George Schroeder MD., M.S., FACEP, FAAUCM
Chief Medical Officer, Magellan Pharmaceuticals, Inc.
International Scientific Advisory Board, Magellan BioScience Corp.
Clinical Assistant Professor of Emergency Medicine, University of Central Florida College of Medicine
AAUCM Executive Council
eJournal Senior Medical Editor
Col. (Ret.) M. Lawrence Kaplan, M.D., DABUCM, DABFM, FACFEI
Clinical Assistant Professor of Emergency Medicine, University of Central Florida College of Medicine
John Spallino, M.D., FACP
Board of Directors eJournal Associate Medical Editor
SCUBA diving has been steadily rising in popularity and most diving injuries are consequences of the significant changes in gases and pressure resulting from expansion of respiratory gases upon descent and ascent. The clinical manifestations of a SCUBA or free diving injury may be seen anywhere during, shortly after a dive or up to 24 hours or later after diving.
Boyle’s Law of Physics states that at constant temperature Volume of gas varies inversely with Pressure applied and physiological consequences explain pressure-related diving diseases (i.e Barotrauma). SCUBA Divers breathing various kinds of compressed gas mixtures , such as Nitrox (Nitrogen + Oxygen), Heliox (Helium + Oxygen) , Trimix ( Helium, Nitrogen & Oxygen), in order to reduce or prevent incidence of pressure-related diving disorders , especially in diving to depth beyond 30 m, or approx. deeper than 100 feet, Divers are subject to risk of pulmonary overinflation, as pressure is reduced, and inversely volume expands on ascent . In accordance with Boyle’s Law:
Volume of Gas @ 30 m (4 bar)
will double@ 10 m (2 bar)
& double again@ 0 m (1 bar) – at surface
Intrapulmonary and environmental pressures are gradually equalized by slow exhalation during ascent from any dive. PBT (Pulmonary Barotrauma) is a direct consequence of: –
Inhaled AIR/GAS = unable to escape through the normal airways (breath-holding on ascent with pulmonary overinflation) leading to > Rupture of parenchymal tissue into one of 3 sites:
- Pulmonary capillaries–causing A.G.E. (ArterialGasEmbolism)
- Intrathoracic Perivascular Sheaths–Mediastinal Emphysema
- Pleural cavity–leading to Pneumothorax
Air/Gas finding its way to the left side of the heart, left atrium, left ventricle > then proceeds to Arterial circulation, and with an upright diver or patient sitting during perhaps a neurosurgical procedure, may very likely be propagated into the carotid arteries which may then lead to Cerebral Air/Gas embolism. Venous Air/Gas embolism is less serious and usually non-fatal unless a significant amount of air/gas bubbles traverse septal defects from right to left side of the heart.
Arterial Gas Embolism is a direct result of expansion of respiratory gases with dangerous entry of gas into the pulmonary circulation as well as a syndrome of paradoxic air embolism via septal defects or a patent foramen ovale. Immersion alone increases cardiac preload with central blood pooling and a rise in cardiac output and increased blood pressure. Pulmonary overpressure or “burst lung” is another mechanism for arterial gas embolism. Baropressure increases as the SCUBA Diver on compressed air ascends with a closed glottis or a free diver takes a breath of compressed air at depth and then ascends. As reviewed above, unavoidable pulmonary overinflation as determined by Boyle’s Law states that with constant temperature, volume of a gas is inversely proportional to pressure directly impacting rising intra- pulmonary pressure on alveolar-capillary interface, upon ascent of any Diver. Henry’s Law states that amount of a gas dissolved in a liquid is directly proportional to the partial pressure of that gas.
When pressure rises due to:
- Breath-hold on ascent
- Dynamic Airway collapse in non-cartilaginous airways
- Low pulmonary compliance, especially when not distributed evenly throughout lungs, dangerous bubbles may form in divers circulation
Experimental findings have revealed that intratracheal pressures of 10 kPa or ascending from 170 feet or 52 m to 120 feet or 36.5m are all that is required for this to occur. Distension of alveoli leads to rupture, alveolar leakage of gas and extravasation of gas into the arterial circuit.
Origin of bubbles in the circulation may arise from 3 sources:
- ParadoxicGasEmbolism=venous gas embolism with breach of pulmonary vascular filter
- Patent Foramen Ovale
- Tear of Pulmonary Parenchyma with entry of gas into pulmonary venous outflow
Typically a small number of systemic venous bubbles enter the pulmonary arterial tree and are then eliminated through the lungs, which are able to trap small amounts of air and excrete it into alveoli, from arterioles. As the diver takes his first breath after surfacing, extra-alveolar gas enters the torn blood vessels, then migrates to the left side of the heart and then air is distributed systemically as emboli are sent to various areas of the body as determined by buoyancy and depth as well as influenced by thermoclines.
Arterial Gas Emboli arise from gas bubbles in pulmonary capillaries – pulmonary veins to the left side of the heart – possible rare Coronary Artery Emboli or Internal Carotid & Vertebrobasilar arteries to the brain – Cerebral Artery Embolism with a clinical presentation of stroke depending on the region of the brain affected.
Cerebral Artery Gas embolism is a consequence of foam or bubbles blocking arteries of 30-60 micron caliber leading to distal ischemia, astrocyte and neuronal swelling. As the gas or air bubble passes over the endothelium, distal cellular effects (within 1-2 minutes) cause release of PMN ( polymorphonuclear WBC’s) . The gas or air bubbles itself has surface effects causing local swelling, downstream coagulopathy with focal hemorrhages. Immediate increase in permeability of the BBB (blood brain barrier), loss of cerebral auto regulation, is associated with a rise in ICP (intracranial pressure) as well as rise in blood pressure. A phenomenon of “NO Re- flow” occurs with post-ischemic impairment of microvascular perfusion, arising from coagulation Factor VIII interacting with prostaglandin system and possibly other blood tissue factors, and therefore, is also sometimes seen during plasmapheresis procedures or in Hemodialysis patients.
- Blurred vision, Auditory & Cochlear dysfunction
- Visual field defect (blank areas in visual field)
- Potential monocular vs. complete binocular vs. cortical blindness
- Cranial nerve involvement – eye movements leading to diplopia, Strabismus – Exotropia or Esotropia, facial asymmetry
- Sudden, unexpected personality change
- Focal or generalized convulsions or seizures
- Sudden loss of sphincter control
- Other neurological abnormalities including sudden onset of Hemiplegia, focal or generalized paralysis
- Focal hypesthesia (reduction, altered or complete loss of sensation)
- Generalized Weakness, Asthenia
- Cognitive Impairment, confusion
- Hemicranial vs occipital, cranio-cervical headache, possibly with nuchal rigidity Horner’s Syndrome
- Vertigo – peripheral vestibular syndrome
- Bloody Froth from nose or mouth
- Liebermeister’s Sign = a sharply defined area of pallor on the tongue
- Lacerated tongue or buccal tissue of inner lip, usually due to seizure
- Air bubbles in Retinal vessels of eye
- Dyspnea, Tachypnea
- Hypoxia, Asphyxia
- Cardiac Dysrhythmias, such as Atrial Fibrillation, PAT, polymorphous VT, VF
- Increased blood pressure, eventually Cardiac Arrest
- Coronary Occlusion – Acute Coronary Syndrome – Myocardial Infraction
- Cardiac Valvular Dysfunction – audible precordial cardiac “machinery” murmur on auscultation, Split S2 (second heart sound)
- Decreased or complete loss of sphincter control > Incontinence
- Diuresis, polyuria
- Marbled, lace-patterned mottled appearance of skin (Cutis Marmorata)
- Central & Peripheral Cyanosis
- Subcutaneous emphysema
- Pulse oximetry
- Chest X-ray – with Inspiration views & Expiration views
- confluent air lucencies filling central vascular bed, heart & great vessels • Doppler Ultrasound, with color-flow imaging studies
- ECG – 12 lead with Lead II – Rhythm strip:
- Atrial Arrhythmias – such as Atrial Fibrillation, – PAT, (WPW = predisposition) – Osborne J Waves – secondary to hypothermia
- Ventricular Arrhythmias: Ventricular Tachycardia Polymorphous VT, VF
- Paced rhythm : as with a variety of transvenous pacemakers, AICD
- 2D Echocardiography – ASD, VSD, Valvular Abnormalities and other possible congenital/ developmental malformations
- E.E.- (Transesophageal Echocardiography)
- may reveal – PFO (Patent Foramen Ovale)
- CT Scan/MRI Scan – in the event of COMA, hemiplegia & other focal neurologic deficits best elucidated with IV Contrast imaging study. CT Scanning is much more sensitive in detecting pulmonary ‘blebs’ than CXR.
- CBC, CMP, ABG, Coagulation studies – PT, PTT, INR !
- UA – may reveal hematuria, proteinuria and ultimately renal failure with occlusion of renal circulation, UDS – toxic substances
- PFT: Comparison of predive lung function showed lower midexpiratory flow rates at 50% and 25% of vital capacity in PBT (Pulmonary Barotrauma p<0.05 p<0.02 respectively) patients. These results indicate that SCUBA Diovers with pre-existing end-expiratory air flow limitation may be at higher risk of PBT, including air embolism.
- Positioning of Patient:
- Immediate Trendelenburg (head-down) position. Keep LV Air or Gas bubble away from Coronary Ostia.
- Left Lateral decubitus position:
- Traps air in non-dependent portion of Right Ventricle therefore preventing entry of air or gas bubble into pulmonary artery
- Also prevents passage of air or gas patients have a potentially patent foramen ovale), thereby enabling gas or air bubbles to enter Left side of heart and gaining access to arterial and possibly cerebral arterial circulation – potentially causing occlusive symptoms such as stroke)
- High flow supplemental oxygen
- Endotracheal Intubation
- Maintenance of a patent Airway free of secretions
- Pulmonary Barotrauma – must be assessed and treated as per ATLS guidelines
- Tension Pneumothorax with Tracheal Deviation Stat needle
- Assessment – Pulmonary Parenchymal injury
- Pleural Trauma
- Sucking external chest wound – providing a prompt completely sealing dressing/bandage to prevent escape of air
- Spontaneous, non-traumatic Pneumothorax
- Mediastinal Emphysema
- IV fluid & electrolyte supportive treatment
- Treatment of potentially dangerous, or fatal cardiac dysrhythmias [esp. with infiltration of air/ gas into neural circuits of brainstem – responsible for neuro-regulation of cardiopulmonary function (brainstem ischemia/infarction)
- Expedient clinical management of focal and generalized seizures. Appropriate selection of anticonvulsant medication
- Rewarming protocols for hypothermic patients
- Hyperbaric Oxygen treatments (H.B.O.T.)
- Delayed Cerebral Edema – may require – steroids, hyperventilation and/or mannitol etc., amidst close monitoring of ICP
- Avoiding Precipitous Rapid Ascent while breath-holding in SCUBA Divers
- Following proper gradual Recompression during Ascent by SCUBA DiversAvoiding Air Travel or High Altitude activities after Diving.
- Avoiding penetrating injuries to Head, Neck , Axilla, Chest , Abdomen and Pelvis
- Proper medical clearance prior to SCUBA Diving in order to ascertain presence of structural intra- cardiac septal defects such as ASD, VSD, PFO
- Avoidance of female orogenital sex and any practices which may lead to forced air or gas entering vaginal space
- Prudent and extremely careful insertion or manipulation of Central Venous Catheters, PICC Lines especially during administration of I.V. fluids, medication, blood and plasma products
- Closely monitored HBOT treatments
- Early recognition and prompt intervention, also to prevent potentially fatal complications,
- such as cerebral edema, stroke, MI, renal failure
- Widespread Education of medical providers:
- Careful practices when using I.V. ports, especially with access to central circulation, and especially during access to head & neck surgery.
- Neurosurgical procedures: Cerebral Gas Embolism include a sudden onset of unconsciousness associated with a generalized or focal seizure. In addition there is confusion, vertigo (extreme dizziness) and Cardiopulmonary Arrest. In a series of 24 US Navy cases in which time was known: 9 occurred during ascent in the water11 within one minute after surfacing from a dive 4 occurred within 3-10 minutes at the surface
- Peri-operative laparoscopic procedures involving air/gas insufflation involving inadvertent injury to vascular structures enabling unintentional entry of air/gas bubbles into blood vessels
- Rapid Triage of Explosive or Blast injuries, both blunt injuries and penetrating trauma secondary to blast waves, resulting in air/gas communicating with torn or lacerated blood vessels
- Emphasizing importance of safe, expedient transport to regional hyperbaric centers for HBOT, after proper recognition, diagnosis, stabilization and triage of all patients identified with A.G.E. (Arterial Gas Embolus) or Air Embolism
- Prompt notification of D.A.N. (Diver Alert Network)
- Maintenance of certification and diver training, with emphasis on strict avoidance of breath- holding on ascent while SCUBA Diving
- Studies have shown decreased incidence of Air embolism, arterial gas embolism in SCUBA Divers, who have engaged in vigorous aerobic activity within 2 hours prior to diving, as well as reducing obesity, which can predispose SCUBA divers
- Death from air, or a mixture of compressed gases inhaled from a SCUBA cylinder, present in the patient’s circulatory system may result from as little as 23 mls of AIR/GAS per pound of body weight (i.e. 350 mls of AIR/Gas in a 155 lb person)
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