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==Overview== | |||
==Differentiating Acute chest syndrome from other Diseases== | |||
* The primary acute pulmonary diseases which affect patients with [[SCD]] include pneumonia, infarction due to in-situ clot, fat / bone marrow emboli and ACS. Patients with [[SCD]] are predisposed to pneumonia due to loss of antibody protection (secondary to auto-splenectomy), and defective opsonization and phagocytosis resulting from a defect in the alternate pathway of complement activation. As blood and sputum cultures are often negative in any patient with pneumonia it is difficult to distinguish infection from ACS. However, unlike children, who have a higher incidence of infectious causes of ACS, adults are thought to have a higher incidence of vascular occlusion. One study that examined the causes of pulmonary infiltrates in patients with ACS with bronchoscopy, found a 21% incidence of bacterial infection. Interestingly, patients with SCD do not have a higher rate of large vessel fibrin thromboembolism compared with the general population. They do, however, have a higher rate of in-situ clot, and fat embolism. In-situ clot results from sickle cells being less deformable than normal cells, an increased adherence of sickle cells to the endothelial cells, and local vasoconstriction secondary to hypoxemia. Patients with SC disease have a higher rate of thrombosis as compared to those with SS disease, due to a higher blood viscosity and hematocrit. [[Fat embolism]] probably results from bone marrow infarction and is often associated with mental status changes, [[thrombocytopenia]], a falling [[hematocrit]] (HCT), [[disseminated intravascular coagulation]] ([[DIC]]), [[hypocalcemia]], [[hyperuricemia]], and severe [[hypoxemia]]. Unfortunately, there is no test that will confirm the diagnosis of fat emboli. Lipemia retinalis and [[petechiae]] on the conjunctiva and upper thorax are suggestive of fat emboli syndrome. Bronchoalveolar lavage findings of greater than 5% lipid laden macrophages, and fat droplets obtained from a pulmonary capillary wedge aspirate are also highly suggestive, however their sensitivity and specificity remain to be define. Rib and sternal fractures or infarction can also precipitate ACS by causing splinting, [[atelectasis]] and hypoxemia. <ref>Hammerman, S.I., Farber, H.W., Pulmonary complications of sickle cell disease, in UpToDate, September 12, 1996.</ref> <ref> Haynes, J. Jr., Kirkpatrick, M.B., The Acute Chest Syndrome of Sickle Cell Disease, Am J Med Sci 1993; 305: 326-330. PMID 8484394</ref> <ref>Oswaldo, C., et.al., The Acute Chest Syndrome in Sickle Cell Disease: Incidence and Risk Factors, Blood 1994; 84: 643-649.</ref> <ref>Vichinsky, E.P. et.al., Acute Chest Syndrome in Sickle Cell Disease: Clinical Presentation and Course, Blood 1997; 89: 1787-1792. PMID 9057664</ref> | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
[[Category:Disease]] | [[Category:Disease]] | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Differentiating Acute chest syndrome from other Diseases
- The primary acute pulmonary diseases which affect patients with SCD include pneumonia, infarction due to in-situ clot, fat / bone marrow emboli and ACS. Patients with SCD are predisposed to pneumonia due to loss of antibody protection (secondary to auto-splenectomy), and defective opsonization and phagocytosis resulting from a defect in the alternate pathway of complement activation. As blood and sputum cultures are often negative in any patient with pneumonia it is difficult to distinguish infection from ACS. However, unlike children, who have a higher incidence of infectious causes of ACS, adults are thought to have a higher incidence of vascular occlusion. One study that examined the causes of pulmonary infiltrates in patients with ACS with bronchoscopy, found a 21% incidence of bacterial infection. Interestingly, patients with SCD do not have a higher rate of large vessel fibrin thromboembolism compared with the general population. They do, however, have a higher rate of in-situ clot, and fat embolism. In-situ clot results from sickle cells being less deformable than normal cells, an increased adherence of sickle cells to the endothelial cells, and local vasoconstriction secondary to hypoxemia. Patients with SC disease have a higher rate of thrombosis as compared to those with SS disease, due to a higher blood viscosity and hematocrit. Fat embolism probably results from bone marrow infarction and is often associated with mental status changes, thrombocytopenia, a falling hematocrit (HCT), disseminated intravascular coagulation (DIC), hypocalcemia, hyperuricemia, and severe hypoxemia. Unfortunately, there is no test that will confirm the diagnosis of fat emboli. Lipemia retinalis and petechiae on the conjunctiva and upper thorax are suggestive of fat emboli syndrome. Bronchoalveolar lavage findings of greater than 5% lipid laden macrophages, and fat droplets obtained from a pulmonary capillary wedge aspirate are also highly suggestive, however their sensitivity and specificity remain to be define. Rib and sternal fractures or infarction can also precipitate ACS by causing splinting, atelectasis and hypoxemia. [1] [2] [3] [4]
References
- ↑ Hammerman, S.I., Farber, H.W., Pulmonary complications of sickle cell disease, in UpToDate, September 12, 1996.
- ↑ Haynes, J. Jr., Kirkpatrick, M.B., The Acute Chest Syndrome of Sickle Cell Disease, Am J Med Sci 1993; 305: 326-330. PMID 8484394
- ↑ Oswaldo, C., et.al., The Acute Chest Syndrome in Sickle Cell Disease: Incidence and Risk Factors, Blood 1994; 84: 643-649.
- ↑ Vichinsky, E.P. et.al., Acute Chest Syndrome in Sickle Cell Disease: Clinical Presentation and Course, Blood 1997; 89: 1787-1792. PMID 9057664