EMBOLISM

Q) Write a note on embolism?

A) (I) Definition - An embolus is defined as a detached intravascular physical mass that is carried by the blood to a site distant from its point of
origin. 95% of all emboli consist of thrombi dislodged from an intravascular thrombus. Some emboli (e g. air embolism) are immediate causes of
deaths from wounds. Other emboli (e.g. thromboembolism, fat etc) cause delayed deaths.

(II) Classification - Emboli may be classified according to their (i) source of origin (ii) their composition.
(A) Classification according to source of origin
(1) Arterial thrombi - Develop in areas where the blood flow is more turbulent (e.g. where blood vessels branch off). They are usually not
traumatic in origin. Usually take many years to build up. Mainly form in –
(i) Left auricle and appendage especially in atrial fibrillation and mitral stenosis,
(ii) Left ventricle [Mural thrombus]
(iii) Aneurysms [especially of aorta]
(iv) Vegetations from valves [SABE, ulcerative endocarditis]
(v) Bullet or stab wounds of carotid arteries injure the intima, stimulating the formation of a thrombus. It can get detached and travel to middle
cerebral arteries as emboli. Arterial thrombosis and embolism is rare.

(2) Venous thrombi- Result from immobilization due to any cause (wounds is just one of the causes)

(B) Classification according to composition - Air, Bullet, Fat, Thrombus, Tissue [amniotic fluid, bone, brain etc]

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(III) Air embolism (write note on air embolism?)

(A) Definition - Air embolism [syn, gas embolism] is entry of air bubbles in vascular system. Air embolism consists of an interruption of the
circulatory system by bubbles of air (or other gas) that gain access to the circulation, usually through the venous side. It is an ‘airlock’, familiar to
plumbers and owners of diesel engines, where the normal flow of liquid through tubes is wholly or partially blocked by air. It is an immediate
cause of death in certain wounds e.g. wounds of neck.

(B) Type of Gas - In most instances, the gas is air, though, in some diagnostic situations, it could be carbon dioxide, nitrous oxide or nitrogen.

(C) Salient features:

(1) While air embolism is an immediate cause of death due to wounds, most other types of embolism (thromboembolism, fat) are remote
(delayed) causes of death due to wounds.
(2) Types:
(i) Venous - more common. So common that when only the phrase “air embolism” is mentioned, it is presumed to be venous air embolism. The
air usually remains in the right side of the heart, pulmonary trunk and arteries, and in the pulmonary vessels, rarely emerging on the pulmonary
vein side
(ii) Arterial — caused when air in sufficient quantities enters –
(a) a vein of the pulmonary system -> reaches left side of the heart -> blocks arterioles and capillaries in different parts of the body [brain, heart]
(b) directly into the arteries of the systemic circulation

(D) Preconditions for air embolism

(1) Direct communication - there should be a direct communication between a source of air and the vasculature
(2) A pressure gradient - favoring the passage of air into the circulation must be present.

(E) Factors favoring pulmonary air embolism

(1) Fixation of walls of veins - This does not allow them to collapse on injury -> -ve pressure develops (e.g., in dural membranes, clavicular and
pelvic regions, upper dorsal spine)
(2) Suction effects of respiratory movements. That is why pulmonary embolism is rarely seen following injury to peripheral veins.

(F) Causes of air embolism

(1) Venous embolism
(i) Artificial respiration - forced respiration by mechanical respiratory aids -> rupture of overinflated alveoli -> interstitial pulmonary emphysema
-> air penetrates pulmonary lymphatic’s -> enters venous system via thoracic duct.
(ii) Criminal abortions - when air or soap solutions are injected in the uterine cavity. At autopsy, air could be seen in the inferior vena cava, right
atrium, and right ventricle
(iii) Crush injuries of chest
(iv) Decompression sickness or Caisson's disease [may cause both arterial and venous embolism]
(v) Oral genital sex, especially in a pregnant woman when partner blows air into the vagina during cunnilingus. [In deaths of pregnant females
during sexual intercourse, one should always suspect air emboli]
(vi) Surgical and other iatrogenic procedures - The true incidence of venous air embolism during surgical and diagnostic procedures is
unknown. 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.
(a) Central venous catheterization (CVC), including central lines, pulmonary catheters, subclavian artery catheterization, hemodialysis catheters
and Hickman (long-term) catheters. With a large-bore channel to a vein, a fatal amount of air can pass quickly into a vessel.
(b) Cesarean delivery, manual extraction of placenta
(c) Refilling of a therapeutic pneumothorax [because the lung is punctured or an adhesion has torn the visceral pleura] and pneumoperitoneum
(d) Hemodialysis [ Patients who disconnected their tubing, with resultant massive air embolus ]
(e) Injection of air under pressure in fallopian tubes (to test patency)
(f) IV injections given with a faulty technique
(g) Neurosurgical procedures, especially those performed in the Fowler's (sitting) position (e.g., air encephalography, posterior fossa
surgeries). Here, air emboli occur in 21 to 29% of all craniotomies and 40% of all occipital craniotomies.
(h) Otolaryngological surgeries
(i) positive pressure ventilation in newborn infants [over distension of airspaces - alveoli rupture+ pulmonary vascular damage entry of air into
pulmonary vasculature]
(j) thoracocentesis
(k) During transfusion, when positive pressure is being used.
(vii) Wounds of –
(a) Neck involving jugular or Subclavian veins - Air enters an open vein whenever there is a negative pressure gradient between the vein and the
right atrium. 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
(b) craniofacial region (especially wounds of sagittal sinus)
(c) Chest and abdomen.

Cerebral embolism - In wounds of neck, air is generally “sucked in” the veins because of -ve pressure. It usually does not enter the arteries
because of +ve pressure. Once in the veins it should theoretically travel downwards along the blood flow and should travel to right side of heart
and embolize the pulmonary arteries. However due to lower sp gr of air bubbles as compared to blood, they would sometimes rise up and
embolize cerebral vasculature.
Preconditions for this to happen are:-
(i) The victim was positioned upright
(ii) Air bubbles move at a velocity greater than that of the opposing blood flow in the vein. This in turn depends on bubble size, vein diameter and
cardiac output.
(iii) Such retrograde cerebral venous air embolism is even possible in the presence of valves in the jugular veins

(2) Arterial embolism

(i) Causes –
(a) Crushing and penetrating wounds the chest [may penetrate a lung vein and a bronchiole and allow air to enter vein]
(b) Surgical procedures on the thorax [any cardiac surgical operation that uses extracorporeal bypass, thoracocentesis, thoracic surgery].
Because the pulmonary vein pressure is low [10 cm H2O, any factor producing a increased pressure gradient between airway and pulmonary
vein allow entrance of air into the vein.
(c) Refilling of an artificial pneumothorax
(d) Paradoxical embolism
(e) Overexpansion of the lung by decompression barotrauma [in a diver who ascends too rapidly from a great depth].Barotrauma is the only
condition when froth may be seen in left heart in air embolism.

(G) Most common cases where forensic pathologist encounters air embolism-
(1) Knife wounds of the neck, and secondary to surgical procedures -.

(H) Pathophysiology:-
(1) If volume of air is large - Air enters venous system -> carried to right heart and pulmonary arteries -> mechanical obstruction and transient
pulmonary vasoconstriction -> leads to churning [turbulent flow] of blood & air -> Production of erythrocyte and platelet aggregates, fat globules,
fibrin and froth [complexes of air bubbles, microbubbles] -> further occlusion of vasculature -> death

(2) If volume of air is smaller:-

(i) Air embolism -> increases microvascular permeability,
(ii) Embolization of RV -> release of endothelin 1 from the pulmonary vasculature -> pulmonary hypertension,
(iii) Microbubbles formed due to turbulent flow -> precipitate platelet aggregation and release of platelet activator inhibitor -> systemic
inflammatory response syndrome
(3) Mechanism of death –
(i) In venous embolism - Almost the only mechanism of death is ‘pump failure’ of the right side of the heart due to obstruction of the pulmonary
arterial system by the air bubbles, the pulmonary vasoconstriction, and the cellular aggregates. With a very large bolus of air, the obstruction
occurs not only in the pulmonary vasculature but also in the right ventricle. Air is not compressible and hence when fills the great veins, right
atrium and right ventricle, causing froth that cannot be pumped on by the heart in systole.

(ii) In arterial embolism - Death can be the result of air locks in the cerebral vessels or of ventricular fibrillation from coronary air embolism

(I) Paradoxical air embolism - occur when air or gas that has entered the venous system crosses over to the arterial system. Arterial tree is
embolized paradoxically. The paradox is how the air entering the veins can embolize arteries.
(1) Occurs when air passes into the arterial system via anomalous structures
(i) Atrial or Ventricular septal defect
(ii) Patent foramen ovale [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]
(iii) Pulmonary AV malformations [AVM].
(iv) In the absence of AVM, gas bubbles may pass when (a) there are large volumes of venous air (b) administration of vasodilators and (c)
volatile anesthetic agents [have a pulmonary vasodilating effect].
(2) Increased right-sided heart pressure also causes air to be forced into the epicardial veins on the surface of the heart
(3) When there is 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

(J) Minimum amount of air that causes fatal air embolism:-

(1) Venous embolism - 100 ml in adults. Several authors give figure ranging from 10 to 480 ml. If the volume of the right side of the heart is
accepted as the minimum space that has to be filled, about 100 ml would appear to be acceptable figure. In children, the figure may be
correspondingly smaller.
(i) Factors influencing volume –
(a) Weight of patient - On translating data from experimental studies on animals, lethal volume has been worked out to be 3-5 ml/kg.
(b) Rate of air entry - If rate of entry is slow, comparatively larger amounts may be tolerated, as the gas is absorbed in blood , as shown in Dogs,
who can withstand up to 1,400 ml of air over a several-hour period.
(c) Proximity of vein of entrainment to the right heart – Closer it is, smaller the required lethal volume. If injected in a limb vessel, comparatively
larger volumes are required, as air is absorbed rapidly.
(2) Arterial embolism - 2-3 ml, because air travels directly from lungs to the left side of the heart, from where it is forced into the coronary or
cerebral arteries

(K) Fatal period - Death from air embolism [venous or arterial] occurs within a few minutes, and is rarely delayed beyond an hour.

(L) Homicide by air embolism - homicide 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 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.
(M) If individuals survive the initial insult of air in the coronary and cerebral circulation, they might develop myocardial or cerebral infarcts.

(N) Demonstration of air embolism:-

(1) In both arterial and venous embolism – Take X-ray and CT Scan of whole body. The first step may be a chest X-ray to look for air in the
heart. Pre-autopsy chest radiograph is the best way of demonstrating air in sufficient quantities to be fatal. A chest radiograph is also essential in
any kind of barotrauma as it may also indicate a pneumothorax, a lesion so often the cause of air embolism.

(2) Body must be carefully inspected for any tissue swelling, especially in the upper thorax and neck region, where crepitant gas bubbles may
form surgical emphysema from leakage from lung damage or pneumothorax, or both, in Dysbarism.

(3) If venous embolism is suspected –

(i) Abdomen opened before any other cavity
(a) Abdominal contents are moved gently out of the way to inspect the IVC closely for bubbles in the lumen through its transparent wall.
(b) Water may be filled up in the abdominal cavity so that IVC drowns under water. Incise IVC carefully to see if air bubbles escape.

(ii) Opening the chest – Care should be taken to avoid pulling the sternum and ribs to avoid creating -ve pressure in the tissues [may result in
sucking in of air, causing artifactual air embolism].

(iii) PM Demonstration of venous embolism:

(a) Air in the right ventricle can be shown
(b) The sternum is removed by dividing the ribs, being careful not to puncture the pericardial sac.
(c) The internal mammary vessels, ascending aorta and IVC are clamped to prevent escape of air from heart into these vessels,
(d) Pericardium is opened anteriorly, and its edges grasped with hemostat on both sides by an assistant and lifted up. This will create a small
sac.
(e) Inspect external epicardial veins for evidence of intraluminal bubbles. In case of air bubbles, they present a beaded appearance, with
numerous air bubbles along the length [One or two bubbles in an Epicardial vein do not make a diagnosis of air embolism]
(f) Water is then poured into the sac
(g) Once the sac is full of water, the coronary arteries are incised and massaged -> escape of gas bubbles noted. Air in arteries indicate systemic
embolism,
(h) Next right atrium and ventricle are incised with a scalpel. If no bubbles escape, twist scalpel a few times. If air is present, bubbles would
escape. It can be collected in a measuring jar and its volume noted
(i) Alternatively, a water-filled 50 ml syringe (minus plunger) is connected to a wide-bore needle, and is inserted into the right ventricle. If air is
present it will be seen in syringe chamber,

(iv) Pyrogallol test – Bacteria may produce gas within the right heart very soon after death [even in the absence of any visible signs of
putrefaction], which may mimic air embolism. This can be distinguished with pyrogallol test,
(a) Principle - (a1) True air embolism contains air with oxygen, while putrefactive gases will not contain any oxygen
(a2) Alkaline solution of pyrogallol, a strong colorless reducing agent turns purple in presence of 02.

(b) Procedure - (b1) 4 ml of 2% freshly prepared pyrogallol soln is collected in two 10 ml syringes
(b2) 1st syringe - add 4 drops of 0.5M NaOH to make it alkaline -> Introduce in right ventricle -> aspirate gas -> take out syringe -> Remove
needle -> seal needle end with a stopper -> shake -> in case of true air embolism there will be 02 and mixture would turn purple; otherwise not.
(b3) 2nd syringe - functions as a control. Introduce some atmospheric air and test as above. It should turn brown in all cases,

(v) Alternative techniques - Useful if facilities for underwater exploration are not there, or autopsy surgeon is inexperienced –
(a) Frothy blood - (a1) Simply lift the heart in-situ, cut apex with knife and look inside left ventricle. If it contains frothy blood, it indicates air
embolism.
(a2) Other conditions presenting with frothy blood - (1) Careless handling of heart before it is opened (2) putrefaction ,

(b) Floatation in water - It has been suggested that if all great vessels of the heart are ligated and heart removed, then it will float in water if it
contains air [much like Breslau’s 2nd life test for stomach and intestines in infanticide ].

(vi) The technique using Aspirometer - This device not only demonstrates the presence of air but measures the amount and stores it for
subsequent analysis by gas chromatography.
(a) 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%.
(b) Detection of CH4 and H2 indicates that decomposition has begun.

(vii) Source of air - should be determined as far as possible. If source of air is neck veins [eg stab wounds of neck], air can be demonstrated in
the SVC; if pregnant uterus, in the large pelvic veins and IVC.

(viii) Composition of air - should be determined by removing air with a syringe and subjecting it to GC-MS. >95% nitrogen indicates nitrogen
narcosis.

(4) If arterial embolism is suspected –

(i) Head should be opened first -> look for air in the cerebral arteries. Cerebral veins may show segmental breakup of blood in the vessels
with collapsed segments in between which represent artifacts.
(ii) Ophthalmoscopy for air bubbles in retinal vessels [may require corneal moistening with isotonic saline to prevent interference from corneal
opaqueness].
(iii) PM demonstration of arterial embolism –
(a) Air in the coronary arteries cannot be identified at autopsy because air bubbles cannot be seen through the wall of these vessels
(b) The basal arteries should be inspected for air. Internal carotid and basilar arteries are ligated before removal of brain
(c) Skull vault removed without damaging the meninges. Dura is opened.
(d) Examine the meningeal vessels for visible air bubbles [if meningeal vessels are damaged during removal of skull cap air bubbles may appear
as artifacts].
(e) The brain is carefully lifted and small artery forceps clamped on the intracranial part of both internal carotid arteries and vertebral arteries.
The vessels are then cut below these before the brain is removed from the skull in the usual manner.
(f) Submerge the whole pluck in water -> release ligatures/clamps -> Cut the vessels -> compress them slightly -> watch for air bubbles,
(g) An air-tight water filled glass syringe with a needle can be used to collect gas from blood vessels, heart or cavities.

(O) Air embolism as artifact –

(1) 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.
(2) 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 does not necessarily indicate
an embolus.
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(IV) Fat embolism - Fat embolism is obstruction of a blood vessel by an embolus made up of fat, occurring especially after fractures of large
bones. In simplistic terms, where skeletal structures containing fatty marrow are damaged or where subcutaneous fat is compressed or
lacerated, fat globules commonly appear in the pulmonary capillaries – and where they are numerous they somehow leak through the lungs into
the systemic circulation where they can cause severe disability or death from impaction in vital organs, such as brain, kidney or myocardium.

(A) Fat Emboli were first noted by F.A. Zenker in 1861 in a railroad worker with a thoraco-lumbar crush injury. The Fat Embolism Syndrome
(FES) was first described by Von Bergman in 1873 in a diagnosis confirmed by post mortem examination. This patient had a fractured femur.

(B) Caused by:

(1) Fracture of a long bone [90–100% of individuals with long-bone or pelvic fractures have fat embolism]
(2) It can also be precipitated by reaming and nailing procedures for long-bone fractures
(3) Injury to adipose tissue [crushing of buttocks or breasts]. Can occur during Liposuction
(4) Injecting oil in circulation (e.g. criminal abortion)
(5) Severe antemortem burns and septicemia
(6) During childbirth
(7) Parenteral infusion of lipids.
(8) Occasionally natural diseases without trauma [e.g., alcoholism (showing fatty changes in liver), Caisson’s disease (acute decompression
syndrome), diabetes mellitus, following blood transfusion, osteomyelitis, pancreatitis (acute and chronic), septicemia, sickle cell disease, steroid
therapy]

(C) Fat is derived from:

(1) The bone marrow after trauma. Bone marrow fat is scanty in children -> fat embolism rare in children.
(2) From the plasma by agglutination of chylomicrons
(3) Infusion of exogenous fat.

(D) Minimum amount of fat necessary to cause fat embolism - 100 ml. About 12–120 ml of free fat causes embolic death.

(E) Conditions simulating fat embolism –

(1) During life: (i) Craniocerebral trauma, (ii) Resuscitation - fracture of sternum or ribs.
(2) At PM examination: (i) Cardiac massage even after death can force fat into capillaries (ii) Charring after death (iii) Putrefaction liquefied fat
enters capillaries

(F) Theories:
(1) Mechanical theory – Fat cells and venous sinuses are disrupted after a bony trauma or injury to adipose tissue. The liberated fat globules
enter the circulation by means of lacerated veins in the traumatized area. Fat droplets of between 20- 40 diameter block the smallest branches
of the pulmonary vasculature whereas smaller fat droplets may pass through the capillaries and enter the systemic circulation. Mechanical theory
is not able to explain convincingly how bigger fat droplets (>20-40 ) can be found in the brain (systemic circulation). Two gateways have been
suggested. They may pass through –
(i) Arteriovenous shunts in the lungs (ii) Patent foramen ovale.
The paradox of how fat can pass from lower pressure right atrium (RA) to higher pressure left atrium (LA) [even if there were a patent foramen
ovale] is explained like this –
(a) Pulmonary emboli with size >20-40  form -> Pulmonary-artery pressure increases -> increases RV pressure -> RA pressure increases ->
Becomes greater than that in LA -> emboli pass into the LA -> get distributed to the brain,
(b) Transient rise of RA pressure (b1) during coughing (b2) after the release phase of the Valsalva maneuver (b3) during mechanical
ventilation. Paradoxical air embolism is also explained in a similar manner. Since fat is readily deformable, it accounts for the passage of masses
larger than the diameter of the patent foramen ovale.

(2) Biochemical theory - Embolic fat is derived NOT from bone marrow or traumatized adipose tissue, but from circulating blood lipids. Trauma
and/or subsequent sepsis -> hormonal changes (most notably catecholamine release) -> mobilization of lipids (chylomicrons) from plasma ->
Acute phase reactants, such as C-reactive proteins (CRP), cause these chylomicrons to coalesce into bigger droplets. CRP is synthesized in the
liver in association with traumatic, inflammatory and malignant processes -> These droplets then travel to lungs, brain and skin and cause fat
embolism. The biochemical theory helps explain several features of fat embolism not properly explained by mechanical theory. For instance -
(i) Why fat embolism is sometimes seen in non traumatic cases, such as diabetes
(ii) How fat emboli greater than 20-40  in diameter escape the lung capillaries to get lodged in brain.

(G) Fat Embolism Syndrome (FES):

(1) The clinical manifestations of fat embolism depend on the volume of fat reaching the lungs.
(2) Fat embolism generally remains undetected clinically, or produces very minor signs and symptoms [cyanosis, precordial pain, and rapid pulse
(tachycardia), and increased temp (fever), petechial hemorrhages especially in the eye, chest and Axilla. Fat globules may be detectable in
urine, sputum and retina].
(3) About 1-2% cases of fat embolism develop Fat Embolism Syndrome (FES). It may manifest as pulmonary fat embolism or systemic fat
embolism depending upon the volume of fat reaching lungs and systemic circulation.
(4) Pulmonary fat embolism –
(i) Fat appears in lungs and can be Histologically demonstrated in majority of cases of fractures and injury to fatty parts of the body such as the
buttocks.
(ii) In 20 – 50 % non-trauma deaths also fat demonstrated in lungs but in lesser quantity.
(iii) Pulmonary fat embolism is merely a phenomenon and not a clinical syndrome unless significant amount of fat is impacted in the lung vessels
which then appear as acute respiratory insufficiency.
(iv) The incidence being up to 2 per cent in long bone fractures and as much as 10 per cent in multiple fractures, especially with pelvic injuries.
(v) Marked pulmonary oedema (shortness of breath, hypoxemia) is the pathological marker for this syndrome, but caution must be
employed, as cerebral fat embolism can also cause pulmonary oedema by its effect upon the brain.

(5) Systemic fat embolism –

(i) Here the fat penetrates the lung capillaries and appears in the major circulation, so that it can be carried to any organ or structure, including
the skin, where it can cause petechial-like lesions.
(ii) Systemic fat embolism is the fatal manifestation, except where pulmonary loading is so great that it causes respiratory distress.
(iii) The brain, kidneys and myocardium are the most vulnerable target organs, the brainstem being the one that is most likely to lead to death
from impaction of fat globules in its capillaries.
(iv) May cause neurological abnormalities (agitation, delirium, or coma), dermatological (petechial rash), and hematological (anemia,
thrombocytopenia) manifestations
(6) Petechial rash - appears on the upper anterior portion of the body, including the chest, neck, upper arm, axilla, shoulder, oral mucous
membranes and conjunctivae, and is considered a pathognomonic sign of FES. However, it appears late and often disappears within hours. It
results from occlusion of dermal capillaries by fat, and increased capillary fragility.
(7) Typically appears 12-72 hours after long bone fractures, especially of the femur or tibia due to delay between trauma and cerebral fat
embolism while fat builds up in the lungs, so that ‘lucid interval’ occurs which may be confused clinically with the development of an extradural
or subdural haemorrhage.
(5) The syndrome is largely self limiting.
(6) Therapy is directed at maintaining respiratory function and early immobilization of fractures
(7) Mortality is 10-20%. Most individuals who die from fat embolism do so as a result of pulmonary failure.
(8) Death usually occurs in about 10 days, but may be delayed upto 3 weeks.
(9) There is, however, a severe fulminating form of fat emboli in which both pulmonary and cerebral deterioration begins within the first 12 h.
Cerebral fat embolism causes death in about 1–2 days.

(H) Postmortem features: When fat is released through the lungs into the systemic circulation, a number of target organs and tissues exhibit
abnormalities demonstrable at autopsy, either by gross or histological examination.
(1) Demonstration of fat embolism - Dissect pulmonary artery under water -> Note escape of fat droplets,
(2) Lungs - (a) Show congestion, edema and slight hypostatic pneumonia
(b) Immediate spot diagnosis - Small piece of lung tissue is put on a glass slide. Add 20% caustic potash and put a cover slip over it. Examine
under microscope. After a few minutes RBCs are lysed and fat is seen lying as highly refractile plugs in the pulmonary capillaries
(c) Frozen sections –
(c1) Brain - Microscopically stained for fat with Sudan III (orange) or osmic acid (black) or Oil Red-O the cerebral petechiae will show a central
fat globule or globules, and others will be visible without haemorrhage
(c2) Heart - In the myocardium, fat may be seen in the interfibre capillaries
(c3) Kidneys - Glomeruli may be stuffed with stained fat.
(c4) There can be fat in the retina and in the optic nerve

(3) Brain, heart, kidneys - show scattered emboli. In the brain, petechial hemorrhages are seen classically in the white matter of cerebrum,
cerebellum and brainstem

(I) Fat embolism as Forensic marker –

(1) Any injury inflicted after cessation of effective cardiac function cannot transmit fat or marrow to the pulmonary capillary bed. This is therefore
a useful forensic marker on some occasions, such as differentiating between ante-mortem and post-mortem fractures in a body recovered from
water.
(2) Systemic embolism is not seen in rapid deaths following trauma - there is an interval averaging 24 hours before lung percolation takes place.

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(V) Thromboembolism - Thromboembolism is the formation in a blood vessel of a thrombus that breaks loose and is carried by the blood
stream to plug another vessel.
(A) Salient features:
(1) Sites - Most common sites of thrombosis are: (i) Deep femoral v. (ii) popliteal v. (iii) posterior tibial v.
Less common sites are (iv) Axillary v. (v) Jugular v. (vi) Iliac v. [external and internal] (vii) Ovarian v. (viii) Prostatic plexus (ix) Subclavian v. (x)
Uterine v. and (xi) Venous sinuses of dura mater

(2) Etiology:
(i) Traumatic – Occurs usually in traumatic lesions of lower extremity especially fractures of long bones
(ii) Non-traumatic - about 10-20% of fatal pulmonary emboli occur in the absence of trauma.

(3) Predisposing factors are:

(i) Virchow’s triad - risk factors for thrombus formation within the venous circulation: (a) venous stasis, (b) injury to the vessel wall, and (c)
hypercoagulability (Virchow triad)
(ii) Tissue trauma increases the coagulability of the blood for several weeks, the peak being between one and two weeks.
(iii) Injury to the tissues, especially the legs or pelvic region, may cause local venous thrombosis in the contused muscles or around fractured
bones)
(iv) Immobility and bed rest - recumbency leads to pressure on the calves and immobility causes reduced venous return and stasis because of
lessened muscular massage of the leg veins.
(v) General debility, especially in the old, leading to poor general circulation and poor cardiac output
(vi) Economy class syndrome - Development of deep venous thrombosis and pulmonary embolism occurring after long duration flights in
economy class with cramped spaces. Predisposing factors are:-
(a) Prolonged immobilization -> venous stasis. Usually postoperative, and due to obesity, stroke
(b) Dehydration -> haemoconcentration. Although not related to trauma in any way, it highlights the importance of immobility and dehydration in
causation of thromboembolism.
(v) Rail coach syndrome - May also occur after long travel in rails and buses [bus travel syndrome] in similar conditions,
(vi) Increased central venous pressure - low cardiac output states, pregnancy
(vii) Hyperviscosity – polycythemia
(viii) Hypercoagulability - medications (OCP, HRT) or disease (malignancy, surgery) or inherited gene defects (resistance to activated protein
C, also known as factor V Leiden). Other major risks for hypercoagulability include the following: deficiencies or dysfunction of protein C, protein
S, and antithrombin; prothrombin gene mutation; hyperhomocysteinemia and the presence of antiphospholipid antibodies (lupus anticoagulant
and anticardiolipin antibody).

(4) Time of formation - thrombus typically forms within 10-20 days of injury

(5) Cause of death in pulmonary thromboembolism (Saddle embolism) : The embolus which blocks the pulmonary trunk causes death in
few minutes due to -
(i) Right sided heart failure [acute cor pulmonale],
(ii) Acute asphyxia
(iii) Vagal inhibition

(6) Autopsy - A noticeable fullness of pulmonary artery is seen before the vessel is opened
(7) Pulmonary emboli may be confused with PM clots. Differences are :-

Characteristic Ante-mortem Embolus Post-mortem clot

Firmness It is firm though brittle It is Soft and jelly-like
Surface Surface is dull, matt, striated surface from fibrin lamination Surface is shiny, glistening surface
Color Older thrombus tends to be greyish-red and varies in colour Dark red, often separated into ‘chicken-fat’ plasma clot and
from place to place dark red-cell clot by sedimentation after death

Shape & May appear to be a cast of the large vessel in which it is
Branching impacted, but may often be unraveled to form a long length that
obviously originated in a leg vein. Side branches, or the stumps
thereof, may be seen that do not correspond to the branches of
the pulmonary artery in which they lie
On Dissection On cutting the lung with a knife, ante-mortem emboli may be
seen in the more peripheral vessels, often standing up slightly
‘proud’ above the surface, like toothpaste coming from a tube.
Obscured Post-mortem clot may be adherent to the ante-mortem embolus
true nature nature is obscured unless a careful examination is made.
When pulled out of the vessels it forms a cast of the
branches, albeit shrunken by clot retraction
Less evident in peripheral branches and, when the lung is
sliced post-mortem, clot does not pour out of cut small
vessels
and sometimes forms a sheath around it, so that the true

(8) Infarction- Pulmonary infarction does not occur from fatal massive pulmonary embolism from blockage of main pulmonary trunk, as death is
too rapid. There may be infarcts present in the lungs but these must be caused by previous smaller emboli due to blockage of artery to a
bronchopulmonary segment or smaller vessel, at least a day earlier and probably much longer.

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(VI) Tissue components - Tissue embolism is obstruction of a blood vessel by a body tissue. Common tissue emboli are:-
(1) Bone marrow embolism – following fractures of bones
(2) Brain embolism - trauma [including gunshot injuries] to head
(3) Chorionic embolism - can cause death during abnormal gestation
(4) Liver embolism-in hepatic trauma
(5) Skin embolism - from venepuncture site
(6) Transition epithelium embolism - from severe ulcerative urethritis
(7) Tumor cell embolism.
(8) Amniotic fluid embolism.
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(VII) Miscellaneous embolic phenomena - Foreign bodies which can get embolized are:
(1) Bones - occurs in trauma-induced septic bone lesions, after bone surgery, after bone marrow transplantation, and normally remains silent, as
bone chips do not usually occlude the vessel lumen. Over time the endothelium covers the bone fragment. Also seen in gunshot wounds of the
head.
(2) Bullets and short gun pellets [most commonly reported]
(3) Iatrogenically introduced objects [hypodermic and radium needles, IV catheters, cotton fibre during angiography]
(4) The lung granulomata of talc, etc., seen in the lungs of intravenous drug users, are emboli from contaminants introduced into the venous
system by syringe and needle
(5) Pins and needles
(6) Thorns and
(7) Wooden fragments.

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(VIII) Amniotic Fluid embolism:-

(A) Definition - Amniotic fluid embolism (AFE) is condition in which amniotic fluid, fetal cells, hair, or other debris enters the mother's blood
stream via the placental bed, with resultant pulmonary microvascular obstruction. It is an uncommon but highly lethal complication of pregnancy.

(B) History - Presence of fetal debris in the pulmonary blood vessels of a mother who had died suddenly in labor was first described by Meyer in
1926. In 1941, Steiner and Luschbaugh were the first to attribute sudden death during labor to AFE.

(C) Salient features:

(1) Occurrence - It occurs not only during (i) criminal abortion, but also during
(ii) first and second trimester abortions (iii) abdominal trauma (iv) Amniocentesis (v) normal labor and delivery (vi) immediately postpartum
[As the pregnancy progresses -> volume of amniotic fluid increases -> risk of amniotic fluid embolism increases -> AFE in 3rd trimester > 2nd > 1st]
(iii) Most cases occur during active labor and shortly after delivery

(2) Risk factors- (i) increased maternal age (ii) augmented labor (iii) cervical laceration (iv) cesarean delivery (v) Diabetes (vi) fetal macrosomia
(vii) induction and augmentation of labor (viii) placenta previa or abruption (ix) Strong uterine contractions (x) uterine rupture, and (xi) vacuum,
and forceps deliveries.

(3) Epidemiology –
(i) Incidence - 1in 8000 to 80,000 deliveries.
(ii) Mortality rate is about 80%.
(iii) In 50% of cases, death occurs within 1st hour of AFE.
(iv) In late deaths, DIC (consumptive coagulopathy) occurs. [AFE is one of potent causes of DIC]

(4) Site of embolization - The solid elements are usually impacted in the lung capillaries, but rarely have been found in the systemic circulation,
including embolization into the kidney, liver and brain.

(5) Etiology-
(i) Mechanical blockage – pelvic trauma of parturition, including rupture of uterus and instrumental interference in late pregnancy -> opens up
venous sinuses in the placental bed -> escape of Amniotic fluid [along with fetal debris] -> enters venous sinuses -> cause’s pulmonary
microvascular obstruction. [Fetal elements identified in autopsy]
(ii) Anaphylactoid syndrome of pregnancy – caused by exposure of maternal circulation to amniotic fluid -> allergic response -> release of
various primary or secondary endogenous mediators [arachidonic acid metabolites, bradykinin, endothelin, histamine, leukotrienes] -> severe
transient vasospasm of pulmonary vasculature, pulmonary hypertension, hypoxia, right heart failure, sudden death. [Fetal elements not found in
autopsy]

(6) Clinical features - (i) altered mental status (ii) DIC (iii) sudden dyspnea (iv) seizures, (v) sudden cardiovascular collapse, (vi) maternal death

(7) Lab diagnosis - (i) Increased Fibrin split products (ii) Decreased Fibrinogen (iii) Prolonged partial thromboplastic and prothrombin times (iv)
thrombocytopenia

(8) Postmortem diagnosis –

(A) Examination of dead body –
(i) Examination of uterus - May reveal entrance site of emboli,

(ii) Histopathology –
(a) Demonstration of (a1) Amniotic and Chorionic cells, (a2) Fat globules, (a3) Fetal squames, (a4) Lanugo hair, (a5) Meconium, (a6) Mucin
and, (a7) Vernix in pulmonary vasculature and in uterine veins. [Mucin is virtually always present, with cellular elements seen less frequently]

(b) Stains used are (b1) Alcian Blue - detects mucin (b2) H&E – routine staining (b3) Attwood's stain - stains the keratin red and the mucus
turquoise blue (b4) Lendrum stain contains Phloxine-Tartrazine. Detects squames by staining them red (b5) Mucicarmine (b6) Sudan Black or
Oil Red – Detects vernix caseosa.

(c) Squamous debris may persist for some weeks after the embolic event, and it is worth looking for even in late deaths,

(d) DIC - deposition of fibrin microthrombi [demonstrated with Martius Scarlet Blue] and extensive bleeding in internal organs.