Since venous blood returns to the right heart and is pumped to the lungs for reoxygenation, the fat globules often get lodged in the pulmonary circulation. Fat globules may also pass through lung circulation back into the left ventricle of the heart to be pumped throughout the body in the systemic circulation. They may also reach the systemic circulation through a patent foramen ovale (a hole communicating the right atrium directly to the left atrium of the heart). If fat globules obstruct 80% of the lung capillary network, the resulting back pressure on the right heart increases workload and causes right heart dilatation through cor pulmonale, leading to acute right heart failure. Biochemical theory - Following trauma, an inflammation causes bone marrow to liberate fatty acids into the venous circulation. This is achieved through the increased activity of lipoprotein lipase which break down triglycerides into free fatty acids. Both the release of fatty acids and the inflammation causes damage to the capillary beds of the lungs and other organs, causing interstitial lung disease, chemical pneumonitis, and acute respiratory distress syndrome (ARDS). This theory can help to explain non-traumatic causes of fat embolism. Diagnosis
Fat embolism is presence of fat particles in the micro-circulation of the body. Meanwhile, fat embolism syndrome is the clinical manifestation as the result of fat particles lodging in the body micro-circulation. There are three major diagnostic criteria proposed for fat embolism syndrome, however, none of them are validated and accepted universally.
Treatment
Stabilization and decontamination
The most important initial treatment for ethylene glycol poisoning is stabilizing the person. As ethylene glycol is rapidly absorbed, gastric decontamination is unlikely to be of benefit unless it is performed within 60 minutes of ingestion. Traditionally, gastric lavage or nasogastric aspiration of gastric contents are the most common methods employed in ethylene glycol poisoning. The usefulness of gastric lavage has, however, been questioned, and it is now no longer used routinely in poisoning situations. Ipecac-induced vomiting is not recommended. As activated charcoal does not adsorb glycols, it is not recommended as it will not be effective at preventing absorption. It is only used in the presence of a toxic dose of another poison or drug. People with significant poisoning often present in a critical condition. In this situation stabilization of the person including airway management with intubation should be performed in preference to gastrointestinal decontamination. People presenting with metabolic acidosis or seizures require treatment with sodium bicarbonate and anticonvulsives such as a benzodiazepine respectively. Sodium bicarbonate should be used cautiously as it can worsen hypocalcemia by increasing the plasma protein binding of calcium. If hypocalcemia occurs it can be treated with calcium replacement although calcium supplementation can increase the precipitation of calcium oxalate crystals leading to tissue damage. Intubation and respiratory support may be required in severely intoxicated people; people with hypotension require treatment with intravenous fluids and possibly vasopressors. Antidotes
Following decontamination and the institution of supportive measures, the next priority is inhibition of further ethylene glycol metabolism using antidotes.