Pulmonary,Air,Fat,Gas Embolism

2017
Pulmonary,Air,Fat,Gas
Embolism

DR. Roman Al
Mamun
Forensic Science,Autopsy
surgeon and Forensic Death
Investigator.
12/2/2017
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Pulmonary Air Embolism:

Pulmonary embolism is a condition in which thrombi are formed in the walls

of the pelvic and leg veins and such thrombi break away and embolise to
the lungs.
Although the thrombosis is the primary event, the embolus itself usually
consists of a tube of thrombus with a central core of clotted blood. When it
reaches the lung, its effect depends on its size, small ones are carried to
the periphery of the lung and causes:

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pulmonary infarcts:

Large emboli reach the bifurcation of pulmonary artery completely blocking

the blood circulation. Most common sites of thrombosis are in deep femoral
vein, posterior tibial vein and popliteal vein.
Intravenous route is the most common recognized source of entry
especially during therapeutic injection. For a serious result, two main
factors are required;
either positive pressure or negative pressures usually at a site near the
heart.
In any event there must be an adequate amount of air, at least 60 ml or
more. Systemic air embolism occurs when an air in sufficient quantity
enters a vein of the pulmonary system and is carried through the
left side of the heart to block arterioles and capillaries in different parts of
the body especially brain and heart.

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One to two ml of air may be enough to produce death because air

travels directly from the lungs to the left side of the heart, from which
it can be forced into coronary or cerebral arteries.
Death from air embolism occurs with in a few minutes, not delayed
beyond 45 minutes. Air entering the venous system is carried to the
heart and pulmonary arteries, which causes mechanical obstruction
of the pulmonary arterial vasculature.
This causes churning of blood and air producing froth. The churning can
result in development of complexes of air bubbles, fibrin,platelet
aggregates, erythrocytes and fat globules thus further occluding the
vasculature, which causes death.
This occurs most commonly in penetrating wounds of chest, crush injuries
of the chest and surgical procedures upon thorax.
Other circumstances under which such accidents occur are:

1. During transfusion when positive pressure is being used

2. During surgical operations especially during those on neck and chest
when negative pressure will produce a ‘suck-in’ effect.
3. During craniotomy in the sitting up position
4. Operations on nasal air sinuses
5. Incised and penetrating wounds of the neck and chest involving jugular
and subclavian veins. Fatal accidental oxygen embolus occurred on one
occasion during an operative procedure.
6. Intravenous drug addicts inject foreign bodies at the time or following
subsequent surgical procedures e.g. metallic mercury embolism.
7. A wound of sagittal sinus inside the skull.
8. Injection of air under pressure in fallopian tube to test the patency
9. Injection of air or fluid mixed with air or soap water in the pregnant uterus
for procuring abortion.
10. Caesarean section, version or manual extraction of placenta may
introduce air into the uterus.
11. Crush injuries of chest
12. Subclavian vein catheterization

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13. Positive pressure ventilation in newborn infant

14. Artificial Pneumothorax and pneumoperitoneum
15. Air encephalography
16. Caisson’s disease.

Autopsy Diagnosis:

Thromboembolism should specially be suspected when death occurs after

a week of trauma. This is seen in upto 65% of such patients who die after a
week of trauma. The thrombus can be demonstrated
by inserting a flexible wire with blunt terminal knob inserted in femoral vein.

1. If air embolism is suspected, head should be opened first and surface

vessels of brain examined for gas bubbles, which must be prominent and

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definite and not the segmental break up of blood in the vessels with
collapsed segments in between.
2. Avoid pulling the sternum and ribs to avoid creating negative pressure in
the tissues, which may result in aspiration of air into vessels.
3. Before handling thoracic organs, the pericardium is opened, heart is
lifted upwards and the apex is cut with a knife.
4. The left ventricle is filled with frothy blood, if air is in sufficient quantity to
cause death.
5. If the right ventricle contains air, the heart will float in water.
6. Air embolism can also be demonstrated by cutting the pericardium
anteriorly and grasping the edges with hemostat on each side.
7. The pericardial sac is filled with water and heart is punctured with the
scalpel and twisted a few times. Bubbles of air will escape if air is present.
8. The amount of air can be measured by placing inverted water filled
graduated glass cylinder, with the mouth of cylinder in pericardial sac.
9. Oxygen in heart indicates air embolism because it is not present in
appreciable quantity if gases were those of decomposition.Frothy blood
resembling air embolism can be found especially in right ventricle due to
handling of heart before it is opened at autopsy, putrefaction, as a
postmortem event and artificial respiration in dying or recently dead.
10. Skull vault be removed without puncturing the meninges.
11. Internal carotid and basilar arteries are ligated before the brain is
removed.
12. Meningeal vessels should be examined for visible air bubbles. In acute
cases, gas bubbles will be visible within the cerebral arteries but not in the
cortical veins.
13. Brain should be submerged in water and ligature should be released.
Then the vessels are cut and slightly compressed to watch for air bubbles.
14. An air tight, water filled glass syringe with a needle can be used to
collect gas from blood vessels, heart or cavities.

Dating of Pulmonary Embolus:

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For dating an embolus, veins along with the thrombi and the muscles
around it are excised as a sample for routine Histopathological
examination.

This tissue can be processed and fibrin can be demonstrated by

phototungstic acid-haematoxylin stain and Martius Scarlet Blue stain. With
phototungstic acid-haemotoxylin acid stain the changes are:

• First day—Purplish strands of fibrin.

• Four days—Thicker strands and sheets of fibrin.
• Two weeks—Fibrin strands are dark purple.
• By twenty-fifth days—Fibrin begins to be absorbed.

With, Scarlet Blue stain, initially the fibrin is

seen as pink coloured that becomes scarlet in
about a week.

Fat Embolism:

Fat embolism is caused by:

• Fracture of a long bone namely, femur and pelvic bones

• An injury to adipose tissue which forces liquid fat into damaged blood
vessels
• Injecting oil into circulation e.g. in criminal abortion
• Occasionally due to natural disease without trauma as in sickle cell
anemia, diabetes,following blood transfusion, fatty change seen in liver as
seen in chronic alcoholics, septicemia, steroid therapy, acute
pancreatitis,osteomyelitis, decompression sickness (Caisson’s disease), in
too rapid ascent to high altitudes without functional pressurized cabin or
under simulated flight conditions in decompression chambers and in burns.

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Two factors favours pulmonary fat embolism:

1.Fixation of walls of veins e.g. in clavicular and pelvic regions, the upper
dorsal spine and dural membranes.
2. The suction effect of the respiratory movements and heart’s actions on
such veins as the jugular, subclavian and vertebral has a tendency to
create a negative pressure in the vessels during phase of inspiration.
Presence of fat droplets in the blood stream indicates that the injury was
produced during life, except in case of burning, advanced putrefaction and
charring after death. Large amounts of liquefied fat are derived from fat
cells.
When cardiac massage is done, fat enters the blood vessels even if the
circulation has stopped. If during resuscitation, the sternum or ribs are
fractured bone marrow embolism is seen in the lungs.

Clinically:
The phenomenon presents as sudden loss of consciousness usually after
a period following the traumatic accident, which need not in itself be serious
such as a fractured tibia and fibula.

Autopsy diagnosis:

Droplets of fat should be demonstrable in the peripheral viscera notably

vessels of kidneys and brain. There are petechial haemorrhages in organs
and punctate haemorrhages in the white matter of brain.

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Fat Embolism Syndrome

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Fat embolism is characterized by the presence of globules of fat in the lung

and peripheral circulation.
Fat embolization occurs in 90–100% of individuals with long-bone or pelvic
fractures.
Following trauma, fat droplets enter the circulation.
The larger droplets are strained out by the lungs, where they lodge in the
vasculature.
The smaller fat globules travel through the pulmonary capillaries, enter the
arterial circulation, and are carried to the brain and other organs. In only a

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small percentage of individuals with fat emboli, however, does this

condition become symptomatic.
This syndrome is characterized by progressive pulmonary insufficiency,
mental deterioration, and a petechial rash. Typically, symptoms do not
appear for 24 to 72 h following injury.
There is, however, a severe fulminating form of fat emboli in which both
pulmonary and cerebral deterioration begins within the first 12 h.
Fat embolism syndrome is rare in children.
The incidence of fat emboli syndrome increases with the multiplicity of the
long-bone fractures.
Noted that the syndrome developed in 3% of patients with a single fracture
of the femur and 33% of patients with two fractured femora.

While the fat embolism syndrome is usually associated with long-bone or

pelvic fractures, it can also be seen in association with acute pancreatitis,
extensive burns, liposuction, decompression sickness, and parenteral
infusion of lipids.

It can also be precipitated by reaming and nailing procedures for long-bone

fractures.

The major clinical signs of fat embolism are respiratory insufficiency,

mental deterioration, and a petechial rash.
The petechiae are typically seen in the conjunctivae, as well as on the chest
and the axillae.
These major signs may be accompanied by fever; tachycardia;
thrombocytopenia; fat globules in the urine, sputum and retina; as well as
renal failure.
Most individuals who die from fat embolism do so as a result of pulmonary
failure. There are two theories as to the cause of pulmonary injury. The first
holds that the injury is caused by the mechanical obstruction of the
pulmonary vasculature by large globules of fat.

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The second theory is that free fatty acids, released from either the marrow
directly or from fat lodged in the lungs, cause direct toxic injury to the
pneumocytes and endothelium, with resultant abnormalities in gas exchange.
Microscopically, there are fat emboli in the pulmonary vasculature, with
edema, transudate, and exudate in the alveoli.
Visualization of fat emboli within the pulmonary vasculature requires the
use of frozen sections and fat stains.
If the individual survives a few days, the brain will show small perivascular
hemorrhages in the white matter around vessels containing fat emboli.
In the early stages, the brain may appear grossly normal.

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Amniotic Fluid Emboli:

 This is an uncommon but highly lethal complication of pregnancy, first
described by Steiner and Lushbough.

 While early studies reported an 86% mortality, more recent work indicates
that the mortality has decreased to 61%.

 Unfortunately, the increased survival was accompanied by a 24% incidence

of permanent neurological injury.
 Thus, only 15% of patients survived neurologically intact.

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 There are no demographic factors predisposing to amniotic fluid embolism

as well as no relationship to route of delivery, prolonged hard labor, or use
of oxytocin.
 Most cases of amniotic emboli occur during active labor, though cases have
occurred as late as 90 min postpartum.
 Ammotic fluid emboli have been reported in first- and second-trimester
abortions as well as following abdominal trauma and amniocentesis.
Clinical Presentation

 The clinical presentation of amniotic fluid emboli is sudden dyspnea,

hypotension, and seizures, followed by cardiovascular arrest.
 If death does not occur immediately, consumptive coagulopathy usually
develops.
 Typically, laboratory studies show decreased fibrinogen, elevated levels of
fibrin split products, prolonged partial thromboplastin and prothrombin
times, and thrombocytopenia.

Etiology:

 The syndrome of amniotic fluid embolism has been attributed to the acute
embolization of amniotic fluid and debris of fetal origin into the maternal
venous circulation, with resultant pulmonary microvascular obstruction.
 On reaching the lung, this material is presumed to produce severe transient
vasospasm of the pulmonary vasculature, pulmonary hypertension, right
heart failure, and hypoxia.
 No matter how small the amount of amniotic fluid involved, simple
exposure of the maternal circulation to amniotic fluid triggers a
pathophysiologic cascade similar to anaphylactic or septic shock generating
the physiological derangements characterizing these syndromes.

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 This would explain the observation that fetal debris is not seen at autopsy in
all cases where there is no doubt, clinically, that the patient had “amniotic
fluid emboli.

Autopsy Findings:

 Traditionally, the diagnosis of amniotic fluid embolism was made at autopsy

by a combination of clinical signs and symptoms and the finding of mucin
derived from meconium, fetal squamous cells, lanugo hair, or vernix fat
globules in the pulmonary vasculature.
 These materials can usually be seen on hematoxylin and eosin slides, though
special stains might better demonstrate individual elements.
 Mucin is virtually always present, with cellular elements seen less
frequently.

 The presence of squamous cells in the pulmonary arterial circulation at

autopsy has traditionally been regarded as one of the pathognomonic
elements of amniotic fluid emboli.

 The detection of squamous cells alone in the pulmonary arterial blood would
not be sufficient for the diagnosis of amniotic fluid embolism.
 Just as the presence of squamous cells is not pathegnomonic of amniotic
fluid embolus, neither is the presence of trophoblastic cells.
 Trophoblastic cells can be found in the blood and lungs of women who do
not have amniotic fluid emboli.

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Gas Embolism
Gas emboli may involve either or both the venous and arterial systems.
In most instances, the gas is air, though, in some diagnostic situations, it
could be carbon dioxide, nitrous oxide or nitrogen.

In the venous system, death from air embolism depends on the size of the
bolus and the rate of delivery.
In arterial embolism, these factors are not as important, because only a small
number of air bubbles occluding a coronary artery or a cerebral vessel can
result in death. In venous air embolism, between 75 and 250 cm of air
delivered rapidly is necessary to cause death.
Venous air embolism may occur during therapeutic or diagnostic procedures
secondary to trauma, during childbirth or abortion, and during oralgenital
sex in a pregnant woman when her partner blows air into the vagina.
Arterial air embolism occurs secondary to cardiopulmonary bypass, arterial
catherization, surgical procedures involving arteries, or injury to the
pulmonary veins after chest trauma.
One might also incur a paradoxical air embolism, that is, air crossing from
the venous to the arterial circulation.
Air entering the venous system is carried to the heart and pulmonary arteries,
with resultant mechanical occlusion of the pulmonary arterial vasculature by
air bubbles.
This is followed by a transient vasoconstriction.
Obstruction of the pulmonary blood flow results in churning of the blood
and air, producing the frothy appearance of the blood seen at autopsy.
This churning can result in the development of complexes of air bubbles,
fibrin, platelet aggregates, erythrocytes, and fat globules, thus further
occluding the vasculature.

Death is caused by obstruction of the pulmonary blood flow secondary to

obstruction of the pulmonary arterial system by the air bubbles, the
pulmonary vasoconstriction, and the cellular aggregates. With a very large

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bolus of air, the obstruction occurs not only in the pulmonary vasculature but
also in the right ventricle.

Paradoxical air emboli

 occur when air or gas that has entered the venous system crosses over to the
arterial system.

 Typically, these have been described in association with septal defects of the
heart. These permit air to go from the right side of the heart to the left
without passing through the pulmonary vasculature.

 If a large air embolism is carried to the heart, the sudden rise in the right-
sided heart pressure may result in a right-to-left shunt through a probe
patent, but physiologically closed, foramen ovale. Increased right-sided heart
pressure also causes air to be forced into the epicardial veins on the surface
of the heart.

 Paradoxical emboli can also occur secondary to arteriovenous anastomoses

in the lung.
 In addition, with sufficiently high pressures and delivery of large quantities
of air, the ability of the lungs to filter out air can be exceeded and bubbles of
gas may traverse the pulmonary circulation and enter the left atrium.

 This has been demonstrated by Butler and Hills in experiments on dogs.

 Air entering the arterial circulation causes death by occluding the cerebral or
coronary arteries.
 Only a very small quantity of air is necessary.

 Forensic pathologists will encounter air emboli most commonly in knife

 wounds of the neck, and secondary to surgical procedures.
 Air enters an open vein whenever there is a negative pressure gradient
between the vein and the right atrium.

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 This is facilitated by the negative intrathoracic pressure generated during

inspiration.
 The higher the open vein is above the right atrium, the greater the pressure
gradient and the more likely air is to enter the vessel.
 This is why wounds to the neck can result in air emboli.

 Thus, in individuals incurring stab or incised wounds of the neck with injury
to the veins, the prosector may want to explore the possibilities of air
embolism at the time of autopsy.

 The true incidence of venous air embolism during surgical and diagnostic
 procedures is unknown, with one exception — craniotomy in the sitting
 position.
 Here, air emboli occur in 21 to 29% of all craniotomies and 40% of all
occipital craniotomies.

 Air emboli have also been reported in a host of other therapeutic and
diagnostic procedures.
 Any surgical procedure that causes a negative pressure gradient between the
right side of the heart and a vein is a potential risk for venous air embolism.
 Individuals have been seated or prone, supine, in the lithotomy position, and
in the lateral knee-chest position at the time they incurred air emboli.

 Air emboli were more common when blood and other fluids were delivered
 in glass bottles rather than the present collapsible plastic bags.
 Even with plastic bags, there is the possibility, though rare, of an air
embolus.

 Air emboli have also occurred following cesarean section, placenta previa,
and
 subclavian venipuncture.

 With a large-bore channel to a vein, a fatal amount of air can pass quickly
into a vessel.

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 Theoretically, 100 cm of air per second can enter through a 14-gauge needle
with a 5-cm water pressure drop across it.
 Fortunately for people with subclavian lines, this is more theoretical than
actual.

 Homicides secondary to injection of air into the venous system using a

 syringe are rare because of the large quantity of air one has to introduce in
 Emboli a bolus (100–250 cm3), the expertise necessary to administer the
injection
 intravenously, and the necessary passivity of the patient.
 Individuals with established intravenous lines, such as hospital patients, will,
of course, be easier to kill in this way.

 When abortions were, for the most part, illegal, occasional deaths caused by
air emboli were encountered.
 This occurred following dilatation of the cervical os, with resultant tears of
the margins of the placenta or the cervical veins.

 In some cases, there was a delay in the air embolus.

 Thus, in one case, after having an illegal abortion, the woman left the
premises, only to collapse and die 2 h later.
 At autopsy, air could be seen in the inferior vena cava, right atrium, and
right ventricle.
 Death caused by air embolism in association with pregnancy may also occur
secondary to cesarean section and placenta previa.

 Just as in an abortion, there can be a time delay prior to the onset of the fatal
air embolus.
 In deaths of pregnant females during sexual intercourse, one should always
suspect air emboli.
 This occurs during oral–genital intercourse, with the partner blowing air into
the vagina during cunnilingus.

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 Suicide from an air embolus is rare.

The broad spectrum of deaths caused by air embolism is illustrated by the
following cases:

 The first involved a 22-year-old woman, 34 weeks pregnant, who was

having intercourse with her husband.
 Her husband blew into her vagina and she suddenly “passed out.”
 She was dead on arrival at the emergency room.
 At autopsy, there was air in the right atrium and ventricle.
 The epicardial veins had a beaded appearance caused by air bubbles.
 Bubbles of air were also present in the pelvic veins.
 The blood of the heart had a frothy appearance.

 The second case involved an obese 40-year-old man who was prone in the
 semi knee-chest position for a lumbar laminectomy.
 Five hours into the procedure, he developed bradycardia and an agonal
rhythm. The autopsy revealed air in the right ventricle, with beading of the
epicardial veins by air bubbles.

 The third case was a 39-year-old woman who went into premature labor.
 She presented with vaginal bleeding.
 On admission to the hospital, she had a complete central placenta previa and
a breech presentation.
 The child was delivered by cesarean section at 8:51 in the evening.
 The operation was over at 9:30 p.m. She then was returned to the recovery
room. At midnight, she was taken to her room.
 As she was being placed into bed, she had a grandma seizure and went into
cardiopulmonary arrest.
 Attempts at resuscitation were unsuccessful.

 At autopsy, there was air in the right atrium and ventricle with beading of
the epicardial veins by massive numbers of air bubbles.

 In a living patient, the diagnosis of venous air embolism to the heart can

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 be made by auscultation of the mill-wheel murmur or by detection of

intracardiac
 air using dopler ultrasonography or transesophageal echocardiography.

 In the deceased individual, to make the diagnosis of air embolism, one must
consider the diagnosis prior to the autopsy.

 The first step may be a chest X-ray to look for air in the heart.

 A Y-shaped incision can then be made into the skin and musculature of the
chest and the skin and muscle retracted.
 Instead of then removing the chest plate in the ordinary way, a “window”
should be cut in the sternum and ribs overlying the heart.
 The bony plate should then be retracted very carefully, so as not to introduce
air into the venous system.
 The pericardial sac can then be cut open and the heart visualized.
 The epicardial veins should be examined for the presence of air.
 One or two bubbles in an epicardial vein do not make a diagnosis of air
embolism.
 Massive air embolus with air in the right atrium and ventricle.
 Note outline of right ventricular wall.

 With air embolism, the epicardial veins usually have a beaded appearance,
with numerous air bubbles the length of these vessels.
 The pericardial sac should then be flooded, the plunger removed from a 50-
 cc syringe, a large-bore needle attached, and the syringe filled with water.

 The tip of the needle can then be pushed into the right ventricle.
 If there is air in this chamber, it will be seen to bubble up through the water
in the syringe.

 The water should then be removed and the right side of the heart opened.
 The blood typically has a frothy appearance.

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 Following this, the incision can be extended through the anterior abdominal
wall to the pubic area.
 If the air entered in the pelvic region, the inferior vena cava is examined for
air bubbles.

 One should be careful about interpreting one or two bubbles in this vessel as
evidence of air embolism.
 If the deceased has been vigorously resuscitated with a thoracotomy and
internal cardiac massage, it is usually impossible to make the diagnosis of air
embolus based on the autopsy, because the air observed in vessels could be
caused by resuscitation.

 Air in the coronary arteries cannot be identified at autopsy because air

bubbles
 cannot be seen through the wall of these vessels.
 In the brain, the process of removing the skull cap, cutting through the dura,
and putting traction on the brain to see the cerebral circulation might
introduce air bubbles into the circulation.

 Thus, the presence of a few air bubbles in the cerebral circulation.

 Air bubbles in epicardial veins of heart in death caused by air embolism does
not necessarily indicate an embolus.
 If individuals survive the initial insult of air in the coronary and cerebral
circulation, they might develop myocardial or cerebral infarcts.

 The technique described to demonstrate air in the heart using a 50-cc syringe
is very basic and very crude.
 A much better and more sophisticated method is to use an aspirometer.
 This device not only demonstrates the presence of air but measures the
amount and stores it for subsequent analysis by gas chromatography.

 Embolized air differs from atmospheric air in that CO2 is less than 15%; N2
is higher than 70% and O2 is reduced, usually measuring between 8 and
15%.

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 Detection of CH and H indicates that decomposition has begun.

 Most individuals feel that decomposition, with its formation of gases of
putrefaction, precludes the diagnosis of air emboli.

 They analyzed gas recovered from the ventricles of 15 individuals, exhumed

after 10–45 weeks burial, who were believed to have been killed by injection
of air. They found that analysis in 8 of the 15 cases gave results typical of air
embolism, with only small amounts of the gases of putrefaction present.

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