Although several theories have been postulated to explain the pathogenesis of the fat embolism syndrome, the end result is the embolization and agglutination of lipids, a process that causes obstruction of local blood flow in end organs (such as the lungs, brain, and skin) and leads to symptoms.
A 46-year-old man had worsening somnolence 1 day after replacement surgery with a femoral endoprosthetic implant. Fever, tachycardia, hypertension, and tachypnea developed, and examination revealed somnolence, gaze deviation, rigidity, and hyperreflexia. A diagnosis was made in a new Case Record.
• What clinical findings are associated with malignant hyperthermia?
Malignant hyperthermia occurs in susceptible persons who have been exposed to halogenated volatile anesthetic agents or depolarizing muscle relaxants. It usually occurs between 30 minutes and 24 hours after such an exposure. Malignant hyperthermia is manifested by marked (sometimes extreme) temperature elevation, tachycardia, profound rigidity, agitation, hypercarbia, and acidosis.
• When would you expect the symptoms of the neuroleptic malignant syndrome to appear in an affected patient?
Neuroleptic agents are sometimes administered in patients who have postoperative delirium, and postoperative use of antiemetic agents is common. Medications from each of these therapeutic classes can be associated with the development of the neuroleptic malignant syndrome. The symptoms typically evolve over a period of 1 to 3 days and include mental-status changes, profound rigidity, bradykinesia, hyperthermia, and autonomic instability, which is manifested by hypertension, tachycardia, and tachypnea.
Morning Report Questions
Q: What are some of the features of the fat embolism syndrome?
A: The classic triad of findings includes respiratory insufficiency (most commonly manifested by hypoxemia), neurologic abnormalities (usually somnolence), and a petechial rash, which typically appears on the head, neck, thorax, and axillae. The fat embolism syndrome has an incidence of 1 to 3% after a single long-bone fracture (most commonly the femur) and a higher incidence after multiple fractures. It is more common among younger patients and those with closed fractures. The syndrome most commonly occurs between 24 and 72 hours after the precipitating injury, but onset between 12 and 24 hours after the inciting event is not uncommon. Eighty-five to 95% of patients with cerebral fat embolism who receive the appropriate supportive care survive.
Q: Is the presence of a petechial rash required for diagnosis of the fat embolism syndrome?
A: Early clinical descriptions of the fat embolism syndrome included the major criteria of respiratory insufficiency, cerebral involvement, and petechial rash; fever and tachycardia, were two minor criteria. However, in a later study involving persons with the fat embolism syndrome, 34% had somnolence as the earliest clinical sign or symptom; 75% had respiratory manifestations, and in 20%, the respiratory manifestations were initially dyspnea or tachypnea rather than hypoxemia. A petechial rash was a sign at presentation in only 17% of patients. Thus, it appears that the absence of hypoxemia and rash at the time of medical consultation does not rule out this diagnosis.