A recent review in KI summarizes the pathophysiology of capillary leak syndrome and numerous etiologies that can cause it along with an interesting management strategy.
Besides sepsis, capillary leak syndrome(CLS) can be seen in:
1. Drug induced CLS—classically interleukin 2, gemcitabine and certain monoclonal antibodies such as OKT3, anti CD-28 antibody TGN1412 ( steroids can help treat)
2. Engraftment syndrome- seen post HSCT ( usually 4-7 days post) with increased inflammatory markers and AKI( 12-25% in most HSCT patients)( steroids can help treat)
3. Differentiation syndrome( retinoic acid) – steroids help in this situation as well
4. Ovarian hyperstimulation syndrome(OHSS)—two variants( early time course, vs late following HCG treatment)—supportive care
5. Hemophagocytic lymphohistiocytosis
6. Hemorrhagic fever( viruses such as Ebola, Marburg, Puumala)
7. Clarkson’s disease( idiopathic CLS)—supportive therapy, IVIG, theophylline
8. Others:- snake bites, Ricin overdose, APLAS, Kawasaki disease
In addition to hypotension, cytokines are likely to be important in the pathophysiology of acute kidney injury in capillary leak syndrome. Fluid management is a critical part of the treatment of capillary leak syndrome; hypovolemia and hypotension can cause organ injury, whereas capillary leakage of administered fluid can worsen organ edema leading to progressive organ injury.
The first phase of treatment is volume resuscitation including fluids, pressors and or IV albumin. The second phase includes loop diuretics, diuretics with albumin and finally renal replacement therapy.
Full article here