SCLS is a rare, potentially fatal disease, with a high mortality rate. It is characterized by hypoproteinemia, acute hypovolemia, and edema of the limbs [
1,
3,
4], however the pathogenesis remains unclear. The capillary leakage leads to a shift of intravascular fluids into the interstitium and extravascular space. This shift may cause severe complications such as compartment syndrome of the limbs or the abdomen, as it did in this case. The most common clinical features described from several case reports are flu-like prodromes including nausea, vomiting, abdominal pain, and myalgia. Further symptoms observed in patients are polydipsia, dizziness, hypotension, generalized edema (as well as cerebral, pulmonary, macular or epiglottic edema), weight gain, pleural or pericardial effusion, and renal dysfunction that could end in renal failure [
5]. Potential laboratory markers found in patients with SCLS are elevated white blood cell count, elevated hematocrit (>55%), low serum total protein and albumin, or monoclonal immunoglobulinopathy such as increased immunoglobulin G (IgG) kappa, IgG lambda, or immunoglobulin A (IgA) lambda levels [
5‐
7]. Most of the patients in the reported cases were previously healthy, indicating that SCLS appears to belong to diseases with an idiopathic genesis. The differential diagnoses that need to be excluded before confirming the diagnosis of SCLS are overwhelming sepsis, dengue shock syndrome, chemotherapy, lymphoma, Sézary syndrome, hereditary angioedema due to C1 esterase deficiency, and carbon monoxide poisoning [
5‐
8].
Most of the reported cases show that the patients were described as previously healthy as was our patient. This indicates that a predisposition for this disease does not yet exist. The mean age for the onset of the disease appeared to be at 47±13.1 years, with a female to male ratio of 1:1.4 [
3]. The pathophysiology of SCLS is still unknown and the process of finding a possible etiopathogenesis appears to be complex.