AUCTORES
Globalize your Research
Case report | DOI: https://doi.org/10.31579/2640-1045/125
1 Medical Officer, Shri Jalaram Arogya Seva Trust Hospital, Meghraj, Gujarat.
2 Medical officer, Siddhi Heart and Medical Hospital, Nirnaynagar, Ahmedabad, Gujarat.
3 Neonatologist, Orange Neonatal and Pediatric Hospital, Ahmedabad, Gujarat.
*Corresponding Author: Shrenil Kavathia
Citation: Shrenil Kavathia, Sharvil Kataria, Nirav Patel, Sagar Patel., (2023), Diabetic Ketoacidosis Induced ‘Terrible Triad’ Associated with Seizures and Acute Renal Failure: A Rare Case Report, J. Endocrinology and Disorders. 7(1): DOI:10.31579/2640-1045/125
Copyright: © 2023, Shrenil Kavathia. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Received: 12 January 2023 | Accepted: 25 January 2023 | Published: 06 February 2023
Keywords: diabetes mellitus; hypertriglyceridemia; diabetic ketoacidosis; acute pancreatitis
We report a case of diabetic ketoacidosis with a severely elevated triglyceride level (25,585 mg/dL) complicated by acute pancreatitis, renal involvement, and generalized seizures. The proposed mechanism is triglyceride excess due to increased lipolysis, resulting in the formation of excess free fatty acids. A 17-year-old male patient came to the emergency department with abdominal pain, headaches for 2 days, lethargy, and Kussmaul breathing. Diabetic ketoacidosis with several complications was diagnosed. The objective of this case report is to present and describe the clinical features, laboratory investigations, case management, and natural course of hypertriglyceridemia in DKA.
An acute metabolic complication known as diabetic ketoacidosis (DKA) primarily affects people with type 1 diabetes mellitus [1]. Type 1 diabetes mellitus results from the destruction of insulin-producing β-cells in the pancreatic islets of Langerhans [2].
DKA is the result of absolute or relative insulin deficiency combined with counter-regulatory hormone excess (glucagon, catecholamines, cortisol, and growth hormone). The decreased ratio of insulin to glucagon promotes gluconeogenesis, glycogenolysis, and ketone body formation in the liver [3]. In DKA, insulin deficiency activates lipolysis in adipose tissue, releasing increased free fatty acids, which accelerates the formation of VLDL in the liver. Additionally, decreased removal of VLDL from the plasma by peripheral tissue lipoprotein lipase results in hypertriglyceridemia [4]. DKA-induced hypertriglyceridemia is a rare cause of acute pancreatitis, which accounts for around 4% of cases [5]. This case involves DKA-induced severe hypertriglyceridemia complicated by acute pancreatitis, acute renal involvement, and generalized seizures.
A 17-year-old boy presented to the hospital with abdominal pain, headache for two days, lethargy, and Kussmaul breathing for the last few hours. The patient was admitted to the ICU for lethargy and severe respiratory distress. The patient was put on ventilator support. Finger stick blood glucose level was more than 500 mg/dL; hence a probable diagnosis of diabetic ketoacidosis (DKA) was made. Glasgow Coma Scale score was 4 (E1M2V1), so he was immediately intubated, commenced on ventilator support, and management of shock was started. Aggressive intravenous (IV) fluids and injection insulin were started after collecting blood samples, as per BSPED guidelines for DKA 2020. Initial laboratory findings were ABGA (pH 6.9, PaCO2 21 mmHg, PaO2 93 mmHg, HCO3- 4 mM/L) which was suggestive of severe metabolic acidosis. Normal saline (NS)bolus of 10 ml/kg was given along with bicarbonate correction. IV antibiotics were started for suspected sepsis. After the initial bolus of 20 mL/kg, the patient was started on noradrenaline for low diastolic blood pressure. Blood investigation reported leukocytosis with a triglyceride (TG) level of 25,585 mg/dL, serum glutamic pyruvic transferase (SGPT) 70.4 U/L, creatinine 1.8 mg/dl with CRP of 42.9 mg/dL. Serum amylase was 394 U/L which implied that the patient had acute pancreatitis.
The patient developed generalized seizures, hence fosphenytoin was administered (20 mg/kg/dose). However, he had persistent seizures, so needed levetiracetam (40 mg/kg/dose) loading dose was dispensed. A neurologist was consulted for the same, who advised an MRI brain which revealed a small acute non-hemorrhagic infarct in the right half of the midbrain without mass effect or midline shift. Electroencephalogram (EEG) report showed abnormal diffuse slow background activity suggestive ofencephalopathy. The patient was continued on fosphenytoin (6 mg/kg/day) and levetiracetam (40 mg/kg/day) maintenance doses. The laboratory parameters were monitored throughout admission (Table 1). On the third day of hospitalization, a nephrologist was consulted due to bilateral mild renal involvement seen on abdominal ultrasonography and for rising serum creatinine and urea levels. A hemodialysis catheter was inserted, and hemodialysis was initiated and continued for four cycles over a week. The TG was 9500 mg/dL, total leukocyte count was 6270 /mm3. On the fifth day of hospitalization, the ABGA revealed a normal pH and normal PaO2 and PaCO2. On the seventh day of hospitalization, the patient was weaned from the ventilator and kept on low-flow oxygen for the next 4 days. The TG level had returned to a normal level of 135 mg/dL.
Table 1: Sequential Laboratory Parameters
Physiotherapy was started during the hospital stay. After [3] days, feeding via Ryles tube was started and was gradually upgraded. The blood culture remained sterile after [5] days of incubation.
An endocrinologist was consulted and the child was shifted to subcutaneous regular insulin injection. Repeat blood investigations showed improvement in serum creatinine levels. The patient developed melena episodes, so Packed Cell Volume was transfused.
The patient was tolerating the management well, so physiotherapy was stopped and he was discharged after 21 days of admission. The patient and his parents were taught how to administer insulin using an insulin pen injection.
This case report describes a patient presenting with symptoms consistent with diabetic ketoacidosis and acute pancreatitis. Blood reports confirmed hypertriglyceridemia and severe metabolic acidosis. Milky blood (Fig.1) as described by Chaurasiya et al.[6], shows a clear supernatant layer of triglycerides above the cellular components of blood. The patient’s clinical course was complicated by generalized seizures, an MRI suggestive of a small acute non-hemorrhagic infarct in the right half of the midbrain without mass effect or midline shift, and a USG suggestive of bilateral mild renal involvement. In this patient, hypertriglyceridemia was well controlled with insulin without lipid-lowering agents. However, in severe hypertriglyceridemia, Furuya T et al. [7] recommended plasmapheresis to avoid severe adverse effects.
Figure 2: Hyperlipidemic blood sample on the day of admission
Diabetic Ketoacidosis is an acute severe complication of Type 1 diabetes mellitus. DKA can be accompanied or complicated by the presence of hypertriglyceridemia and pancreatitis. This is known as the ‘Terrible Triad’ or ‘Enigmatic Triad’ which can be an unusual presentation of Type 1 and Type 2 diabetes mellitus [8]. The actual trigger is not known, but after onset, it creates a ‘domino effect’ [9]. The triad can lead to a continuous loop of events (Figure.2).
Figure 2: Complex interrelationship between the Terrible Triad
While one case reports Hypertriglyceridemia to be the trigger of Acute Pancreatitis which then causes DKA1 [1], in another case DKA is suggested to be the cause of hypertriglyceridemia and acute pancreatitis [12].
Several neurologic deficiencies have been associated with DKA, including cerebral edema with increased intracranial pressure resulting in a coma; partial and generalized seizures; and cerebrovascular occlusive disease resulting in motor and/or sensory dysfunction [13]. Neurological deterioration during an episode of DKA is usually assumed to be caused by cerebral edema, but hemorrhagic infarction is an infrequent cause. During an episode of DKA, increased inflammation increases the risk of vascular disruption and also due to hyperglycemia and acidosis-induced oxidative injury [14]. Acute renal involvement in DKA is probably affected by multiple factors, but it is most likely due to hypotension and hypovolemia [15]. Myers et al [16] found an association between renal involvement and signs of cerebral injury with DKA.
To our knowledge, this is a very rare case involving the Terrible Triad and required immediate medical management for the control of DKA as well as hypertriglyceridemia.
We report a rare case of DKA with extremely high triglycerides complicated with acute pancreatitis, renal involvement, and a hemorrhagic infarct which was managed with fluids and insulin. Early diagnosis of the Terrible Triad helps in identifying the complications and proper management helps in preventing its long-lasting adverse effects. Further research into this triad is required to completely understand its pathophysiology and the effects it has on the human body.
Clearly Auctoresonline and particularly Psychology and Mental Health Care Journal is dedicated to improving health care services for individuals and populations. The editorial boards' ability to efficiently recognize and share the global importance of health literacy with a variety of stakeholders. Auctoresonline publishing platform can be used to facilitate of optimal client-based services and should be added to health care professionals' repertoire of evidence-based health care resources.
