Fat Embolism

Chapter 170 Fat Embolism



Alan M. Klide, VMD, DACVA



KEY POINTS



• There are many causes of fat embolism, but it most commonly results from traumatic injuries, especially long-bone fractures.

• Fat embolism is often a diagnosis of exclusion.

• Fat embolism often is not considered a cause of morbidity and mortality in veterinary patients and is reported infrequently in animals.

• Fat embolism is easily and consistently created in dogs with procedures that mimic clinical orthopedic procedures.

• The vast majority of reports and investigations concern endogenous fat as the source of embolus, but there are a few reports of fat embolism from exogenous sources.

• Clinical signs of fat embolism may include right ventricular failure, cardiovascular collapse, hypoxemia, neurologic changes, fever, petechial rashes, tachycardia, retinal changes, renal failure, tachypnea, and dyspnea.

• Treatment of fat embolism is somewhat controversial and is mostly nonspecific and supportive.

• Pulmonary contusions combined with fat embolism produce a greater degree of pulmonary change than either alone.


INTRODUCTION


Fat embolism is a frequently overlooked but important subject in veterinary medicine. In human medicine, the detrimental effects of embolic fat have been recognized for almost 200 years.1 Wars have provided much material and information.1 There are many possible causes for its occurrence, and the fat sources have been studied but are not always clear. It has been said that fat embolism does not occur in animals or that it has not been reported in animals. Both of these statements are incorrect. Fat embolism can be a severe, life-threatening event that should be considered in the proper patients and circumstances.



DEFINITIONS


There are two definitions related to the subject.2 The first is the term fat embolism. It usually is used to mean fat within the circulation that can produce embolic phenomena that may or may not lead to clinical sequelae. The second term is fat embolism syndrome, which refers to fat in the circulation that is associated with an identifiable pattern of clinical signs that typically occurs 24 to 72 hours after the event. It is a collection of respiratory, hematologic, neurologic, and cutaneous signs associated with trauma or other surgical and medical conditions.2



CAUSES



Predisposing Causes


The incidence of fat embolism is highest following trauma, especially lower limb fractures. However, it can be associated with many other conditions such as soft-tissue injury, liposuction, acute pancreatitis, burns, diabetes mellitus, joint reconstruction, cardiopulmonary bypass, and decompression sickness.2-3


When considering fat embolism as a rule-out, it should be remembered that the source of the fat may be exogenous or endogenous. The vast majority of the literature on the subject relates to endogenous sources of fat; however, there are a few reports regarding exogenous sources. These are related to relatively new drugs and techniques such as propofol,2,4 total parenteral nutrition,2,5 and transcatheter arterial chemoembolization with lipiodol.6



Actual Causes


The sources of the endogenous fat have been variously reported. Incriminated1 factors include alterations of lipid metabolism, changes in the coagulation mechanisms that affect lipids, shock, or atraumatic perturbations in the physical state of the blood. Another possible cause is mechanical,1 also called the infloating theory,2 which states that the fat is physically forced into the venous system following trauma. Capillaries in bone are relatively wide compared with those in the systemic circulation. These capillaries empty into wide sinusoids that are supported by a fibrous network attached to the intramedullary trabeculae. After trauma, many of these sinusoids remain distended rather than collapsing as do veins in soft tissue. Rupture of these delicate structures and increased pressure can force marrow or fat, or both, into the sinusoids.1 Intramedullary manipulations,2 such as reaming and increased pressure (i.e., following cementing) have been shown to cause fat embolism as well.


Systemic embolization without pulmonary effects has been seen and is somewhat confusing.2 The most commonly cited explanation is passage of the emboli through a patent foramen ovale,2,7-9 but there are many reports of fat in the systemic circulation in patients without a patent foramen ovale.2,8,10,11


A possible biochemical mechanism is known as the lipase theory: elevated plasma lipase following trauma destabilizes circulating fats by demulsification, saponification, and mobilization of lipid stores.2 Another, less proven, biochemical mechanism is called the free fatty acid theory, in which circulating free fatty acids directly damage pneumonocytes and create gas exchange abnormalities.2


There may be multiple mechanisms acting synergistically to cause fat embolism syndrome and perhaps also explain the delay in clinical signs. Trauma leads to catecholamine release, which promotes the release of free fatty acids.12 Human patients with trauma or sepsis have elevated C-reactive protein levels that cause chylomicrons to coalesce and form fat globules.13 Therefore factors related to lipid metabolism may provide a connection between the traumatic and atraumatic forms of the fat embolism syndrome. Interestingly, the mechanisms that cause acute respiratory distress syndrome (ARDS) in animals with severe pancreatitis may resemble those causing ARDS associated with fat embolism syndrome.

Related posts:

  1. Deteriorating Mental Status
  2. Hyperthermia and Fever
  3. Ventilator-Associated Lung Injury
  4. Allergic Airway Disease in Dogs and Cats and Feline Bronchopulmonary Disease

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Sep 10, 2016 | Posted by in SMALL ANIMAL | Comments Off on Fat Embolism

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