Chyluria is the excretion of chyle from the urinary tract [1]. Chyle is defined as the lymphatic fluid in the intestinal lacteals that contains absorbed fat in the form of chylomicrons, giving the intestinal lymph a milky appearance [2]. Chyluria is associated with abnormal retrograde or lateral flow of lymph from the intestinal lymphatics of the kidney, ureter or bladder, allowing chylous material to be discharged into the urinary collecting system [3]. On an anatomical basis, the renal lymphatics follow the renal vein and end in the lateral aortic glands as efferents which flow to the lumbar trunks. The intestinal trunks receive lymph from the stomach, intestine, pancreas, spleen and liver. Pathological obstruction and/or insufficiency of the valvular system of the lymph channels leads to retrograde flow of lumbar lymph glands draining into renal lymphatics [3].
The etiology of chyluria can be classified as either parasitic or non-parasitic [4]. Lymphatic filariasis is the most common cause of parasitic chyluria in persons living in endemic areas, namely tropical and subtropical regions between latitude 40° North and 30° South [5]. Wuchereria bancrofti infection accounts for most of the lymphatic filariasis worldwide [6]. Chyluria can be a late and uncommon manifestation of chronic lymphatic filariasis [5]. The diagnosis of lymphatic filariasis is usually made by the detection of microfilariae on thick Giemsa-stained blood smears. In recent years, circulating filarial antigen detection tests using polyclonal and monoclonal antibodies have been introduced [6].
The non-parasitic causes of chyluria are rare, and various causative factors have been implicated. Passage of chyle into the urine has been related to rupturing of the lymphatic varices, leading to the aperture of one or more perirenal lymphatic vessels into the pyelocaliceal system. The non-parasitic causes of chyluria also include granulomatous disease (such as tuberculosis and leprosy), malignancy, trauma, venous stasis and aortic aneurysm [7]. In traumatic or congenital communication between the lymphatic system and the urinary tract, lymphatico-urinary fistulae have been detected at the level of the kidney, ureter or bladder. In children, chyluria due to a congenital fistulous communication between the lymphatic system and the bladder has been described [8].
The evaluation of chyluria includes localization of lymphaticourinary fistula and the assessment of the underlying etiology. Lymphangiography is the imaging procedure of choice since it demonstrates the site, the calibre and the number of fistulous communications. In patients with chyluria, lymphangiography typically shows marked dilatation and tortuosity of the lymphatics around the hilar regions of the kidneys, followed by opacification of the calyceal systems [9].
A cystoscopy performed after a fatty meal allows the identification of the ureteral orifice that is passing milky urine or the site of chylous efflux into the bladder or urethra [2].
The prognosis of non-parasitic chyluria is usually very good, and the treatment is mostly conservative with adequate dietary modification, medical management and two or more instillations of sclerosants. Surgery is the treatment of choice in severe forms of chyluria that involve significant weight loss, hypoproteinemia, anasarca and/or severe anemia, recurrent clot retention and hematochyluria and refractory chyluria (failure of conservative treatment) [8].
B.
Propofol anesthesia:
The appearance of milky urine has been rarely noted during surgical procedures under intravenous general anesthesia with propofol, but the real incidence of this urine discolouration is not known [10‐13]. A number of hypotheses have been formulated to explain the phenomenon. Nates et al. reported white urine in four patients and speculated that the vehicle of the propofol emulsion was responsible for the colour change of the urine [10]. Masuda et al. attributed the urine feature to intraoperative hypotension and oliguria that could cause the accumulation of propofol and its metabolite in urine [11]. These authors also showed that patients under total intravenous anesthesia had increased urine uric acid and observed the appearance of milky colour urine more frequently in operating theatres with an ambient temperature of less than 24 °C. The reason attributed to this was that decreased temperature caused decreased solubility of uric acid crystals [12].
However, in all described cases urine discolouration was transient and self-limiting, the renal function was normal and no long-term renal damage was reported.
C.
Complication of central venous catheterization:
Many complications of central venous catheters (CVC), which include perforation of the vessel walls and extravasation of the infusate into a body cavity, have been reported. Delayed effusion into pericardial, pleural and peritoneal cavities is not a rare occurrence. Perforation of the renal pelvis is a very rare complication, reported in few cases of neonates with abdominal malformation [14, 15]. In this situation the milkiness is due to the presence of lipid in the total parenteral nutrition (TPN) extravasated, which is mixed with the urine. To our knowledge there are no reports of perforation of a CVC into the renal pelvis in a non-malformed neonate.
2.
In our case the appearance of milky urine was iatrogenic, due to the dislocation of the long line and perforation of the right renal pelvis. As previously reported, the milkiness of urine is due to the presence of lipid in the total parenteral nutrition extravasated.
3.
To confirm the diagnosis we performed an abdominal radiograph during the instillation of 0.5 ml of contrast (Omnipaque 140; Nycomed NZ Ltd, Auckland, NZ) through the CVC. Contrast was seen to flow into the right renal pelvis (Fig. 1). The line was removed and a new CVC was reinserted in the upper limb. The baby’s further course was uneventful.
Fig. 1
Abdominal X-ray with instillation of contrast through the central venous catheter, flowing into the right renal pelvis
