Baylor University Medical Center Proceedings July 2017 - 359

Figure 1. (a) Initial plasmapheresis session with lipemic, opaque effluent. (b) Translucent change of effluent after second plasmapheresis session with reduction
in triglyceride levels.

examination and return of her studies, her cumulative Ranson
score was 5 out of 11. With any Ranson score above 4, the risk
of morbidity and mortality is high (1). The patient was aggressively rehydrated with Ringer's lactate solution and was started
on an intravenous insulin infusion.
Plasmapheresis was performed with one calculated plasma
volume exchange using 5% albumin replacement within 24
hours of admission. After the initial session, the patient's triglyceride level was reduced to 1026 mg/dL, a 74% reduction.
The following day, a second plasmapheresis was performed with
a reduction in triglyceride level to 360 mg/dL, an overall 90%
reduction. The eﬄuent of the initial exchange transitioned from
lipemic and opaque to translucent after two sessions (Figure 1).
Her ﬁnal measured triglyceride level was 280 mg/dL, a 93%
reduction, and her serum lipase was 399 U/L. By hospital day
5, she was tolerating a solid diet without abdominal pain and
was transitioned to subcutaneous insulin.
DISCUSSION
HTGP is a well-established cause of acute pancreatitis, accounting for 1% to 4% of cases (2). HTGP is most common
in patients with diabetes mellitus, diabetic ketoacidosis, chronic
alcoholism, and women with increased estrogen (2). The risk
of developing acute pancreatitis increases in proportion to the
serum triglyceride level once a threshold of 1000 mg/dL is
reached. However, the severity of acute pancreatitis does not
correlate well with the serum triglyceride level (3). The exact
mechanism by which elevated triglyceride levels trigger acute
pancreatitis remains largely unknown (3). One theory behind
HTGP is that pancreatic lipase hydrolyzes the excess triglycerides into free fatty acids, which subsequently produce injury
July 2017

to the pancreatic acinar cells. Ischemia is theorized to be from
either hyperviscosity of excess chylomicrons or hyperviscosity
of serum itself in the pancreatic capillaries (2).
Several modalities exist for treating HTGP. Maintenance of
triglyceride levels below 500 mg/dL has been shown to greatly improve outcomes (4). In extreme levels of hypertriglyceridemia with
life-threatening symptoms, plasmapheresis is recommended. This
was ﬁrst described as a treatment modality in 1978 by Betteridge
(5). Plasmapheresis oﬀers several advantages, including removing circulating triglycerides and chylomicrons, reducing blood
viscosity, and lowering cytokines associated with pancreatitis (6).
Published experience with the use of plasmapheresis to
treat HTGP remains scarce (7). This case is novel in that the
patient presented twice within the same year with HTGP and
responded well to prompt plasmapheresis therapy.
1.

3.
4.
5.

6.
7.

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