Using fresh frozen plasma as an emergency treatment modality for hypertriglyceridaemic acute pancreatitis in a resource-constrained environment: A case report and review of literature

Clinical case

A 49-year old man presented with a three-day history of severe epigastric pain, abdominal distension, nausea and vomiting. He was a known hypertensive and a newly diagnosed type 2 diabetic. He was not known to have hypertriglyceridaemia or cholelithiasis.

On initial examination, he had a tachycardia (138 beats per minute) and blood pressure of 166/86. His general examination was normal. There were features of cardiac failure. The abdomen was distended with severe epigastric tenderness.

A basic blood panel was drawn with lipid profile, lipase and an arterial blood gas analysis (Table 1). The blood in the test tubes was lipaemic. Plain radiographs showed no obvious pathology.

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Table 1.

Relevant blood results during hospital admission.

	Before FFP	After 2 units FFP	After 4 units FFP	On discharge	Normal range
Lipase (U/L)	561	108		49	13–60
Total cholesterol (mmol/L)	22.05	12.89	9.37
Triglyceride (mmol/L)	75.37	23.36	8.00	5.57
HDL (mmol/L)	0.17	<0.08	0.28
Calcium (mmol/L)	1.49			2.09	2.15–2.50
Lactate (mmol/L)	4.2	2.1	1.5	0.8	0.5–1

The patient was diagnosed with hypertriglyceridaemic acute pancreatitis on the basis of a serum lipase value of 561 U/L and a triglyceride level 75.37 mmol/L (N < 1.7 mmol/L). Abdominal ultrasound was normal. Subcutaneous insulin was commenced together with oral hypoglycaemic agents to control the uncomplicated hyperglycaemia. Heparin was initiated in an attempt to lower triglyceride levels, and a low lipid diet was implemented. These measures did not lower his hypertriglyceridaemia.

A lactic acidosis suggested end organ dysfunction, evidenced by an acute kidney injury and early stage heart failure. Four units of fresh frozen plasma were infused over two days, after conventional treatment failed to lower the hypertriglyceridaemia. Within two days, he improved considerably, with minimal symptomatology, and complete alleviation of abdominal tenderness. His lactic acidosis and end organ failure subsided, and he could be discharged on the fourth day after initiating fresh frozen plasma therapy.

Discussion

Hypertriglyceridaemia accounts for up to 10% of all cases of acute pancreatitis, but the exact mechanism is not well understood. ^1,2 With increased levels of free fatty acids and chylomicrons, the plasma viscosity increases and can cause ischaemic injury to the pancreas and therefore trigger further inflammation. ²

Severe hypertriglyceridaemia is defined as a serum triglyceride level > 55 mmol/L.^3,4 Its cause may be primary or secondary. The latter are due to inadequately controlled diabetes, obesity, excess alcohol use, pregnancy or medications.

We believe our patient had type IV primary hyperlipidaemia. These patients usually present in adulthood and are characterised by a precipitant, in this case acute pancreatitis. Genetic defects that cause severe hypertriglyceridaemia include lipoprotein lipase deficiency, lipoprotein lipase gene mutation and Apolipoprotein C2 deficiency. ⁵ Our diagnosis is based on the unresponsiveness to insulin and heparin treatment together with a dramatic response to fresh frozen plasma which contains the very element that is deficient, namely lipoprotein lipase.

The treatment of hypertriglyceridaemic acute pancreatitis is similar to the treatment of pancreatitis of other causes. However, the primary focus is to lower triglycerides as fast as possible.^2,4 Insulin has been documented to do this ⁵ by activating lipoprotein lipase activity which in turn accelerates chylomicron degradation, and heparin by causing stored lipoprotein lipase to be released. ⁵

Plasmapheresis works by rapidly removing triglycerides and chylomicrons from the circulation and therefore removing the inciting factor which stops inflammation and damage to the pancreas. ⁵ A single cycle of plasmapheresis can lower blood triglyceride levels by 50–80%. ⁵ The incidence of adverse events is low, but the primary problem is access to blood products and funding. ⁵