Rabu, 28 Desember 2011

Diving Accident Management

Introduction
It  is  desirable  to  have  a  standard  approach  to  the  initial  management  (i.e. first-aid)  of  an  injured  diver.
Coincidentally, a diver may have a non-diving related illness or injury, but in general, symptoms and signs following a dive are likely to be due to that dive.



Rescue
An injured diver must be removed from the water as quickly as possible. If the diver is unconscious and beneath the surface of the water, then they should be surfaced and decompressed in the head upright, normal anatomic position with special attention being paid by the rescuer to the maintenance of a patent airway. Surfacing feet first would delay the initiation of mouth to mouth for a short period. Air would continue to be forced from the lungs by ascent either way you raise the diver. PADI states that head up is the appropriate method. On the surface, the 'do-ci-do' left sided position is what is being taught for mouth to mouth initiation of breathing.
Getting the unconscious diver to the surface as fast as reasonably possible, head up and with the regulator in place would be my recommendation. NOAA does not address this in their new manual and I cannot find any reference to position of retrieval
in the Navy manual.
A SCUBA diver in this context should have their regulator placed in their mouth, but no attempt at "purging" gas into the injured diver should be made. Divers using rebreathing systems, full-face masks, band masks or helmets should be "flushed-through' with fresh gas, preferably from an alternative emergency gas supply, before swimming them to the surface or recovering them to a platform or bell. Specific techniques for recovery of a diver into and resuscitation of a diver in a bell or hyperbaric rescue vessel are needed and must be practiced.
In the absence of such a platform, the injured diver should be made positively buoyant by removing their weight-belt and perhaps by inflating their buoyancy-compensator (providing it neither limits access for the rescuer nor causes the injured diver to float "face-down'). The injured diver's air tank should be left in-situ as it acts as a keel. The rescuer should adjust their own buoyancy by buoyancy-compensator inflation and not by dropping their weight-belt in case they lose hold of the injured diver and have to recover them again from underwater.
The utility of expired-air-resuscitation (EAR) in the water, either directly or via a snorkel, is debatable. Certainly there is a significant difference between conducting EAR in a swimming pool and in the ocean in this context, effective in-water EAR is only possible with continual practice in the ocean and, in general, an injured diver's best interests are usually served by protecting their airway and getting them out of the water as quickly as possible.



RESUSCITATION
 
 
Effective  EAR  and  chest  compression  ( which  obviously  should  not  be  attempted in  the  water )  are  life-saving  if  cardiorespiratory  arrest  occurs,  regardless  of  the cause  of  the  injury.
Techniques  should  not  vary  between  the  diver  who  has  drowned  and  the  diver who  has  been  envenomated,  nor  should  it  be  altered  for  a  hypothermic  diver  (in whom  it  must  never  be  abandoned  until  after  re-warming  has  been  completed).



POSITION
If any form of decompression illness (DCI) is suspected, then the diver must be laid flat and not allowed to sit-up or stand as this may cause bubbles to distribute from the left ventricle and aorta to the brain. Although such posture-induced phenomena are unusual (rare), they have a very poor outcome. This posture must be maintained until the injured diver with DCI is inside a recompression chamber (RCC). A headdown posture is no longer advocated as it may increase the return of and subsequent "arterialization" of venous bubbles, it causes cephalic-venous engorgement such that subsequent middle-ear inflation (e.g. in a RCC during treatment) is very difficult, it limits access for resuscitation and assessment, and, in animal-model studies it actually retards the recovery of brain function in comparison to the horizontal posture.



OXYGEN
With the exception of oxygen toxicity, administration of 100% oxygen is useful in all diving accidents. Although divers who have pulmonary oxygen toxicity need to breathe a PiO2 of less than 0.6 Bars, many of those who have had an oxygen-induced convulsion will subsequently become hypoxic and need oxygen administration.
To administer 100% oxygen, a sealing anesthetic-type mask is needed (unless a mouthpiece and nose-clip in a conscious diver or an endotracheal tube is used) and a circuit with high gas flow-rates and a gas reservoir must be used. Air breaks, to retard pulmonary damage, may be needed, but should be minimized as must all other interruptions. This is one of the reasons why oral rehydration is not particularly useful.
It is noteworthy that administration of 100% oxygen is the definitive treatment of the salt-water aspiration syndrome and most pulmonary barotrauma, including the majority of pneumothoraces. Indeed, chest cannulation is rarely needed.



IV fluids
As with oxygen, aggressive intravenous rehydration is probably of benefit to all injured divers, even those who have drowned. Certainly, such therapy is of considerable benefit in DCI. Isotonic solutions should be used. Glucose solutions should be avoided as they have been shown to increase damage in neurological trauma.
An indwelling catheter should be inserted (filled with water, not air) and an accurate fluid balance is essential. A persistent poor urinary output despite adequate fluid replacement may indicate either persistent hemoconcentration or bladder dysfunction. Either indicates severe DCI and warrants both bladder catheterization and further fluid replacement.



Medications
There are no drugs of proven benefit in the treatment of DCI. Corticosteroids, anti-platelet drugs, aspirin have been tried without success. Lignocaine has been shown to improve neurological outcome of DCS, particularly when added to oxygen. Diazepam is used to prevent and treat oxygen convulsions and to control vestibular symptoms. It makes titration of treatment almost impossible because it masks the symptoms. Indomethacin is useful only when used in combination with prostaglandin and heparin.
Nasal decongestants and analgesics are useful in many divers with aural barotrauma, and, rarely, antibiotics may be indicated.
Some chemotherapy is useful for marine animal injuries. Many coelenterate (jelly-fish) tentacle nematocysts are inactivated by being doused with vinegar. Fish-sting pain is markedly reduced by immersion of the sting-site in hot water.
Box jellyfish stings
Box jelly fish injury
 
 
Box jellyfish
   Box jelly fish
Compression-immobilization bandages should be used where possible. Analgesia often requires regional or local anesthetic-blockade and there are specific anti-venoms available for the box jelly fish (Sea wasp), the stone fish and for sea snakes




In-Water Treatment
In-water treatment of DCI is practiced and advocated by some, but is logistically difficult, requires dedicated and effective equipment (e.g. full-face mask; umbilical and breathing system cleaned for oxygen; cradle, chair or platform that can be lowered to the desired depth; warm, calm water without current and dangerous marine animals; and, adequate supplies of oxygen), and clearly should not be used for unconscious, confused or nauseated divers. In general, the diver should be retrieved as quickly as possible to a definitive treatment facility.



Transportation
As for any retrieval of an injured person, stabilization of the diver must precede transportation. This will include resuscitation, delivery of oxygen, insertion of an intravenous line, correction of hypothermia (in divers in the field this should be based on passive re-warming using dry clothes and blankets) or hyperthermia (most likely in closed-diving systems and again the response will need to be specifically developed and practiced), control of hemorrhage and splinting of fractures. A record of oxygen administration and fluid balance is essential.
If DCI is suspected, then the retrieval must not exceed 1000 ft above sea level. A transportable recompression chamber is ideal, but hyperbaric transportations are logistically difficult and considerable time-savings are needed to justify this activity. Many aircraft can be pressurized to "sea-level' during flight, although this usually limits the altitude at which they can fly (and hence makes the retrieval slower and more fuel-expensive). Unpressurized aircraft are intrinsically unsuitable and must fly at less than 1000 feet, which is often not possible. Road transport may also be inappropriate depending upon the road's altitude, contour and surface.



Summary
It is desirable to have a standard approach to the initial management (i.e. first-aid) of an injured diver.  An injured diver must be removed from the water as quickly as possible. An injured diver usually requires oxygenation and rehydration. Attention to these, and early adequate retrieval can significantly improve outcome.


Management where no chamber is available
a.     100% O2 by tight-fitting mask in all cases. Continue to   treat and transport even if becomes asymptomatic!

b.     Oral fluids - 1 liter (non-alcoholic)per hour.

c.     IV fluids as soon as possible. Avoid over-loading. One to         2 liters in first hour, then 100 cc per hour. Glucose       containing fluids should not be given in the event of   neurological DCS.
        Hyperglycemia increases the chance of neurological        damage.
        -Ringer's solution without dextrose. Hartmann's,     Lactated Ringer's or Normal saline preferred.
        -Normal saline
        -LMW Dextran (Dextran 40, Rheomacrodex) in saline    (alters the charge of the RBC, preventing Rouleaux   formation). 500 cc twice daily. Beware of adverse effects     of anaphylaxis and pulmonary edema.

        d. Medications
    1. Glucocorticoids in neurological DCS.
    2. Diazepam (Valium) 10-15 mg IV or per rectum to    control seizures and severe vertigo.
    3. Aspirin is given by some.
    4. Lidocaine is being used by some but is still not yet   proven.

e.     Catheterization for the paraplegic. Use water in the        balloon rather than air. Protect pressure points.

f.  Pleurocentesis, if indicated.

        Transport, transport, transport! Fly in aircraft        pressurized at sea level or as low as possible. Beware        driving through mountain passes. Have diver         accompanied by a person familiar with the facts.
D tampilkan ulang oleh dr. Erick Supondha ( hyperbaric & diving medicine consultant)  dokter ahli hiperbarik dan kesehatan penyelaman , Jakarta Indonesia , telepon 99070050 , sumer by Ernest S Campbell, MD, FACS

Selasa, 20 Desember 2011

Oxygen Resuscitation Equipment

Oxygen should be an absolute necessity on a dive boat and would certainly be helpful on any boat. Knowledge is needed as the appropriate local emergency information number to call and this information should be readily available in the First Aid kit.. If the kit is used, it should be immediately replenished and should be up dated every 6 months to a year depending on the types of medications it contains.
Oxygen Resuscitation Equipment
The DAN Oxygen System provides an O2 cylinder in a case with appropriate pressure regulator, flow meter, tubing, airways and ventilation devices. Other oxygen sources are available-but the important thing is that the equipment should be up-to-date, readily available and someone should know how to use it properly.
Oxygen is the one first aid treatment that can be used with the full knowledge that it can only help and usually is the one treatment that will turn a serious diving injury around. It is the first thing you should think of in all serious decompression illness and should be used even if you're uncertain of its need.
It probably would be a good idea to have a backup kit-since most dives are 40-60 minutes away from the shore and the O2 tanks hold generally only 20 minutes of oxygen. A larger O2 tank would solve this problem but in most boats the space is limited.
If possible, have your divemasters take a DAN oxygen course or at least have studied their oxygen manual.
DAN now offers 'Remo2', a partial rebreathing apparatus that prolongs the oxygen supply of the O2 bottle.

Senin, 12 Desember 2011

I. First Aid Kit
The following items are offered as an example of a list of first aid supplies which can be modified according to your needs and experience:
  1. Gloves
  2. Deodorant cleansing soap (antibacterial)
  3. Household Vinegar solution (neutralize jellyfish stings)
  4. Household ammonia
  5. Antibiotic Ointment
  6. Cortisone Cream 1%
  7. Non-aspirin pain reliever
  8. Hot packs
  9. Cold packs (pain relief)
10. Denatured alcohol, 12 oz. bottle (sterilizing instruments)
11. Telfa pads or plastic wrap (cover burns)
12. Absorbent dressings (control severe bleeding with pressure)
13. Squeeze bottle of water, 6 oz. (irrigating eyes and wounds)
14. Squeeze bottle of sterile saline
15. Sterile cotton, gauze pads, and adhesive tape
16. Band-Aids and butterfly bandages
17. Q-TipsTongue depressors
18. Disposable cups
19. Razor blades, single edged
20. Shaving cream
21. Tweezers or forceps
22. Needle nosed pliers with wire cutters (to remove fishhooks)
23. Bandage scissors
24. Lighter or waterproof matches
25.Space blankets
26. Backboard, splints and neckbrace, if space permits
27. Penlight
28. Seasickness medication
29. Pocket mask (eliminates direct contact while resuscitating a person)



Jumat, 25 November 2011

HATI HATI TIDAK SEMUA HIPERBARIK AMAN DAN LAYAK UNTUK MANUSIA

HATI HATI TIDAK SEMUA HIPERBARIK AMAN DAN LAYAK UNTUK MANUSIA
                Ilmu Kesehatan Penyelaman dan hiperbarik sampai saat ini masih belum banyak dilirik dan diminati oleh banyak kalangan medis terutama para dokter. Secara jalur akademis di Indonesia belum ada terbentuk program studi spesialisi kedokteran hiperbarik, Tetapi program studi Magister kedokteran kesehatan penyelaman dan hiperbarik telah lama ada di Fakultas Kedokteran Universitas Indonesia Jakarta. Sampai saat ini masih sedikit lulusan yang dihasilkan. Karena belum terbentuknya program studi spesialisasi Hiperbarik dan kesehatan penyelaman maka pendidikan program magister ini memiliki bobot dan beban praktek yg tinggi saat perkuliahan sehingga para lulusan program magister ini memiliki kemampuan praktisi yg tinggi dan mumpuni di bidang hiperbarik dan kesehatan penyelaman.
                Kita ketahui bahwa Indonesia sangat luas bahkan 2/3 dari wilayah Indonesia adalah perairan dan sangat banyak kekayaan alam yg terkandung didalamnya yang sampai saat ini masih dikuasai oleh pihak asing, dalam hal ini saya menuliskan tentang bidang kesehatan penyelaman dan hiperbarik di seluruh wilayah Indonesia masih dikuasai oleh pihak asing, dan kita terlena , tidak mau  melihat dan berjuang keras agar semua kekayaan dan kesempatan keilmuan yang ada di Indonesia bisa dimiliki dan di kuasai oleh rakyat Indonesia. Ilmu adalah sesuatu yang sangat bermanfaat dalam hidup kita, apapun bentuk dan jenis ilmu itu, jika kita mendalami dan menekuni dengan sungguh sungguh maka tidak ada ilmu yang sia sia atau mubajir, terlebih lagi ilmu kesehatan penyelaman dan hperbarik ini sudah marak dikuasi oleh pihak asing di Indonesia. Mari bersama kita kembangkan bidang keilmuan ini.
                Sayangnya dengan berjalannya hari  adalah segelintir orang yang memiliki kekuasan dan permodalan yang kuat sehingga bisa merekayasa dengan mengembangkan hiperbarik di Indonesia, walaupun saat ini masih seputar Jakarta. Sangat disayangkan dari mereka yang mengembangkan hiperbarik ini bukan semata mata secara keilmuan tetapi dari segi bisnis semata, mengeruk nilai ekonomi dari ketidak tahuan banyak orang bahkan juga  para dokter ahli dan spesialis di Indonesia.Mereka mengembangkan hiperbarik dengan tidak ada satupun orang yang mengerti dan membidangi bahkan pendidikan formal baik secara medis maupun tehnik yang berhubungan dengan kedokteran hiperbarik ataupun tehnik hiperbarik.Sehingga sudah barang tentu hasil akhirnya adalah tidak sesuai dengan yang seharusnya.
                Kami para dokter dan komunitas kedokteran hiperbarik dan kesehatan penyelaman sangat menyayangkan kondisi ini, dan juga ketidaktahuan dari pemerintah tentang bidang keilmuan ini dan peraturan yang tidak ada dan tegas mengatur tentang permasalahan ini membuat peluang yang sangat lebar bagi para spekulan spekulan ini. Menjadi sebuah pemikiran dan juga mungkin olok olok di komunitas kami adalah beberapa alat ini berada di beberapa rumah sakit besar dan mewah bahkan dokter spsesialis yang berpraktek didalam sana banyak para doctor dan professor dan para spesialis senior dan sangat berkompeten di bidang masing masing tetapi didalam sana ada alat hiperbarik yang secara tehnik dan medis kedokteran hiperbarik sangat tidak layak dan aman dipakai untuk pelayan terhadap manusia, jangan kan Izin operasional alat ini, izin kelayakan sebuah alat hperbarik dapat dipakai oleh manusia juga belum ada. Terlebih lagi karena masih sangat terbatas nya para dokter ahli kedokteran hiperbarik dan kesehatan penyelaman maka banyak rumah sakit yang memiliki alat hiperbarik ini tidak memiliki dokter yang kompeten di bidangnya. Hasil akhir tentu anda dapat menilai sendiri.
                Melihat Fenomena seperti ini dan semakin dalamnya jerat dan pengaruh pengaruh yang salah tentang hiperbarik dan kesehatan penyelaman, Kami dari komunitas dokter ahli kedokteran hiperbarik dan kesehatan penyelaman bersepakat untuk terus memasyarakatkan bidang keilmuan hiperbarik dan kesehatan penyelaman baik untuk kalanagan awam, para penyelam dan juga para dokter dan calon dokter, kami terus melakukan kampanye , seminar, dan bahkan bebrapa dari kami aktif sebagai pengajar di fakultas kedokteran untuk memberikan bekal tentang hiperbarik dan kesehatan penyelaman yang sebenar benarnya. Kami saat ini juga telah memiliki sebuah perusahaan yang khusus memproduksi alat tabung hiperbarik dan membentuk sebuah lembaga usaha dalam rangka memberikan pendidikan dan pelatihan kepada para dokter dan tenaga medis di seluruh Indonesia tentang hiperbarik yang baik dan benar.
                Saat ini sudah beberapa tabung hiperbarik di produksi oleh perusahaan ini tentunya dengan standar yang benar sesuai dengan diving medicine dan memiliki sertifikasi internasional dan juga sertifikasi bahwa alat hiperbarik ini layak dipakai dan aman untuk manusia. Lebih penting lagi  perlatan hiperbarik ini di awaki dan diawasi oleh para dokter ahli hiperbarik dan kesehatan penyelaman, serta secara tehnik semua pealatan di rawat dan di kalibrasi oleh para tehnisi yang khusus di bidang hiperbarik.
                Terlebih penting adalah semua peralatan yang dipakai adalah bahan dan peralatan yang sesuai dengan diving medicine dan aman untuk manusia, system filterisasi sangat berlapis dan terawatt dengan baik, tekanan yang dicapai sesuai dengan teori teori hiperbarik. Intinya kami memberikan dan mengembangkan ilmu yang dapat dimanfaat secara medis dengan benar oleh masyarakat luas, bukan hanya semata mencari nilai ekonomis, kami para dokter di komunitas kedokteran hiperbarik dan kesehatan penyelaman tidak ingin citra baik dan manfaat yg tinggi dari hiperbarik rusak dan buruk akibat ulah segelintir orang yang bermain secara ekonomis bukan berlandaskan keilmuan.
                Terakhir kami dari komunitas kedokteran hiperbarik dan kesahatan penyelaman menghimbau kepada seluruh masyarakat luas, para penyelam professional, rekreasi, dan komersial, serta para dokter dan guru besar agar teliti dan hati hati saat akan melakukan terapi hiperbarik, jangan sampai bermaksud untuk sehat malah sebaliknya. Kami siap memberikan informasi kepada seluruh masyarakat yang membutuhkan dalam rangka usaha kami untuk mensosialisasikan hiperbarik yang benar dan aman untuk manusia. Silahkan hubungi kami melalui blog ini atau dapat melalui web di :
                Salam ,semoga bermanfaat info hati hati dari kami. Terima kasih.      

Jumat, 11 November 2011

Percutaneous Transthoracic Needle Biopsy Complicated by Air Embolism Blake W. Arnold1 and William J. Zwiebel + Author Affiliations 1 Both authors: VA Salt Lake City Health Care System Imaging Services, 500 Foothill Dr., Salt Lake City, UT 84148. Next Section Percutaneous transthoracic needle biopsy is a common procedure for evaluating pulmonary and mediastinal lesions. The most frequent complications include pneumothorax (27-49%), hemorrhage (11%), and hemoptysis (7%) [1,2,3]. Air embolism resulting from thin-needle biopsy is a rare (incidence of ≈ 0.07%) but potentially life-threatening complication [1]. In this article we report a case of air embolism to the heart that was confirmed on CT. Previous SectionNext Section Case Report A 60-year-old man with a 10-year history of corticosteroid-dependent chronic obstructive pulmonary disease presented with three episodes in the preceding 5 months of left lower lobe “pneumonia” accompanied by recurrent hemoptysis and a segmental left lower lobe opacity on chest radiography. The patient was further evaluated with chest CT that showed a focal 2.5-cm mass in the posterior segment of the left lower lobe and adjacent ground-glass opacity that was attributed to resolving pneumonia. No hilar or mediastinal adenopathy was present. Several low-density liver lesions were also seen that were too small to characterize on CT. Because the liver lesions were small and inaccessible and because the lung mass could be approached easily, percutaneous transthoracic needle biopsy was attempted. This procedure was performed 2 weeks after the diagnostic chest CT scan was obtained. In the interval, the appearance of the left lower lobe mass and ground-glass opacity did not change, and the patient's clinical condition remained stable. His medical history was remarkable for asthma treated with steroids and a melanoma of the right cheek that was removed 4.5 years previously. The differential diagnosis of the lung lesion was metastatic melanoma or bronchogenic carcinoma. The patient was placed in right lateral decubitus position and the lesion was localized using CT. A 19-gauge Chiba-type needle was placed into the lesion on the first pass during a single inspiratory breath-hold (Fig. 1A). This needle was not moved until the end of the procedure, and scans obtained at intervals during the procedure showed its position to be unchanged relative to the pulmonary mass. A coaxial 21-gauge needle was inserted through the 19-gauge needle, and three aspiration biopsy specimens were obtained using suction with a 10-mL syringe. The 19-gauge needle stylet was inserted between obtaining the specimens with the 21-gauge needle. With the 21-gauge needle removed, a final specimen was taken without aspiration using the 19-gauge needle. The patient was entirely cooperative during the procedure. The insertion of the needle and the aspiration biopsy were conducted during suspended inspiration. At no time did the patient cough or breathe inappropriately while the needles were in his chest. Fig. 1A. View larger version: In this page In a new window Download as PowerPoint Slide Fig. 1A. —60-year-old man with left lower lobe mass who underwent percutaneous lung biopsy. Axial CT images show percutaneous biopsy needle positioned at periphery of lesion (A), air—fluid level in left ventricle (arrow) after biopsy (B), and small bubbles of air (arrows) in coronary arteries after biopsy (C). At the end of the procedure, after the removal of the 19-gauge needle, the patient briefly coughed and expectorated a small amount of bright red blood. Immediately afterward, a 10-slice CT scan was obtained to assess whether pneumothorax was present. At the end of this scanning, the patient again coughed and expectorated a small to moderate amount of bright blood. While he was being moved to prevent aspiration, he abruptly became unresponsive, and respiratory arrest occurred. Resuscitative efforts were started immediately and the cardiac arrest team was called. Resuscitative efforts were unsuccessful and the patient died on the CT table. Because of the acute need to prevent aspiration and the subsequent cardiac arrest, the CT scans obtained after the procedure were only briefly examined; they showed a very small left pneumothorax. After the cardiac arrest team arrived, a more careful review of the postprocedure CT scans revealed an airfluid level in the left ventricle and small bubbles of air along the presumed course of the coronary arteries (Figs. 1B and 1C). Fig. 1B. View larger version: In this page In a new window Download as PowerPoint Slide Fig. 1B. —60-year-old man with left lower lobe mass who underwent percutaneous lung biopsy. Axial CT images show percutaneous biopsy needle positioned at periphery of lesion (A), air—fluid level in left ventricle (arrow) after biopsy (B), and small bubbles of air (arrows) in coronary arteries after biopsy (C). Fig. 1C. View larger version: In this page In a new window Download as PowerPoint Slide Fig. 1C. —60-year-old man with left lower lobe mass who underwent percutaneous lung biopsy. Axial CT images show percutaneous biopsy needle positioned at periphery of lesion (A), air—fluid level in left ventricle (arrow) after biopsy (B), and small bubbles of air (arrows) in coronary arteries after biopsy (C). An autopsy was performed, and subsequent microscopic analysis and immunofluorescent staining showed that the left lower lobe mass was malignant melanoma. Autopsy of the chest revealed that the portion of the lung traversed by the needle was chronically inflamed and friable, apparently because of recent pneumonia. The left lung was removed en bloc, and the bronchus was injected with water-soluble contrast material under fluoroscopic visualization. A fistula from a bronchus to a pulmonary vein could not be defined. Previous SectionNext Section Discussion Percutaneous transthoracic needle biopsy is a frequently performed procedure that is accepted as a standard method for the diagnosis of pulmonary lesions. Pneumothorax is reported in 27-49% of cases and is the most frequent complication [1,2,3]. Intraparenchymal hemorrhage is also a frequent complication, occurring in about 11% of cases, and hemoptysis occurs in about 7% of cases [1,2,3]. The mortality of the procedure is unclear, although Berquist et al. [3] reported two deaths resulting from hemorrhage after biopsy. With respect to air embolism, Sinner's review of the literature [1] found two suspected cases in 2726 patients. We have found seven additional reports of air embolization during percutaneous needle biopsy of lung lesions [4,5,6,7,8,9,10]. These cases resulted in neurologic morbidity or death. To our knowledge, the case reported here is the first to show gas in the heart and coronary arteries. The formation of a communication between an airway and a pulmonary vein is the assumed mechanism of air embolization during percutaneous lung biopsy. It is not difficult to understand how this might occur, considering that pulmonary vein pressure is normally only 10 cm H2O. It is possible that the coughing episodes in this patient contributed to the entry of air into the pulmonary veins by increasing air pressure in the pulmonary airways. Other factors such as chronic obstructive pulmonary disease and air trapping may have also contributed to increased airway pressure, resulting in an increased pressure gradient between the airway and the pulmonary vein. An alternate mechanism for air embolization is communication between the needle and a pulmonary vein if the patient breathes while the needle hub is open to the air. This cause seems unlikely in this case, because the needle and stylet were inserted directly into the mass during a single breath-hold and the patient did not breathe while the needle hub was open to the air. The friability of tissues and vessels is an indication that the patient's corticosteroid dependence may have contributed to the air embolization in this case. The vascular nature of this lesion was shown on autopsy, and the increased vascularity of the mass may have increased the risk of air embolism. Another contributing factor may have been postinflammatory changes in a portion of the lung traversed by the needle. At autopsy, the left lower lobe was easily torn and friable, possibly contributing to the formation of an airway—vein fistula. This case raises several practical points. First, serious complications can occur during percutaneous lung biopsy, even when the technique is excellent and patient cooperation is perfect. Second, some practitioners perform percutaneous lung biopsies with the patient in sustained expiration, rather than inspiration, in an attempt to prevent air embolization. Such is not the prevailing practice in our department, because in our experience many patients cannot suspend respiration as well in expiration as in inspiration. Therefore, the potential benefit of expiratory biopsy must be judged against the risk of uncontrolled respiration during manipulation of the needle. Third, the use of the outer 19-gauge needle in obtaining a final biopsy specimen may result in an increased risk of an airway—vein fistula formation because of the larger diameter of the needle (compared with the usual 21-gauge biopsy needle). Although this possibility is theoretic, we have stopped using the 19-gauge needle as a biopsy device and simply use it as a conduit for the 21-gauge needle. Fourth, passage of the needle through diseased lung, as in this patient, may increase the risk of complications, including hemorrhage and air embolus. This potential risk should be considered in planning the access route to a lung lesion. In this instance, no other practical approach to the mass was present. Finally, if it had been recognized that gas was present in the left ventricle before it embolized to the brain, the patient might have been quickly placed in Trendelenburg's position and right-side down. However, to do so was not possible in this case because the patient suffered cardiac arrest immediately after the CT images were acquired and before they could be examined. The tr

Percutaneous Transthoracic Needle Biopsy Complicated by Air Embolism

  1. Blake W. Arnold1 and
  2. William J. Zwiebel
+ Author Affiliations
  1. 1 Both authors: VA Salt Lake City Health Care System Imaging Services, 500 Foothill Dr., Salt Lake City, UT 84148.
Percutaneous transthoracic needle biopsy is a common procedure for evaluating pulmonary and mediastinal lesions. The most frequent complications include pneumothorax (27-49%), hemorrhage (11%), and hemoptysis (7%) [1,2,3]. Air embolism resulting from thin-needle biopsy is a rare (incidence of ≈ 0.07%) but potentially life-threatening complication [1]. In this article we report a case of air embolism to the heart that was confirmed on CT.

Case Report

A 60-year-old man with a 10-year history of corticosteroid-dependent chronic obstructive pulmonary disease presented with three episodes in the preceding 5 months of left lower lobe “pneumonia” accompanied by recurrent hemoptysis and a segmental left lower lobe opacity on chest radiography. The patient was further evaluated with chest CT that showed a focal 2.5-cm mass in the posterior segment of the left lower lobe and adjacent ground-glass opacity that was attributed to resolving pneumonia. No hilar or mediastinal adenopathy was present. Several low-density liver lesions were also seen that were too small to characterize on CT.
Because the liver lesions were small and inaccessible and because the lung mass could be approached easily, percutaneous transthoracic needle biopsy was attempted. This procedure was performed 2 weeks after the diagnostic chest CT scan was obtained. In the interval, the appearance of the left lower lobe mass and ground-glass opacity did not change, and the patient's clinical condition remained stable. His medical history was remarkable for asthma treated with steroids and a melanoma of the right cheek that was removed 4.5 years previously. The differential diagnosis of the lung lesion was metastatic melanoma or bronchogenic carcinoma.
The patient was placed in right lateral decubitus position and the lesion was localized using CT. A 19-gauge Chiba-type needle was placed into the lesion on the first pass during a single inspiratory breath-hold (Fig. 1A). This needle was not moved until the end of the procedure, and scans obtained at intervals during the procedure showed its position to be unchanged relative to the pulmonary mass. A coaxial 21-gauge needle was inserted through the 19-gauge needle, and three aspiration biopsy specimens were obtained using suction with a 10-mL syringe. The 19-gauge needle stylet was inserted between obtaining the specimens with the 21-gauge needle. With the 21-gauge needle removed, a final specimen was taken without aspiration using the 19-gauge needle. The patient was entirely cooperative during the procedure. The insertion of the needle and the aspiration biopsy were conducted during suspended inspiration. At no time did the patient cough or breathe inappropriately while the needles were in his chest.
Fig. 1A. 60-year-old man with left lower lobe mass who underwent percutaneous lung biopsy. Axial CT images show percutaneous biopsy needle positioned at periphery of lesion (A), air—fluid level in left ventricle (arrow) after biopsy (B), and small bubbles of air (arrows) in coronary arteries after biopsy (C).
At the end of the procedure, after the removal of the 19-gauge needle, the patient briefly coughed and expectorated a small amount of bright red blood. Immediately afterward, a 10-slice CT scan was obtained to assess whether pneumothorax was present. At the end of this scanning, the patient again coughed and expectorated a small to moderate amount of bright blood. While he was being moved to prevent aspiration, he abruptly became unresponsive, and respiratory arrest occurred. Resuscitative efforts were started immediately and the cardiac arrest team was called. Resuscitative efforts were unsuccessful and the patient died on the CT table.
Because of the acute need to prevent aspiration and the subsequent cardiac arrest, the CT scans obtained after the procedure were only briefly examined; they showed a very small left pneumothorax. After the cardiac arrest team arrived, a more careful review of the postprocedure CT scans revealed an airfluid level in the left ventricle and small bubbles of air along the presumed course of the coronary arteries (Figs. 1B and 1C).
Fig. 1B. 60-year-old man with left lower lobe mass who underwent percutaneous lung biopsy. Axial CT images show percutaneous biopsy needle positioned at periphery of lesion (A), air—fluid level in left ventricle (arrow) after biopsy (B), and small bubbles of air (arrows) in coronary arteries after biopsy (C).
Fig. 1C. 60-year-old man with left lower lobe mass who underwent percutaneous lung biopsy. Axial CT images show percutaneous biopsy needle positioned at periphery of lesion (A), air—fluid level in left ventricle (arrow) after biopsy (B), and small bubbles of air (arrows) in coronary arteries after biopsy (C).
An autopsy was performed, and subsequent microscopic analysis and immunofluorescent staining showed that the left lower lobe mass was malignant melanoma. Autopsy of the chest revealed that the portion of the lung traversed by the needle was chronically inflamed and friable, apparently because of recent pneumonia. The left lung was removed en bloc, and the bronchus was injected with water-soluble contrast material under fluoroscopic visualization. A fistula from a bronchus to a pulmonary vein could not be defined.

Discussion

Percutaneous transthoracic needle biopsy is a frequently performed procedure that is accepted as a standard method for the diagnosis of pulmonary lesions. Pneumothorax is reported in 27-49% of cases and is the most frequent complication [1,2,3]. Intraparenchymal hemorrhage is also a frequent complication, occurring in about 11% of cases, and hemoptysis occurs in about 7% of cases [1,2,3]. The mortality of the procedure is unclear, although Berquist et al. [3] reported two deaths resulting from hemorrhage after biopsy.
With respect to air embolism, Sinner's review of the literature [1] found two suspected cases in 2726 patients. We have found seven additional reports of air embolization during percutaneous needle biopsy of lung lesions [4,5,6,7,8,9,10]. These cases resulted in neurologic morbidity or death. To our knowledge, the case reported here is the first to show gas in the heart and coronary arteries.
The formation of a communication between an airway and a pulmonary vein is the assumed mechanism of air embolization during percutaneous lung biopsy. It is not difficult to understand how this might occur, considering that pulmonary vein pressure is normally only 10 cm H2O. It is possible that the coughing episodes in this patient contributed to the entry of air into the pulmonary veins by increasing air pressure in the pulmonary airways. Other factors such as chronic obstructive pulmonary disease and air trapping may have also contributed to increased airway pressure, resulting in an increased pressure gradient between the airway and the pulmonary vein. An alternate mechanism for air embolization is communication between the needle and a pulmonary vein if the patient breathes while the needle hub is open to the air. This cause seems unlikely in this case, because the needle and stylet were inserted directly into the mass during a single breath-hold and the patient did not breathe while the needle hub was open to the air.
The friability of tissues and vessels is an indication that the patient's corticosteroid dependence may have contributed to the air embolization in this case. The vascular nature of this lesion was shown on autopsy, and the increased vascularity of the mass may have increased the risk of air embolism. Another contributing factor may have been postinflammatory changes in a portion of the lung traversed by the needle. At autopsy, the left lower lobe was easily torn and friable, possibly contributing to the formation of an airway—vein fistula.
This case raises several practical points. First, serious complications can occur during percutaneous lung biopsy, even when the technique is excellent and patient cooperation is perfect. Second, some practitioners perform percutaneous lung biopsies with the patient in sustained expiration, rather than inspiration, in an attempt to prevent air embolization. Such is not the prevailing practice in our department, because in our experience many patients cannot suspend respiration as well in expiration as in inspiration. Therefore, the potential benefit of expiratory biopsy must be judged against the risk of uncontrolled respiration during manipulation of the needle. Third, the use of the outer 19-gauge needle in obtaining a final biopsy specimen may result in an increased risk of an airway—vein fistula formation because of the larger diameter of the needle (compared with the usual 21-gauge biopsy needle). Although this possibility is theoretic, we have stopped using the 19-gauge needle as a biopsy device and simply use it as a conduit for the 21-gauge needle. Fourth, passage of the needle through diseased lung, as in this patient, may increase the risk of complications, including hemorrhage and air embolus. This potential risk should be considered in planning the access route to a lung lesion. In this instance, no other practical approach to the mass was present. Finally, if it had been recognized that gas was present in the left ventricle before it embolized to the brain, the patient might have been quickly placed in Trendelenburg's position and right-side down. However, to do so was not possible in this case because the patient suffered cardiac arrest immediately after the CT images were acquired and before they could be examined. The treatment for other cases of air embolism has been a decompression chamber, and that may have been an option in this case had the presence of air in the left ventricle been discovered earlier.

Footnotes

  • Address correspondence to B. W. Arnold.
  • Received September 7, 2001.
  • Accepted December 6, 2001.

References



Articles citing this article

Rabu, 05 Oktober 2011

The Impacts Of Smoking On Diving

The Impacts Of Smoking On Diving

By Art Ranz, DDS

Cigarette smoking is one of the largest preventable health and death risks in the United States. It receives enormous amounts of negative media attention and yet millions of people start smoking every year. Unfortunately, it is frequently difficult to have a prudent, scientific discussion about the risks of smoking with someone who is addicted to nicotine. The addiction leads smokers to rationalize or deny the risks of smoking. However, this `head in the sand` response allows them to ignore the obvious impact that smoking has upon their bodies and the more subtle ways it effects many aspects of their lives, such as scuba diving.
The effects of smoking are especially significant for persons who participate in scuba diving. A review of scientific literature about the body's reaction to smoking and nicotine addiction illustrates how smoking can effect diving performance. While the diving and health limitations imposed by tobacco use vary according to the degree of use, tobacco always has some impact on individual health.
The most extensive, long-term, prospective study on smoking and other health issues is the Framingham study. This ongoing study has followed 5,000 people for more than 34 years, providing a wide range of statistical information. For instance, the 30-year-old who smokes 15 cigarettes a day - or less than one pack - shortens his life by five years. Smokers experience a 20-fold increase in lung cancer and greatly increased cancer rates in other organs, including skin, bladder, pancreas, mouth and throat. Smokers have twice the risk of cardiovascular disease, 2.2 times the number of strokes and 3.5 times more intermittent claudication expressed as leg cramping due to a lack of circulation. At any given age, the risk of dying for any reason is twice that of a non-smoker. Smokers have seven times the normal incidence of airway damage and respiratory distress. Children who smoke beginning at age 14 only develop 92 percent of the lung function, on average, that a non-smoking child does. This loss of function is permanent. Obviously, efficient lung function is essential to managing stressful situations and promoting efficient inert gas removal from a diver's blood. Poor circulatory efficiency can have dangerous impacts on inert gas elimination and oxygen delivery to needy muscles, greatly effecting a diver's personal safety. Atherosclerotic plaques in blood vessels form twice as fast when smoking is added to a high fat diet.
There are great increases in the LDL (`bad cholesterol`) that reduces circulatory efficiency and complicates inert gas removal. Inert gas (especially nitrogen) appears to lodge in fatty deposits, creating likely sites for bubble congregation and growth. Furthermore, 90 percent of patients with infections after spinal surgery are smokers and bone marrow density in men is decreased almost 20 percent and in women 25-30 percent, while the incidence of back pain from a work related injury increases from one in five to one in two for smokers. Hyperbaric bone damage (osteonecrosis) has gained increasing concern among medical professionals as researchers strive to demonstrate the cause of occasional bone degradation. To be sure, reduced bone density due to smoking aggravates the problem and some researchers are suggesting a more careful analysis of the relationship between hyperbaric damage and tobacco smoking.

How does tobacco cause such dangerous repercussions?

There are four groups of dangerous substances present in cigarette smoke:
  1. Carcinogens and co-carcinogens are mostly polycyclic aromatic alcohols that directly initiate cancer formation. These affect areas in direct contact with the smoke and also distant organs through absorption into the bloodstream.
  2. Irritants cause immediate coughing and broncoconstriction, inhibit cilliary action in the lung and stimulate mucus secretion.
  3. Chronic exposure to nicotine induces an increase in the number of nicotinic cholinergic receptors in the brain, causing structural and functional changes in the brain and nervous system. It induces tolerance and physical and psychological changes upon withdrawal. These are classic developments from an addictive drug.
  4. Toxic gases are inhaled, including carbon monoxide, hydrogen sulfide and hydrogen cyanide.
Smoking related cancer is tragic, costly and largely preventable, but the direct impact to diving is often less obvious. By way of illustration, the irritants present within smoke induce a chronic inflammation of the alveoli causing the body to produce proteolytic enzymes that eat away at the alveolar wall. Cilia are microscopic hairs that fan and carry harmful particles out of the lung. The irritants present in smoke impede these cilliary actions. With the addition of increased secretions, the lung has now lost a significant part of its defenses from outside agents. Chronic bronchitis develops, making smokers more susceptible to emphysema, viral and bacterial infections. As this process continues over the years and more alveolar damage occurs, there is a loss of capillaries in the walls which causes `ventilation-perfusion abnormalities.`
This damaging chain of events leads to a reduction in the area of alveolar membrane available for gas exchange and also to perfusion of unventilated areas and ventilation of unperfused areas. In simple terms, gas exchange is compromised and air (or other gases) is not reaching the blood for exchange. General lung function is often severely compromised in the smoking population as is evidenced by several clinical measurements in the lung. The standard measure of lung function is the forced expiratory volume in one second or FEV1. This is the amount of air that can be exhaled in one second.
The Framingham study showed the FEV1 to be decreased to 80 percent of expected values in smokers. This decrement in lung function creates less efficient ventilation on exertion and decreases the force of the cough (a vital protective mechanism for the lung) and may indicate a general degradation of lung health. The forced vital capacity (FVC) is another common measure of lung function and measures the amount of air one can expel from a full inhale to a full exhale. On average, smoking reduces FVC by 10 percent in moderate smokers. A 10 percent reduction in vital capacity is a significant indication of lung dysfunction and an obvious deterrent to pulmonary exchange in decompression.
Nicotine is not only a powerfully addictive drug, but a potent pharmacological agent. Nicotine promotes platelet aggregation and fibrinogen formation, which are precursors to the clots that obstruct small blood vessels. An obstruction initiates negative repercussions that increases the risk of diving and decompression. The heart rate increases, elevating oxygen consumption and the shrinking of small blood vessels increases total peripheral resistance. The resistance, in turn, causes more problems such as increased blood pressure and poor circulation in the periphery of the body. Peripheral circulation involves the miles of very small blood vessels all over the body. The vessels are problematic in efficient inert gas elimination. For example, the extremities contain numerous areas of reduced circulatory efficiency such as the joints (responsible for the majority of decompression sickness). When divers begin to get chilled, a natural reduction in blood circulation to the peripheral system occurs to maintain a reasonable core temperature. Smoking exacerbates this problem as studies show that the circulation in small blood vessels is reduced 19 percent after just two cigarettes. Poor gas exchange and increased risk of decompression sickness results.

The Problem with Carbon Monoxide

It is important to understand the Oxygen Dissociation Curve when reviewing the impact of smoking on oxygen transport mechanisms. This curve illustrates the assimilation of oxygen in large amounts even with low oxygen pressures in the lungs. Hemoglobin picks up the oxygen from the lungs and transports it to the tissues where it is released. Several factors control how easily the oxygen is released from its hemoglobin carrier. Higher concentrations of carbon dioxide in the blood cause the body to react as if there is poor ventilation and a greater need for oxygen. This environment initiates the release of more oxygen to the tissues. Under these conditions the hemoglobin affinity for oxygen is reduced, making it easier for oxygen to be released. In reference to the Dissociation Curve, this condition is sometimes referred to as a `shift to the right` and results in a greater supply of oxygen to the tissues. However, a `shift to the left` prevents oxygen from being released to the tissues. This condition is prominent with the carbon monoxide accumulation that results from smoking.
The primary mechanism behind the risk of carbon monoxide impact is twofold. First it binds to hemoglobin 250 times better than oxygen, making a compound called carboxyhemoglobin. This compound replaces the oxygen in the hemoglobin molecule and prevents the leftward shift of the Oxyhemoglobin Dissociation Curve. The increased affinity of hemoglobin for oxygen results in a decrease in oxygen carrying capacity and impaired release of the oxygen once it reaches the tissues. Non-smokers have about one percent carboxyhemoglobin while smokers have close to 15 percent. To illustrate the severely harmful effects of CO in the blood, imagine that an individual has 50 percent of their hemoglobin bound to CO. Compare this individual with another person who has lost half of their hemoglobin (due to severely bleeding ulcers, chronic gastrointestinal bleeding or massive injuries, for instance).The individual who has 50 percent of their hemoglobin bound with CO will die. But, the person who has a 50 percent loss of hemoglobin will still not experience hypoxia while in a resting state.
Furthermore, chronic hypoxia (reduced oxygen) results from the smoking induced impairment of oxygen transport and causes the production of more red blood cells. The red blood cells are the containing mechanism for oxygen transport in the hemoglobin. The Framingham study has shown that smokers have a significant increase in the percentage of red blood cells in the blood (increased hematocrit). Normally the red blood cells are about 35-40 percent of the blood by volume. Smoking can cause this to increase by 20 percent, making the blood much more viscous, inducing obvious complications to efficient circulation. This problem is further aggravated by the pressures found below the surface and causes sludging of the red blood cells in the small capillaries, damaging the cells lining the blood vessels (endothelium).
The transport of hydrogen cyanide to the lungs during smoking creates additional decrements to health and diving safety. This noxious gas directly prevents use of oxygen by the cells by interfering with the cellular engine- the mitochondria. Even small amounts of hydrogen cyanide are deadly. The presence of this toxic substance causes direct injury to the lung by interfering with the alveolar enzymes normally responsible for maintaining the integrity of the alveolar membranes. Hydrogen sulfide is another dangerous substance in cigarette smoke and is a direct toxin to most all cell life, especially to tissues it directly contacts such as the lungs. The numerous impediments to a healthy circulatory and respiratory system establish an insidious cycle of unacceptable risk to safe diving practices.
For instance, when increasing environmental demands require the delivery of more oxygen, the smoker is at a serious disadvantage. An increased supply of oxygen in the inspired air does not help delivery of more oxygen to the tissues where it is needed. There are two ways to increase oxygen delivery with increased demand: increasing blood flow through the tissue and raising the coefficient of oxygen usage. The former is compromised by the inferior cardiovascular condition of the smoker (consider the number of serious atheletes who smoke). The latter is increased by two things that happen automatically: greater partial pressure of oxygen between blood and tissue (resulting from the increase in oxygen consumption in the tissues) and the rise in carbon dioxide as a byproduct of increased metabolism. This increase in carbon dioxide causes the hemoglobin curve to shift to the right and allow more release of oxygen. This typically beneficial reaction is countered by the smoker's CO poisoning and the shift back to the left. The really adverse effect of smoking is the 20-30 percent rise in peripheral resistance (closing or restriction of small blood vessels) caused by the presence of nicotine. Small blood vessels are where the exchange of gases takes place and a reduction of circulatory efficiency in this area may be significant. Reduced blood flow and impeded oxygen release prevent efficient oxygenation especially when it is needed most. Therefore, the simple act of smoking initiates circulatory reactions that place divers in harm's way. Whether from decompression illness risk or ineffectual response to stressful environments, the smoker intentionally places himself and his team at greater risk.

Understanding Smoking's Short Term Impact on Diving

Smokers and those who choose to dive with them should consider not only the long-term health impacts, but the immediate implications of smoking and diving. Consider the increase in sudden cardiac death, the reduced ability to absorb and deliver oxygen to the cells, the obvious cognitive impairment, the likely increased risks of decompression illness, the increased likelihood of lung overpressurization injuries and the many other dangerous effects of smoking and diving. With all of the damage and risk associated with smoking and diving, what possible justification (save addiction) can there be to continue? Individuals with drug addictions, which is clearly what smoking is, must be encouraged to seek assistance and be freed from this damaging habit.
Consider that many `diving deaths` are thought to be cardiovascular in nature: cardiac arrhythmias, myocardial infarcts and strokes just to name a few. The smoker's incidence of these maladies is much higher. With this in mind, can a smoker be a responsible diving buddy? Can they help other divers out of trouble or are they merely likely to create problems? With increased anxiety, the heart beats faster and the breathing rate increases. Increased heart rate is the number one cause of increased oxygen use by the heart muscle and the heart of a smoker has a reduced ability to deal with the increased demand for oxygen. As a result, pulmonary exchange is poorer and utilization of breathed gases is compromised, leading to greater gas consumption and reduced ability to assist other divers. All dives are decompression dives. The list is long on how smoking causes decreased gas exchange and potential for decompression sickness. The ability of the lungs to filter bubbles is a major reason that every dive does not result in clinical decompression injury. The lungs are directly damaged by smoking. Ventilation, monitored by FEV1, is decreased, and the Forced Vital Capacity, or FVC, is decrease by at least 10%. With decreased pulmonary function, the lungs' function as a big bubble trap is compromised and the risk of decompression illness is increased.
Nicotine causes significant peripheral constriction, further compromising elimination of gas in the areas most difficult to get the inert gases out the small vessels and the area they perfuse. It causes increased platelet aggregation and fibrinogen production which only gives the body a head start on the same process that bubbles produce in occluding vessels and damaging vessel walls. One prominent theory of decompression illness suggests that bubbles in the bloodstream cause damage to the endothelium, the lining of the blood vessel walls, setting off a cascade of body reactions to repair itself. With nicotine in the body this process is aggravated and accelerated, causing platelets and blood clots to clog the small blood vessels. This reduces the body's ability to get rid of inert gasses. Nicotine gives the body a head start on the bad things that happen with bubble formation. The smoker has increased numbers of red blood cells per volume, or increased hematocrit, which sounds good, but actually makes the blood `thicker.` Increased atmospheric pressure from diving causes sludging of red blood cells in small vessels and the clogging of these vessels is aggravated by the increased hematocrit of the smoker. This is more bad news for perfusing the small vessels in the decompression part of the dive. Increased hematocrit may be directly involved with the endothelial damage which has been implicated in DCS. Carbon monoxide inhibits the transportation of oxygen mostly in its effect upon the hemoglobin and the hemoglobin disassociation curve. Smoking directly reduces pulmonary blood volume and the number of open capillaries in the lung, causing a ventilation to perfusion impairment with the obvious impairment of gas transfer at a time when every little bit is vital.
Acute nicotine withdrawal causes severe performance degradation, memory impairment, confusion, impulsiveness and slowed reaction time, just to name a few. Any of these are serious problems when simple decisions become life or death decisions under water. In a recent study of `undeserved hits` (a dive where supposedly all decompression limits are met and ascent rates are appropriate, but the diver still suffers from decompression illness), smoking and lung damage from smoking seemed to play a key role. Two groups emerged, those with intra-cardiac shunts and those without. Those with shunts had more brain symptoms and none smoked, while those without shunts, 50 percent smoked, a remarkable number. These divers experienced mostly spinal neurological sequelae and had deficits identical to divers with rapid ascents and pulmonary barotrauma. This implies that the smokers had occult lung disease that precipitated the pulmonary barotrauma giving more evidence of hindrance on the body's bubble filter. This makes perfect sense when considering the damage caused by smoking on the small airways and the alveolar walls which allow bubble to pass though the system instead of being filtered. Please think about these facts before picking up that next cigarette or diving with someone who smokes. If you smoke, see your doctor for help with overcoming the addiction. Make your diving safe and fun.

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