Ascriptin, Bayer aspirin)

Aspirin blocks prostaglandin synthetase action, which, in turn, inhibits prostaglandin synthesis and prevents the formation of platelet-aggregating thromboxane A2. By inhibiting prostaglandin synthesis, aspirin may also inhibit key steps in the inflammation process.

Pseudoephedrine (Silfedrine, Sudafed)

Pseudoephedrine stimulates vasoconstriction by directly activating alpha-adrenergic receptors of the respiratory mucosa. It induces bronchial relaxation and increases the heart rate and contractility by stimulating beta-adrenergic receptors.

Acetaminophen with codeine (Tylenol #3)

Acetaminophen with codeine is indicated for mild to moderate pain.

Methylprednisolone (Solu-Medrol, Depo-Medrol)

By reversing increased capillary permeability and suppressing PMN activity, methylprednisolone may decrease inflammation. It may also prevent neuronal damage by inhibiting prostaglandin synthesis.

Helium-oxygen (heliox)

Helium-oxygen consists of 50% helium and 50% oxygen.