Arterial Gas Embolism
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Pulmonary Barotrauma
References to Pulmonary Barotrauma
Reducing the Risks of PBT
Board Prep Summary

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Arterial Gas Embolism

Pathophysiology

Arterial gas embolism is a major cause of death in diving and the initiating cause (pulmonary barotrauma) usually goes undetected. Caused most often by the expansion of respiratory gases during ascent, it also occurs when the breath is held during ascent from a dive, when there is local pulmonary pathology, when there is dynamic airway collapse in the non-cartilaginous airways and if there is low pulmonary compliance, particularly if this is not distributed evenly throughout the lungs. Boyle's law is the physical law controlling the event. Experimental evidence indicates that intratracheal pressures of about 10 kPa  (4 fsw or 1.22 m. or ascending from 170 feet or 51.82 m. to 120 feet or 36.58 m.) are all that's needed for it to happen. Distention of the alveoli leads to rupture, alveolar leakage of gas, and extravasation of the gas into the arterial circuit.

Origin of Bubbles

Bubbles in the arterial circulation can arise from basically three sources: venous gas embolism with breach of the pulmonary vascular filter (paradoxic gas embolism), patent foramen ovale (paradoxic gas embolism) and tear of the pulmonary parenchyma with entry of gas into pulmonary venous outflow. Studies show that systemic venous bubbles are trapped in the pulmonary arterial tree and are usually completely eliminated from that site. The lung traps the air and excretes it into alveoli from the arterioles. (RG Presson, J Appl Physiol; 1989;67(5),1898-1902)

The syndrome of paradoxic air embolism (from septal defects) was first described by J. Cohnheim in 1877. (J Cohnheim, ZV Berline, Hirschwald, 1877;1:134). Hagan at the Mayo Clinic reported on 965 normal hearts and showed that more than 25% of patients with a history of cardiac disease have a 'probe patent' foramen ovale at autopsy. (PT Hagan, Mayo Clinic Proc, 1984; 59:17-20.).

The other main mechanism for arterial gas embolism is by way of the pulmonary overpressure syndrome or 'burst lung'. This occurs from baropressure increases as the diver on compressed air ascends with a closed glottis or a free diver takes a breath of compressed air at depth and ascends. Because of Boyle's law, maximal changes in volume occur in the 4 feet (1.22 m.) closest to the surface and the diver sustains a tear in the pulmonary parenchyma with the escape of air into the pulmonary venous outflow. This can result in several outcomes: pneumothorax (collapsed lung), pneumomediastinum (air in the space around the heart), subcutaneous emphysema (bubbles of air in the fatty tissues under the skin) and air into the pulmonary capillaries.

As the diver takes his first breath after surfacing, the extra-alveolar gas enters the torn blood vessels, migrates to the left side of the heart and is distributed systemically as emboli sent to areas determined by buoyancy.

Arterial gas emboli arise from gas bubbles in the pulmonary capillaries => pulmonary veins to the left side of the heart =>possible coronary artery emboli (rare) or internal carotid and vertebro-basilar arteries to thebrain => cerebral artery embolism (blockage) with the clinical picture of a stroke.

The foam or bubbles block arteries of the 30-60 micron caliber and cause distal ischemia, with astrocyte and neuronal swelling. As the bubble passes over the endothelium, there are direct cellular effects (within 1-2 minutes) causing PMN stimulation. The bubble itself has surface effects causing local swelling, downstream coagulopathy with focal hemorrhages. There is immediate increased permeability of the blood-brain barrier, loss of cerebral auto-regulation, rise in CSF and a rise in the systemic blood pressure. A phenomenon called 'no-reflow' occurs with a post-ischemic impairment of microvascular perfusion. This is thought to be the result of FactorVIII interacting with the prostaglandin system and possibly other blood/tissue factors.

Clinical Manifestations

The clinical manifestations of cerebral gas embolism include a sudden onset of unconsciousness associated with a generalized or focal seizure. There is often confusion, vertigo (extreme dizziness) and cardiopulmonary arrest. In a series of 24 USN cases in which the time was known, 9 occurred during ascent in the water, 11 within one minute at the surface and 4 occurred within 3-10 minutes at the surface.

Other clinical manifestations include the sudden onset of hemiplegia (paralysis on one side), focal weakness, focal hypesthesia (loss of feeling), visual field defect (blank areas in vision), blindness, headache and cranial nerve defects (vision, hearing, eye movements, facial muscles and feeling). The operative word here is "sudden"--nearly all of these symptoms can also be caused by neurological decompression sickness. Less common manifestations are chest pain and bloody, frothy sputum.

Management Outline

Recognition *This usually occurs during or immediately after surfacing*
 

A 25 year old divemaster made one dive to 40 feet for 38 minutes and then spent 3 hours and 45 minutes on the surface. His second dive was to 55 feet for 27 minutes, at the end of which he struggled with a heavy anchor, swimming with it to the surface. At the surface he raised out of the water, yelled, became comatose and was pulled from the water. apparently convulsing. He was placed in the head low position, given O2 by mask and on arrival at a recompression chamber 50 minutes later, he was alert, oriented and really felt well. He complained of a slight numbness of both right extremities but otherwise had a normal exam. Is this DCS, epilepsy or pulmonary over-pressure? What is the one clue you need to make the diagnosis?

This diver obviously had a pulmonary overpressure accident with arterial gas embolism and was treated by placing him on Table 6A ( 165 feet for 30 minutes) and then on Table 6. The fact that it occurred immediately on surfacing indicates that it's not DCS and surely a person with epilepsy should never have been certified as a divemaster.

Prevention

This episode underlines the potential risk of pulmonary overpressure accidents on every compressed gas dive regardless of depth and time. Prevention of pulmonary overpressure accidents starts with a good diving physical exam to ensure no history of pulmonary pathology which would prevent free pressure equilibration of all parts of the lungs as well as psychological evaluation of propensity to panic. The scuba instructor has in his hands the final prevention by teaching the dangers of breath-holding.

Mechanisms of Action

The mechanisms that occur when a pulmonary overpressure accident occurs are directly related to Boyle's Law, and the greatest danger is at shallow depths-with the greatest gas volume expansion near the surface. Boyle's Law states that with the temperature constant, the volume of a gas is inversely proportional to the pressure. When pressure differential between gas in alveoli and water (or chamber gas pressure in a compression chamber) exceeds 50-100 mmHg (3 to 5 FSW),free gas can be forced across the fine alveolar membrane into pulmonary interstitial tissues, pulmonary capillaries or rarely through the path of greatest resistance, the visceral pleura.

Arterial gas emboli arise in the gas bubbles in the pulmonary capillaries -> pulmonary veins to the left side of the heart->possible coronary artery emboli or internal carotid and vertebro-basilar arteries to the brain-> cerebral artery embolism with the clinical picture of a stroke.

The clinical manifestations of cerebral gas embolism include a sudden onset of unconsciousness associated with a generalized or focal seizure. There is often confusion, vertigo and cardiopulmonary arrest. In a series of 24 USN cases in which the time was known, 9 occurred during ascent in the water, 11 within one minute at the surface and 4 occurred within 3-10 minutes at the surface.

Other clinical manifestations include the sudden onset of hemiplegia, focal weakness, focal hypesthesia, visual field defect, blindness, headache and cranial nerve defects. The operative word here is "sudden"-nearly all of these symptoms can also be caused by neurological decompression sickness. Less common manifestations are chest pain and bloody, frothy sputum.

An Unusual Case of Cerebral Gas Embolism
A snorkeler takes a breath from a compressed air regulator at depth.

Mediastinal and subcutaneous emphysema, due to bubbling in the tissues, cause substernal pain, subcutaneous crepitus (a crunching feeling ), a definite x-ray appearance and occasionally circulatory embarrassment (rare).

Pneumothorax occurs when the visceral pleura is ruptured by the air pressure and the lung collapses. When this occurs there is pain, decreased respiration on the affected side, changes to auscultation and percussion on physical exam with typical x-ray findings. If the opening is large-a tension pneumothorax can occur, requiring tube decompression of the chest before treatment with the compression chamber.
Spontaneous pneumothorax

All of these things can happen when two precipitating factors occur:

1). Breath-holding ascent

2). Local air trapping

A breath-holding ascent occurs in association with panic, buddy-breathing and acute laryngospasm (a breath of sea water). Local air trapping is the result of bronchospasm (asthma), mucous plugs (post-bronchitis), blebs (blisters on the surface of the lung), air-containing pulmonary cavities(as in scarring from TB), and very often no reason whatsoever.

Sarcoidosis
Marfan's Syndrome
Cystic Fibrosis
Asthma

Treatment of these three entities varies from the simple ( bedrest, O2, and observation for the emphysema) to immediate compression to 6 ATA and resuscitation while in transport for the arterial gas embolism. A chest tube is standard care for pneumothorax with a good neurological exam to rule out cerebral embolism.

Compression takes precedence over treatment of the pneumothorax and mediastinal emphysema and frequently attendants must also treat coexistent near-drowning, using endotracheal tube, 100% oxygen and IV fluids and dexamethasone.

Our young divemaster had a close encounter with the ghost of Sir Robert Boyle when he apparently held his breath while straining to swim to the surface with the anchor. The lessons of this episode should be readily apparent and can be acted upon by all of us, no matter how experienced we think we are.

Coxson HO, Rogers RM, Whittal KP, et al: A
Quantification of the Lung Surface Area in Emphysema Using
Computed Tomography. Am J Respir Crit Care Med
159(3):851-856, 1999.

J Emerg Med 1998 May-Jun;16(3):413-7
Fatal pulmonary barotrauma due to obstruction of the central circulation with air.
Neuman TS, Jacoby I, Bove AA

Hyperbaric Medicine Center and Department of Emergency Medicine, University
of California Medical Center, San Diego, USA.

Cardiac arrest in cases of barotraumatic arterial gas embolism (AGE) is usually
ascribed to reflex dysrhythmias secondary to brainstem embolization or secondary
to coronary artery embolization. Several case reports suggest that obstruction of
the central circulation (i.e., the heart, pulmonary arteries, aorta, and arteries to the
head and neck) may play a role in the pathogenesis of sudden death in victims of
pulmonary barotrauma. We report three consecutive cases of fatal AGE in patients
in whom chest roentgenograms demonstrated confluent air lucencies filling the
central vascular bed, the heart, and great vessels. In none of the victims was there
evidence by history or at autopsy that the intravascular gas was iatrogenically
introduced. Total occlusion of the central vascular bed with air is a mechanism of
death in some victims of AGE, and resuscitation efforts for such patients should take this possibility into consideration. 

Undersea Hyperb Med 1997 Winter;24(4):301-8
Recompression treatments during the recovery of TWA Flight 800.
Leffler CT, White JC
Medical Department, Naval Amphibious Base Little Creek, Virginia, USA.

After the crash of TWA flight 800, U.S. Navy (USN) and civilian divers recovered
the aircraft and the victims' remains from 117 feet of sea water (fsw). Safety
information was gathered from observations, interviews, and medical and diving
records. Of 752 dives employing surface decompression using oxygen (SDO2), 10
divers required recompression treatments, mainly for type 2 decompression
sickness (DCS). When using hot water heating, the DCS risk was high until the
dive profiles were modified. Divers made nearly 4,000 no-decompression scuba
dives. In eight scuba divers and one tender treated with recompression, the
diagnoses included DCS (3), arterial gas embolism (AGE) (1), and vascular
headache (2). All USN divers recovered fully. The experience is consistent with
previous work suggesting an increase in DCS risk in warmer SDO2 divers. The
USN SDO2 tables can be made safer by limiting bottom time and extending
decompression. Even under stressful conditions, rapid ascents resulting in AGE are
uncommon. Vascular headaches can mimic DCS by responding to oxygen.

Aviat Space Environ Med 1997 Nov;68(11):1025-8
Neurological manifestation of arterial gas embolism following standard altitude chamber
flight: a case report.
Rios-Tejada F, Azofra-Garcia J, Valle-Garrido J, Pujante Escudero A
Centro de Instruccion de Medicina Aeroespacial (C.I.M.A.), Madrid, Spain.

In the course of a decompression at flight level 280 (28,000 ft) in an altitude
chamber flight, a 45-yr-old cabin air traffic controller developed sudden numbness
in his left upper and lower extremities and, soon after, complete paralysis in the
left side, dysarthria and left facial palsy. A presumptive diagnosis of arterial gas
embolism (AGE) was made and hyperbaric oxygen therapy (HBO) was given after
airevac of the patient to the closest compression facility. Complete resolution of
the symptoms was obtained after treatment Table VI-A (extended), plus 3
consecutive HBO treatments (90 min of Oxygen at 2.0 ATA). AGE is a rare event
in the course of regular altitude chamber flight and diagnosis should be done in the
context of the barometric pressure changes and an acute cerebral vascular injury.
Risk factors and follow-up diagnostic procedures are discussed.

Chest 1997 Sep;112(3):654-9
Risk factors for pulmonary barotrauma in divers.
Tetzlaff K, Reuter M, Leplow B, Heller M, Bettinghausen E
Department of Diving and Hyperbaric Medicine, Naval Medical Institute, Kiel,
Germany.

STUDY OBJECTIVES: Pulmonary barotrauma (PBT) of ascent is a feared
complication in compressed air diving. Although certain respiratory conditions are
thought to increase the risk of suffering PBT and thus should preclude diving, in
most cases of PBT, risk factors are described as not being present. The purpose of
our study was to evaluate factors that possibly cause PBT. DESIGN: We analyzed
15 consecutive cases of PBT with respect to dive factors, clinical and radiologic
features, and lung function. They were compared with 15 cases of decompression
sickness without PBT, which appeared in the same period. RESULTS: Clinical
features of PBT were arterial gas embolism (n=13), mediastinal emphysema
(n=1), and pneumothorax (n=1). CT of the chest (performed in 12 cases) revealed
subpleural emphysematous blebs in 5 cases that were not detected in preinjury and
postinjury chest radiographs. A comparison of predive lung function between
groups showed significantly lower midexpiratory flow rates at 50% and 25% of
vital capacity in PBT patients (p<0.05 and p<0.02, respectively).
CONCLUSIONS: These results indicate that divers with preexisting small lung
cysts and/or end-expiratory flow limitation may be at risk of PBT.

Medical Factors

  History
The same conditions that cause  spontaneous pneumothorax can be deadly in the increased ambient pressures of diving - and even in the pressure changes that take place in pressurized aircraft. Awareness of these conditions that can lead to spontaneous pneumothorax might aid in the reduction of the risk of 'burst lung' and cerebral arterial gas embolism.

Some of these conditions and diseases include:

Asthma, COPD, mucoviscidosis (cystic fibrosis), Pneumocystis carinii, tb, bronchiolitis (smokers), viral lower airway disease, HIV infection, bronchial atresia, sports blunt trauma, weight lifting, metastatic tumors, catamenia (perimenstrual), empyema, bullous emphysema (juvenile, apical, generalized), Marfan's syndrome, Schistosome infestation, Pregnancy, cryptogenic fibrosing alveolitis, and pulmonary histiocytosis X, Congenital bronchopulmonary cystic disease, vibroacoustic disease, alveolar proteinosis, bronchiectasis

     Symptoms of emphysema include:
     Cough
     Wheezing
     Shortness of breath
     Blue or pink discoloration of the nail beds or lips (blue bloater or pink puffer)
     Smoking
     Exposure to chemical or commercial agents

Awareness of cause of problem (ascending from depth with a closed  air-containing chamber)
Gear failure
Breath holding on ascent
'Sipping' from a regulator by a free diver
Weight lifting from depth
Boat exits in heavy wave action
   -ascend anchor line for stability
   -continue to breathe via regulator until you are out of the water
Straining while removal of gear (fins, weight belt) in the water
Poor air management, avoid running out of air
Panic ascents
Faulty buddy breathing practices

Title
     Air trapping on expiratory high-resolution CT scans in the absence of inspiratory scan
     abnormalities: correlation with pulmonary function tests and differential diagnosis.
Author Arakawa H; Webb WR
Address Department of Radiology, University of California, San Francisco 94143-0628, USA.
Source AJR Am J Roentgenol, 170(5):1349-53 1998 May
Abstract
     OBJECTIVE: We wish to describe the differential diagnosis and pulmonary function
     correlates of patients with normal findings on inspiratory high-resolution CT (HRCT) scans
     who showed air trapping on expiratory scans. CONCLUSION: Air trapping on expiratory HRCT scans in patients with normal findings on inspiratory scans is most often associated with bronchiolitis obliterans and asthma. Obtaining expiratory scans in patients who may have one of these diseases recommended.

     CONCLUSION: Quantitative chest CT assessment of disease severity is correlated with the
     degree of airflow limitation and exercise impairment in pulmonary emphysema.