Monday, January 5, 2009

ARTERIAL GAS EMBOLISM

ARTERIAL GAS EMBOLISM - Jacqueline J. Wu, MD; Ruben Peralta, MD, FACS
BASICS
DESCRIPTION
• Arterial gas embolisms are caused by the entry of gas into the pulmonary veins or directly into the arteries of the systemic circulation.
- Gas may enter arteries as a result of overexpansion of lungs by decompression barotraumas.
- May result from paradoxical embolus
• Emboli can travel to any artery, but the most serious consequences occur when they affect the cerebral or coronary circulation.
• Synonym(s): Gas embolism; Air embolism
ALERT
Any diver who has an onset of new symptom(s) or sign(s) after recently completing a Self-Contained Underwater Breathing Apparatus. SCUBA dive of any type, to any depth, for any period of time: Serious consideration must be given that such a patient sustained a dive-related injury.
GENERAL PREVENTION
• Strict adherence to diver safety protocols, especially including the buddy system
• No diving after any dive injury or with any medical condition until evaluated and approved by a physician knowledgeable about diving medicine
EPIDEMIOLOGY
• Predominant age: Young adult
• Predominant sex: Male > Female
Prevalence
Estimated (based on injury/mortality reports collected by Divers Alert Network) to occur in approximately 4 per 100,000 sport divers per year
RISK FACTORS
• Surgery: Recent craniotomy with patient in upright position, cardiothoracic (with cardiopulmonary bypass), hip replacement, Caesarian section
• SCUBA: Arterial gas embolism is the most serious and rapidly fatal of all SCUBA diving injuries and is second only to drowning as the leading cause of death associated with sport diving. Arterial gas embolism occurs on ascent; from alveolar rupture; time to the manifestation of symptoms is nearly always 10 minutes.
• History of patent foramen ovale has been associated with a >4-fold increase in decompression illness events and 2-fold more ischemic brain lesions than in divers without this condition.
ETIOLOGY
• Cerebral air embolism
- Air bubbles occlude the brain vasculature
- ICP increases
- Unequal distribution of blood in the brain causes hyperemia and ischemia.
- Small bubbles irritate vascular wall causing breakdown of blood-brain barrier; small size allows rapid absorption and may cause only brief interruption of cerebral blood flow.
- Larger air bubbles take longer to absorb (up to several hours) and can cause primary ischemic injury with diffuse brain edema and increased ICP.
• Coronary air embolism: Caused by obstruction of coronary arteries by an air bubble
- Temporary ischemia of myocardium
- Labile BP
- Dysrhythmias
- Cardiac failure and/or arrest
• Obstruction is possible in any artery.
- Small emboli in the vessels of skeletal muscles and viscera are well-tolerated.
- Arterial gas embolisms to coronary and cerebral arteries are especially serious or fatal because of the vulnerability of heart and brain to short periods of ischemia.
ASSOCIATED CONDITIONS
• Pulmonary barotrauma leading to arterial gas embolism can also cause pneumomediastinum, subcutaneous emphysema, pneumopericardium, pneumothorax, and pneumoperitoneum.
• Always consider the possibility of decompression sickness in addition to arterial gas embolism in any SCUBA diver who has recently completed a dive.


DIAGNOSIS
SIGNS AND SYMPTOMS
• Cerebral air embolism
- Dizziness
- Chest pain
- Cardiac arrythmia
- Paresthesias
- Minor motor weakness
- Convulsions
- Paralysis
- Nausea
- Visual disturbances
- Gas bubbles in vessels of retina
- Headache
- Asymmetric pupils
- Hemianopia
- Bradypnea
- Cheyne-Stokes breathing
- Aphasia
- Mental status changes ranging from subtle to total lack of consciousness
• Coronary arterial embolism
- Cardiac arrythmias
- Cardiac arrest
ALERT
Anesthesia and/or analgesics alter the symptomatology and may complicate evaluation of the patient's clinical status. Delayed recovery from general anesthesia may be a clue to cerebral arterial embolism.
TESTS
Lab
• Hematocrit: Increased, indicating volume depletion and extravascular shift of fluid into injured tissues
• Serum creatine kinase: Correlation between creatine kinase activity and outcome suggests that elevated serum level of this enzyme may be a marker for size and severity of arterial gas embolism.
• Urinalysis: Increased specific gravity indicates volume depletion.
Imaging
• Chest radiograph to rule out pneumothorax
• ECG
• CT scan: Changes often very subtle
• MRI: Can sometimes show increased volume of water in injured tissue (not very reliable)
DIFFERENTIAL DIAGNOSIS
Decompression sickness
TREATMENT
PRE-HOSPITAL
• General
- Life-saving measures (e.g., CPR) must take precedence to sustain life.
- Endotracheal intubation for somnolent or comatose patient
- Highest possible concentration of oxygen: Eliminates gas in the bubbles by establishing diffusion gradient that favors egress of gas from bubbles
- Place patient in flat, supine position (head down position may aggravate cerebral edema that develops).
• Hyperbaric oxygen
- 1st-line treatment of choice for arterial gas embolism: Immediate transport to a suitable hyperbaric chamber for recompression as soon as possible; do not delay because of nonessential procedures
- 100% oxygen at pressure above that of the atmosphere at sea level
- Decreases bubble size
- Prevents cerebral edema
- For assistance and advice in locating the nearest treatment chamber in your area (worldwide), call Divers Alert Network (DAN) at any hour (919) 684-4326.
• IV fluids
- To counteract hemoconcentration seen in gas embolism
- Colloids preferred over crystalloid (latter may promote cerebral edema)
- Goal is normovolemia
STABILIZATION
• See"Treatment" and "General Measures."
• Hospital-based hyperbaric chamber capable of performing a U.S. Navy Table 6A recompression (165 feet of seawater)
GENERAL MEASURES
• CPR
• Keep patient recumbent while maintaining patent airway.
• Maintain hydration with IV fluids.
• Frequent neurologic checks in the acute pretreatment and treatment phases
Diet
Nothing to be consumed until after treatment
Activity
None until after treatment
SPECIAL THERAPY
IV Fluids
• Colloids preferred over crystalloid
• Achieve normovolemia
MEDICATION (DRUGS)
First Line
Oxygen
• As high a concentration as possible
• Transfer to facility with hyperbaric chamber as soon as possible
Second Line
• Heparin
- Prevents platelet clumping
- Studies of its use are inconsistent.
• Barbituates (if indicated)
- For suppression of seizures
- Reduce ICP
- Decrease cerebral oxygen consumption
• Lidocaine
- Decreases ICP
- Improves recovery of somatosensory evoked potential following cerebral air embolism
- Preserves cerebral blood flow
FOLLOW-UP
PROGNOSIS
Complete to partial resolution with adequate treatment
COMPLICATIONS
• Long-term serious neurologic impairments
• Death
PATIENT MONITORING
Complete neurologic assessment at 1, 3, 6, and 12 months
REFERENCES
1. Muth CM, Shank ES. Gas embolism. N Engl J Med. 2000; 342:476-482.
2. Vann RD, Dovenbarger JA. Reports on decompression illness. Diving fatalities and project dive exploration, the Divers Alert Network Annual Review of Recreational Scuba Driving Injuries and Fatalities. 2002 Data Durham: Divers Alert Network. 2004:1-152.
3. Van Hulst RA, Klein J, Lachmann B. Gas embolism: Pathophysiology and treatment. Clin Physiol Funct Imaging. 2003;23:237-246.
4. Davis J. Medical Examination of Sport Scuba Divers, 2nd ed. San Antonio, TX: Medical Seminars; 1986.

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