Plasma exchange for the treatment of severe hypertriglyceridemia pancreatitis with diabetic ketoacidosis: a case report from sub-Saharan Africa.

The triad of acute pancreatitis, diabetic ketoacidosis, and hyperlipidemia is extremely rare. A case report describing this unusual triad has been successfully managed with insulin infusions alone. Here, we highlight the challenges in making this diagnosis and the therapeutic potential in sub-Saharan Africa in the management of hypertriglyceridemia pancreatitis associated with diabetic ketoacidosis that was initially refractory to insulin infusion alone. I present my first experience with plasmapheresis.


Severe acute pancreatitis (AP) is associated with significant morbidity and mortality, with mortality estimates as high as 30-40% in hospitalized patients with organ dysfunction or pancreatic necrosis. [1]Hypertriglyceridemia is the third most common cause of pancreatitis after gallstones and chronic alcohol abuse, and is estimated to account for approximately 5% of cases. [2]An assessment of global temporal trends indicates an increase in the incidence of hypertriglyceridemia AP (HTGP) due to increased obesity-related dyslipidemia. [3]Compared with other etiologies of AP, HTGP, especially with triglyceride (TG) levels above 5.6 mmol/l, is associated with greater clinical severity and higher complication rates. [4]Furthermore, despite similar initial management approaches to AP irrespective of etiology (i.e., fluid resuscitation, pain management, and nutritional support), definitive HTGP management includes insulin or heparin infusions, or therapeutic plasmapheresis may be required. [5]There are no clear evidence-based guidelines for the ultimate management of HTGP. [6].

Studies from Africa on the epidemiology of AP are lacking.South African studies [7] Dyslipidemia accounted for approximately 8% of cases and showed an epidemiological profile similar to that in the Western world. However, compared with the West, most deaths in African studies tended to occur earlier, highlighting the need for rapid, improved, supportive and definitive management. The syndrome, the global epidemiology of diabetes, is showing a worrying increase, especially in developing countries. [8]HTGP is bound to become a growing concern in Africa.

To our knowledge, there is no documented experience with therapeutic plasmapheresis (TPE) for the management of HTGP in Africa. Furthermore, there is little literature on HTGP with diabetic ketoacidosis (DKA). Here we share our experience with this unique presentation. This was initially unresponsive and necessary to insulin infusions and responded well to TPE.

case presentation

A 38-year-old man with no known comorbidities urgently with a 1-week history of polydipsia and polyuria and a 1-day history of sudden-onset severe epigastralgia with nonradioactive nausea and vomiting introduced to the treatment room. A psychosocial history revealed occasional alcohol consumption, which he described as “about five beers every weekend” and a score of 0 on the screening CAGE questionnaire. He did not indicate a history of inflammatory drug (NSAID) use. There was no known family history of chronic diseases, including dyslipidemia. On examination, he appeared ill, dehydrated and alert despite being visibly tachypnea. His body mass index he was 25.5 kg/m2 (height = 177 cm, weight = 80 kg). His blood pressure he had 127/66 mmHg, pulse rate he had 110/min and respiratory rate he had 34/min. There were no physical signs of hyperlipidemia. A general examination revealed severe epigastric tenderness with decreased bowel sounds. His chest was evident on auscultation. An initial impression of DKA was made based on bedside elevation of blood glucose and ketone levels. The patient started his 0.1 U/kg/h insulin infusion after an initial 0.1 U/kg bolus and intravenous fluids.

In the first hours of patient management, there was a noticeable delay in laboratory reporting of some patients, with the laboratory requesting multiple repeat samplings for “hyperlipidemic samples.” As shown in the table, it took about 12 hours before the lab was finally able to process and report the full first set of labs (marked as Day 1). 1.

Survey/Date First day the 2nd day Third day 1 month after discharge reference range
total cholesterol 28.12 8.3 6.2 2.06 3-5.5mmol/L
HDL cholesterol 4.17 0.33 0.2 0.3 >0.9mmol/L
LDL-cholesterol 10.84 1 1 0.57 < 3.37mmol/L
Triglyceride >12.44 >6.22 >6.22 3.21 0.3-1.7mmol/L
Lipase 1616 1450 1000 56 10-150U/L
serum sodium 116 137 141 141 136-146mmol/L
serum potassium 4.47 3.59 3 3.52 3.5-4.5mmol/L
serum creatine 111 98 58 49 62-133 μmol/
serum bicarbonate <10.0 18 twenty three 26.9 18-22mmol/L
Blood urea nitrogen (urea) 3.7 3.5 2.3 3.1 1.2-3mmol/L
White blood cell count (total) 15.41 8.68 7.8 7.5 4 to 10×10^9/L
hemoglobin 13.6 8.6 7.4 8.5 13-17 grams/day
platelet count 73 129 172 648 150~400×10^9/L
random blood sugar 27.8 8.1 7.5 6.8 < 6.7mmol/L
serum ketone 3 0.2 0.1 0.1 < 0.6mmol/L
Serum Ph 7.28 7.34 7.41 7.43 7.35-7.45

At this point, the patient was receiving approximately 6 liters of intravenous fluids. Glycated hemoglobin (HbA1C) he rose to 8.3%.Abdominal CT showed an edematous pancreas with acute free peripancreatic fluid and no evidence of pseudocyst formation (Fig. 1).

A diagnosis of severe HTGP was made and high-dose statins and fenofibrate were added to his management.

Despite adequate fluid resuscitation and insulin infusion with adequate reduction of serum glucose and ketone levels, the patient’s clinical status was now concerned with decreased blood pressure and urine output, metabolic acidosis, and pulmonary edema. A decision was made to initiate continuous renal replacement therapy (CRRT), which proved futile due to hyperlipidemic blood. To avoid this, his TPE was initiated to periodically interrupt his CRRT under the advice of the nephrology team. Exchanges were performed at a blood flow (Qb) of 200 ml/min for 4 hours and were planned to displace 3 liters of fluid configured as 200 ml albumin and 800 ml lactated Ringers. Heparin was used, but plasmapheresis failed in him twice because hyperlipidemic blood clogged the filter, resulting in increased transmembrane pressure (Fig. 2). 2).

Plasmapheresis clogging with hyperlipidemic blood

TPE was retried and its duration was reduced to 2 hours before completing successfully. The patient was then able to benefit from her CRRT. By hospital day 3, the patient reported significant improvement in epigastric pain and improved urine output. After plasmapheresis, serum triglyceride levels were reduced by half. There were no additional TPE sessions for her. The patient was discharged on a basal bolus insulin regimen, statins and fenofibrate. Two months after discharge, the patient was performing well with adequate glycemic control as seen by self-monitoring of blood glucose and an improved lipid profile. He found inpatient care and outpatient follow-up care satisfactory.

Informed consent was obtained from patients for the use of anonymized medical history and clinical information.


The AP, DKA, hyperlipidemia (HL) triad is rare and only a few cases have been reported to date [9-13]This has been described as a cryptic triad by previous authors who hypothesized that DKA was the first event leading to transient HL followed by AP. AP was also seen in his DKA at low triglyceride levels (<3.4 mmol/L) and these authors suggested that in the DKA setting either very low levels of TG were required to trigger HTGP or that DKA itself We speculate that is a rare cause. AP's [10]Even more mysterious is the diagnosis of AP in the setting of DKA. For example, epigastralgia and elevated serum amylase and lipase levels typical of AP may also occur in her DKA in isolation. [14]Worse, the 3-fold increase in serum lipase specific for AP diagnosis may not be present in HTGP [15]Finally, the delay in measuring TG levels could lead to falsely low assays in HTGP as levels tend to normalize after 72 hours of fasting. [16]Therefore, management of patients with HTGP can be complicated by laboratory assay interference resulting from hyperlipidemia in the blood, as demonstrated in our case. This can significantly delay the administration of both DKA and HTGP.

Nonetheless, it is generally believed that a serum triglyceride level of 11.42 mmol/L or higher is required to induce HTGP, and several population-based studies have shown that for every 1.142 mmol/L increase in triglycerides It has been shown to increase the risk of AP by 4%. [17]Not all HTG patients develop AP. HTGP is a combination of HTG and one or more, including poorly controlled diabetes (possible in our case), alcoholism, pregnancy, and certain medications (estrogen therapy, olanzapine, protease inhibitors). It tends to occur in patients with secondary factors. DKA causes HTG by inhibiting lipoprotein lipase (LPL) activity and being in an insulin-deficient state that promotes lipolysis. [18]Lipolysis releases free fatty acids that are eventually converted to HTG. Certain theories have been proposed to explain the pathophysiology of HTGP. [19], the most common being the effects of elevated free fatty acid levels on acinar cells and the process of capillary plugging following plasma hyperviscosity resulting from elevated chylomicrons levels. Both of these processes cause ischemia and acidosis, ultimately activating trypsinogen and causing AP.

Therefore, final HTGP administration involves activation of LPL activity, such as by insulin infusion, heparin infusion, or fibrates. Plasmapheresis has been demonstrated to rapidly reduce serum chylomicron and triglyceride levels. Some literature cites an approximately 80% reduction in his TG levels after TPE compared to the 40% seen with insulin infusions. Furthermore, TPE is associated with rapid improvement in clinical symptoms. [2], especially epigastric pain, is also indicated in our case. However, there is no high-quality evidence showing improved clinical outcomes with TPE, and outcomes are similar in her HTGP patients managed with or without TPE. [20].

A case report describing this triad of AP, DKA, and HL in adults is, in theory, managed entirely by insulin infusions, as this therapy may address both DKA and HTGP. Here we present a scenario where clinical deterioration necessitates early access to a TPE with good response.


Our case demonstrates potential challenges in the management of HTGP and highlights the role of TPE in severe HTGP associated with DKA.

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