Case Reports in Medicine Pregnancy Increased plasma oestrogen Increased plasma HPL Increased VLDL synthesis Figure 2: Schematic representation of HTG-related hormonal changes during pregnancy. Hypertriglyceridaemia Increased plasma HPL Increased serum FFA levels Increased hepatic TG synthesis TG hydrolysis by pancreatic lipase Accumulation of FFA Acinar cell and capillary endothelial damage Increased chylomicron levels Capillary plugging Ischaemia and acidosis Acidosis Trypsinogen activation Acute oedematous and necrotising pancreatitis Figure 3: Pathophysiology of acute pancreatitis secondary to HTG. Kadikoylu et al. and Bae et al. both state that there is no diﬀerence in the clinical course, complications, and physical ﬁndings of acute pancreatitis induced by HTG and acute pancreatitis secondary to other factors [4, 18]. However, the latter article does suggest that the HTG element may 3 sometimes contribute to the development of respiratory failure, echoing Warshaw et al. [19]. One essential component in the treatment of acute pancreatitis presentations is the classiﬁcation of severity at presentation. This is important as, although 80% of pre- sentations are self-limiting mild interstitial pancreatitis that respond satisfactorily to conservative management, a signif- icant minority develop a severe form, with a 10–30% mor- tality within this cohort [20, 21]. Those patients predicted to develop acute severe pancreatitis normally require high- dependency/intensive-level management, as well as possible intervention. Both clinical and radiological scoring systems have been developed to classify pancreatitis severity [5]. However, in this case, the clinical systems (Ranson’s, acute physiology and chronic health evaluation (APACHE)) were unsuitable given the diﬃculty processing the patient’s blood samples on admission. We utilized the radiologically based Modiﬁed CT Severity Index [8], which grew out of the initial CT Severity Index described by Balthazar et al. [6, 22]. This scoring system incorporates radiographic features of organ failure and extrapancreatic complications as a means of determining condition severity [8]. However, in this case, the CT was performed within forty-eight hours of onset of symptoms. Warshaw et al. [19] suggested 48–72 hours as an appropriate imaging interval to detect evidence of pancreatic collections and necrosis. While in some cases this may account for the marked inconsistency between the clinical and radiological ﬁndings, the clinical team was cognizant of this discrepancy, obtaining interval abdominal imaging to assess the evolution of the condition during the patient’s hospitalisation. This emphasized the parallel and complementary nature of clinical and radiological severity scoring and the need to incorporate both into clinical decision making [7]. In fact, this area of acute pancreatitis management remains an evolving ﬁeld, with continual amendments to the diagnostic criteria and severity classiﬁ- cations being suggested [23]. The initial management of HTG-induced acute pancre- atitis is similar to other causes of acute pancreatitis: fasting, intravenous ﬂuids, analgesia, and monitoring for evidence of renal failure or septic shock [4, 18]. Dominguez-Munoz et al. found that serum lipid levels fall in the acute phase of acute pancreatitis, emphasizing the need to check lipid levels early during presentation [24]. Rapidly falling levels of triglycerides may mask the aetiology if investigations are delayed. Yadav and Pitchumoni suggest dietary restriction of fats and lipid-lowering agents (preferably ﬁbrates) [14]. How- ever, these methods may take days or weeks before an eﬀect is seen [11]. Gan et al. advocate active steps to lower the levels of precipitating lipid, most notably by removing chylomicrons via plasmapheresis/therapeutic plasma exchange (TPE) [10]. Although ﬁrst described by Betteridge et al. [25], experience of this method to treat HTG-associated pancreatitis remains limited [14]. The mechanism involves reducing triglyceride levels and circulating activated enzymes, proteases, and inﬂammatory mediators by physically ﬁltering out these toxic substances from the blood [12]. Chait and Brunzell found that this process could signiﬁcantly lower plasma lipid