2 dilatation consistent with ileus, and bilateral pleural eﬀusions with associated atelectasis. There was no radiological evi- dence of any pancreatic pathology at this stage. As a result, mild acute pancreatitis was predicted as per the Modiﬁed CT Severity Index [8]. Despite aggressive resuscitation, the patient remained haemodynamically unstable after transfer (tachycardic and hypotensive), requiring signiﬁcant vasopressor support. As a result of the associated pulmonary oedema and inotropic dependent cardiac failure, she developed type 1 respiratory failure necessitating intubation and ventilation. In addition, a persistent oliguria secondary to acute renal failure was noted with concomitant metabolic acidosis, and it was felt that dialysis would be appropriate. As a result of this mul- tiorgan failure, the patient was transferred to the intensive care unit. In spite of this, she demonstrated persistent organ failure during her ICU stay [7]. Three sessions of plasmapheresis were performed during a progressive deterioration in the patient’s condition, using 5% human albumin solution as replacement ﬂuid. She rapidly improved, both clinically and biochemically (random Chol: 3.1 mmol/L, TG: 6.4 mmol/L), was extubated and maintained on supportive care (gastric decompression, jeju- nal feeding tube, total parenteral nutrition, and haemodialy- sis), returning to the ward nine days after admission. Once the patient was stabilised, she continued to expe- rience intermittent temperature spikes. Blood cultures were positive for Staphylococcal and Candida spp. Interval imaging over four weeks showed an evolving ascites (Figure 1) and loculation. No evidence of pancreatic or peripancreatic collections or necrosis was noted during this period. Samples of the ascitic ﬂuid obtained under ultrasound guidance grew Escherichia coli. After detailed discussion with the microbiology service, appropriate parenteral antibiotics and antifungals were commenced. The ascitic collections were not amenable to radiological drainage due to their highly loculated nature. A decision was made not to proceed to laparotomy and surgical drainage, as the ascites promptly resolved, and her inﬂammatory markers quickly fell with the commencement of targeted antimicrobial therapy. The patient’s clinical condition continued to improve until the time of her discharge. 3. Discussion Of particular relevance in this case study is the association between acute pancreatitis and HTG. There is a small, but signiﬁcant, increased risk of developing acute pancreatitis in individuals with a greatly elevated plasma triglyceride level (greater than 10 mmol/L) [9]. Between 1.3 and 7% of all cases of acute pancreatitis have been attributed to HTG [10, 11], with 1.7–6% of cases of acute pancreatitis in pregnancy attributed to hyperlipidaemia [1, 2]. Interestingly, Syed et al. stated that it is HTG itself that causes acute pancreatitis and not hypercholesterolaemia [12]. HTG can be categorized as primary and secondary, although an underlying molecular basis can be found in less than 5% of cases [9]. The secondary forms of hyperlipidemia normally associated with pancreatitis include types I, IV, Case Reports in Medicine Figure 1: Axial contrast-enhanced CT abdomen 14 days after-ad- mission showing gross ascites and pancreatic parenchymal enhance- ment. and V of the Frederickson Classiﬁcation [13]. Gan et al. also state that 60% of the variability of serum lipid levels is determined by genetic factors [10]. In fact, the typical clinical proﬁle of pancreatitis induced by HTG is someone with a preexisting lipid abnormality in the presence of a precipitant of elevated lipid levels (e.g., poorly controlled diabetes, alcohol use, or a medication) [14]. Pregnancy is a well-known cause of secondary HTG, with cholesterol sometimes increasing by 25–50% and triglycerides by 200– 300%, respectively [15]. Ramin et al. found that 53% of all cases of acute pancreatitis in pregnancy, regardless of cause, occurred in the ﬁnal trimester [16]. The mechanism behind gestational HTG has been widely described. Saravanan et al. suggests that increased levels of serum triglyceride in the third semester of pregnancy can be associated with a similar increase in plasma oestrogen and human placental lactogen (HPL) levels [3]. The increased oestrogen levels lead to increased VLDL production [17], while elevated HPL increases adipose tissue lipolysis and consequently free fatty acid levels in serum [3]. This allows for increased hepatic triglyceride synthesis. Sivakumaran et al. also states that lipoprotein lipase activity is reduced during pregnancy [17]. These factors lead to increased VLDL production and reduced elimination of triglycerides, culminating in elevated serum triglyceride levels (Figure 2). This is exacerbated in individuals with familial HTG, as this additional VLDL production cannot be reversed [3]. The exact pathogenesis behind HTG-induced acute pan- creatitis is not yet fully understood. Kadikoylu et al. suggested that triglycerides accumulating around the pancreas were hydrolysed by pancreatic lipase seeping out of acinar cells, leading to the accumulation of high levels of free fatty acids [4]. These are believed to be toxic and are thought to damage acinar cells and capillary endothelium. This can occur alongside increased chylomicron concentrations, which can cause capillary plugging, ischaemia, and acidosis. In this acidic environment, free fatty acids activate trypsinogen and trigger acute oedematous and necrotizing pancreatitis (Figure 3).