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[cmdzstyle;1][cmdigt;perm4jcaselg] In order to maintain the educational aspects of these cases, the abstracts and files will be printed at the end of the article. This case was prepared by WILLIAM P. BUTLER, M.D.

Resident in Aerospace Medicine, School of Aerospace Medicine, Brooks AFB, TX {HD2;1}Part I--Initial Clinical Presentation {/HD2;1} A 39-yr-old male pararescueman was on temporary duty (TDY) in Florida. Training during this TDY included 2 d of scuba diving. He performed three dives on the first day and two dives on the second day. The sequence of dives and the dive profiles are as follows:

Day 1 [cmdix]Dive 1 - 115 ft for 18 min (safety stop at 15 ft   for 5 min) Surface Interval - 37 min Dive 2 - 30 ft for 30 min (safety stop at 15 ft for   4 min) Surface Interval - 26 min Dive 3 - 30 ft for 30 min (safety stop at 15 ft for   4 min) Surface Interval - approximately 20 h[cmdin;0]

Day 2 [cmdix]Dive 1 - 110 ft for 18 min (safety stop at 15 ft   for 5 min) Surface Interval - 37 min Dive 2 - 40 ft for 40 min (safety stop at 15 ft for   4 min) He experienced no difficulties on the first day of diving. However, on the second day during the 110-ft dive, he noticed a "small" sharp pain over his heart. This pain was localized just below the left nipple in the intercostal space. Despite the pain, he completed the required training dives. On a scale of 1-10 (10 being the worst pain ever experienced), he rated this pain a 2-3.

The next morning he embarked on a 6-mi run. At the 0.25-mi mark, he noted a "sudden sharp stabbing pain in my heart." This was like an "ice pick" in the chest. Although he aborted the run, the pain persisted. He now rated the pain at 6 out of 10. No shortness of breath, air hunger, or cough accompanied the pain and deep breaths did not exacerbate the pain. Of note, he described extreme fatigue.

Question 1: What is your differential diagnosis?

Question 2: What physical findings do you anticipate and what ancillary tests do you want? {HD2;1}Part II--Additional Information {/HD2;1} At this point, decompression sickness (DCS) is a primary consideration. It is a clinical entity that is dependent on residual tissue nitrogen. In fact, this malady might be thought of as "too much nitrogen" disease. Normally, blood and tissue contain a certain amount of inert nitrogen. The amount is dependent on the nitrogen partial pressure in the ambient atmosphere. The greater the pressure, the greater the level of nitrogen in blood and tissue. At a stable pressure, equilibrium is reached. Rapid changes in the ambient pressure alter this equilibrium. Sometimes the blood and, especially, the tissue can not adequately respond to a pressure drop (a rapid ascent from depth or a rapid ascent to altitude). As a result, the blood and tissue become supersaturated with residual or excess nitrogen. And, should critical supersaturation be reached, bubbles of nitrogen will evolve. These bubbles can produce clinical signs and symptoms-decompression sickness. Joint pain is the "bends," nerve dysfunction is "neurologic DCS," and pulmonary DCS is the "chokes" (1).

Because DCS is a clinical syndrome without a pathognomonic laboratory indicator, risk factors must be carefully examined. Without a change in ambient pressure there can be no DCS. Obviously, the pararescueman experienced ambient pressure changes during his dive training. Additionally, multiple dives over multiple days predisposed him to decompression sickness. Each dive exposes the diver to an increased ambient, as well as nitrogen, pressure. Tissue nitrogen equilibrium is disrupted. To re-establish the equilibrium, tissues on-load nitrogen (Henry's Law). After multiple dives, the tissues develop a significant nitrogen burden thus increasing the diver's risk for DCS.

Further scrutiny of this case elicited no other significant predisposing factors. The pararescueman was relatively youthful, being in early middle age. In contrast, most authorities agree that DCS risk markedly rises at a 40-42-yr threshold (6). This observation holds true for both diving and altitude-induced DCS. His dives during this training session were not overly strenuous. In contrast, vigorous exercise (while diving) increases tissue perfusion, nitrogen on-loading, and DCS risk. He had no recent injuries. In contrast, injury alters local tissue perfusion increasing risk. He was not dehydrated. In contrast, dehydration reduces tissue perfusion slowing nitrogen off-loading. This increases DCS risk. He was not obese. In contrast, fat stores act as a nitrogen sink. Fat has a five-fold affinity for nitrogen and is poorly perfused. These attributes reduce nitrogen off-loading and increase DCS likelihood. Significantly, the pararescueman was extraordinarily fit. In fact, he routinely competed as a triathlete.

Since the pararescueman's only risk factor is the diving profile, it must be carefully examined. The decompression burden, or excess tissue residual nitrogen, can be estimated with the US Navy's Standard Air Decompression Table (USN Diving Manual; Revision 3, February 1993). When his profile is scrutinized, interesting findings are unearthed. The pararescueman did not exceed the table limits, nor did he accumulate an excessive degree of residual nitrogen. In addition, there was no missed decompression time. Indeed, he performed unrequired decompressing safety stops with every dive. These observations sharply diminish the likelihood of DCS.

In this case, however, if DCS is contemplated, chokes must be considered. There was no joint pain suggesting bends and there was no neurologic deficit suggesting neurologic DCS. There was only chest pain. And, chokes is generally characterized by a high residual nitrogen burden and the clinical triad of shortness of breath, nonproductive cough, and substernal chest pain. Clearly, the pararescueman did not easily fit this diagnosis. On evaluation, DCS (chokes) was initially considered low probability. Since palpation of the area produced local pain, muscle strain was diagnosed and non-steroidal anti-inflammatories were prescribed.

On day 4, the pararescueman returned home by commercial aircraft. He reported to his Flight Surgery Clinic the next day. Now, he described persistent midsternal chest pain that felt "like I had swallowed a large ice cube." He also discussed his condition (by telephone) with a local recompression chamber facility. Both the flight surgeon and recompression facility felt the process was probably unrelated to diving.

Question 3: Do you agree with their opinion? {HD2;1}Part III--A Change in Symptoms {/HD2;1}

On Day 6, he developed the urge to cough. And, on Day 7, the chest pain changed: "It now feels like I have a small weight tied to a string in my chest and, when I move about, it swings freely." On the following day, the flight surgeon's exam was unremarkable. Again, the problem was felt unrelated to diving.

For 3 d, he noted little change. On Day 10, he attempted a 4-mi run. He felt out of shape, out of breath, and very weak. Remember, he is a very active triathlete. On Day 11, he attempted a 6-mi run. After only 1.5 mi, he turned around and returned home. Interestingly, he timed the third/final mile; it was 7:40 min. He was fatigued, short of breath, and alarmed. For the first time in years he had taken over 7 min to run a mile. In frustration, he contacted the USAF Davis Hyperbaric Laboratory. This facility mans a year-round 24-hour Hyperbaric Medicine consultation service. Ostensibly military, its services remain available to any caller.

Question 4: What testing would you perform?

The telephone conversation raised little suspicion for decompression sickness (chokes) or musculoskeletal strain. Pulmonary barotrauma, however, was strongly suspected. An immediate chest X-ray (CXR) was recommended. Subsequently, a 60-70% left pneumothorax was discovered (Fig. 1).

He was then admitted to the hospital following emergency department insertion of a left tube thoracostomy. His chest pain, shortness of breath, and fatigue completely resolved. Two days later, the chest tube was successfully removed. He remained asymptomatic.

Question 5: Was this a spontaneous pneumothorax or a "deserved" pneumothorax?

Question 6: Was any further treatment necessary? {HD2;1}Part IV--Definitive Treatment {/HD2;1} Spontaneous pneumothorax is an unprovoked rupture of the lung resulting in migration of intrapulmonary air into the extrapulmonary thorax. This air produces a positive intrathoracic pressure. Thus, the normally negative intrathoracic pressure is reversed. As a result, the soft, spongy lung tissue is compressed by the positively pressured air. And, pulmonary function is compromised.

Spontaneous pneumothorax is not uncommon-9 per 100,000 people annually. It is most frequently seen in tall, thin males (5-10 males : 1 female) between 16-24 yr of age. Chest pain and shortness of breath are common. Other symptoms (such as fatigue) are infrequent. Of note, only about 10% present while exercising (5,7).

Generally, treatment is tube thoracostomy. Applied suction removes the extrapulmonary air allowing the lung to re-expand and seal itself. Occasionally, the lung does not seal and operative therapy must be pursued. Similarly, recurrent pneumothoraces may require surgery. In fact, there is a 20-50% recurrence rate and most of the recurrences occur within 2 yr. In addition, the recurrence of a third or fourth pneumothorax is very high-about 60% and 80%, respectively (5,7).

Definitive surgery requires removal of offending pulmonary tissue such as blebs (surface "blisters" on the lung). If there are no blebs, pleurodesis is recommended. Pleurodesis is operative scarification of the parietal and visceral pleura effectively obliterating the pleural space. Without this space, there is no place for air to go-a recurrent pneumothorax is minimized. Mechanical, or abrasive, pleurodesis (up to 6% recurrence) appears superior to chemical pleurodesis (up to 25% recurrence). Today, thoracoscopic pleurodesis is the preferred technique. The ease of recovery and the success of this procedure has led some to suggest that surgery is indicated following even an initial pneumothorax (3).

To contrast, a "deserved" pneumothorax is not spontaneous. There is a good physiologic reason it happens. In this case, the chest pain began during a dive. This strongly suggests a pulmonary overpressure etiology. Normally, the lung can tolerate only a mild amount of positive intra-alveolar pressure. Indeed, a study using fresh cadavers suggested that an overpressure of 80-100 mm Hg will rupture the alveolus (4). This is a very important concept. Ascending from a depth of as little as 4 ft of water (reflecting a pressure change of ~80 mm Hg or ~1.5 psi) can rupture an alveolus. And, with alveolar rupture, there are three potential consequences.

Air released from the alveolus can track into the mediastinum. This results in a relatively mild degree of chest pain that resolves with rest and supplemental oxygen. Air released from the alveolus can enter the pulmonary veins, be transported to the left heart, and enter the systemic arterial circulation. This air gas embolism (AGE) characteristically presents as a coronary blockage (analogous to a myocardial infarction) or, more commonly, a central neurologic blockage (analogous to a stroke). Emergent recompression with hyperbaric oxygen is mandatory. Unfortunately, residua are common. And, finally, air released from the alveolus can track into the pleural space causing a pneumothorax. Not infrequently, investigation will uncover an emphysematous bleb. Presence of such a bleb solidly suggests etiology. In this case, a CT scan (performed about 3 weeks after the hospitalization) revealed an apparent intraparenchymal lung cyst (Fig. 2) (2).

Since this pathology probably contributed to the pararescueman's pneumothorax and since it was a job disqualifier, further definitive treatment was pursued. One month later, he underwent a left mini-thoracotomy with a wedge resection of a small emphysematous bulla from the superior surface of the left lower lobe. Mechanical pleurodesis was also carried out. He was discharged without sequelae 3 d later.

Question 7: Would you permit the pararescueman to resume his duties in Special Operations? {HD2;1}Part V--Aeromedical Disposition {/HD2;1} The impact of a pneumothorax on Special Operations personnel can be devastating. In the U.S. Navy, a spontaneous pneumothorax is a disqualifying event. However, waiver of a deserved pneumothorax can be obtained (6 mo after the incident) with a normal CXR, normal ventilation-perfusion scan, normal pulmonary function testing, and a normal evaluation by a pulmonologist (USN BUMED Notes 61-20).

In the U.S. Air Force, retaining flight status is the key to returning to Special Operations. Following full recovery from an initial spontaneous pneumothorax, return to flight status requires no waiver if the CT scan is normal. However, a second pneumothorax or a CT scan demonstrating blebs requires definitive surgery. Within 6 mo of successful surgery, a waiver for full duty can be obtained if pulmonary function testing is normal (USAF AFI 48-123). Not infrequently, an altitude chamber challenge flight is queried. Since there has never been a challenge failure, this is no longer required. In this case, the pararescueman fully recovered from definitive surgery, successfully passed pulmonary function testing, and even endured an uneventful altitude chamber flight to 25,000 ft (with rapid decompression). He has since returned to full pararescue duty and remains in excellent health.

One final note is requisite. It is extremely important to remember that Special Operations personnel are world class athletes. Not only was this military man one of the elite USAF pararescue force, but he was also an accomplished competitive triathlete. Such individuals possess an incredible physical reserve; they are better able to withstand physical insult than average people. As a result, they do not necessarily demonstrate expected symptoms and signs. Physicians caring for these individuals must recognize this phenomenon. The presented case is a clear demonstration of this tenet. {ABS;1}BUTLER WP.

Cases from the Aerospace Medicine Residents' Teaching File: Unsuspected Pulmonary Barotrauma. [cmdzid]

A USAF pararescue specialist developed chest pain during scuba diving duty. Initial evaluations considered decompression sickness and musculoskeletal etiologies. Pulmonary barotrauma was not contemplated because of the relatively mild presentation. Later, a very significant pneumothorax was discovered and successfully treated without sequelae. Decompression sickness is briefly discussed followed by a more in-depth examination of the presentation, diagnosis, treatment, and aeromedical aspects of spontaneous and "deserved" pneumothoraces. {/ABS;1} REFERENCES

  • 1. Bennett PB, Elliott DH, eds. The physiology and medicine of diving. 4th ed. Philadelphia: WB Saunders Company, 1993: 454-541.
  • 2. Bove AA, ed. Bove and Davis' diving medicine. 3rd ed. Philadelphia: WB Saunders Company, 1997: 176-204.
  • 3. Hopkirk JAC, Pullen MJ, Fraser JR. Pleurodesis: the results of treatment for spontaneous pneumothorax in the Royal Air Force. Aviat Space Environ Med 1993; 54:158-60.
  • 4. Malhotra MC, Wright HC. The effects of a raised intrapulmonary pressure on the lungs of fresh unchilled cadavers. J Pathol Bacteriol 1961; 82:198-202.
  • 5. Paape K, Fry WA. Spontaneous pneumothorax. Chest Surg Clin N Am 1994; 4:517-37.
  • 6. Sulaiman ZM, Pilmanis AA, O'Connor RB. Relationship between age and susceptibility to altitude decompression sickness. Aviat Space Environ Med 1997; 68:695-698.
  • 7. Voge VM, Anthracite R. Spontaneous pneumothorax in the USAF aircrew population: a retrospective study. Aviat Space Environ Med 1986; 57:939-49.


    Fig. 1. [cmderror: could not locate figure number for placement]

    Chest X-ray reveals an almost total collapse of the left lung (see arrows) from a large pneumothorax. It is important to appreciate that the pararescueman ran a 7:40 min mile with this pneumothorax.



    Fig. 2. [cmderror: could not locate figure number for placement]

    Chest CT scan demonstrates moderate sized emphysematous bleb within the left lung. Although this pulmonary defect appears intraparenchymal, in reality, it was situated on the superior surface of the left lower lobe.[cmd/FIG1]


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    Table of Contents for Volume 71, Number 11 of the ASME journal.