A 48-Year-Old Man With Diabetic Ketoacidosis, Hypothermia, and Cardiac Arrest Managed With Veno-Arterial Extracorporeal Membrane Oxygenation

Introduction

Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes mellitus characterized by hyperglycemia, acidosis, and ketonemia [1]. Although most commonly seen in type 1 diabetes, DKA can also occur in type 2 diabetes during periods of physiological stress [1]. Standard management includes intravenous fluid resuscitation, insulin therapy, and electrolyte replacement [1].

DKA occasionally presents with hypothermia, creating a uniquely challenging clinical scenario [2]. Hypothermic patients face risks that can trigger life-threatening arrhythmias [3], which compound DKA-associated circulatory collapse. Additionally, cerebral edema can develop as a rare but potentially fatal complication of DKA [4]. The combination of DKA with severe hypothermia leading to cardiac arrest appears to be very rare, with available evidence limited to isolated case reports [2].

Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is a form of mechanical circulatory support that drains venous blood, oxygenates it extracorporeally, and returns it to the arterial circulation [5]. VA-ECMO is indicated for refractory cardiogenic shock and cardiac arrest unresponsive to conventional resuscitation [5]. In the setting of accidental hypothermia with cardiac arrest, VA-ECMO additionally enables controlled extracorporeal rewarming [6]. A previous case of VA-ECMO resuscitation in DKA with hypothermic cardiocirculatory instability was reported by Lin et al [7], who described successful management using veno-arterial ECMO in a patient presenting with similar hemodynamic compromise. This report describes the case of a 48-year-old man with diabetic ketoacidosis, hypothermia, and cardiac arrest managed with VA-ECMO.

Case Report

A 48-year-old man had a history of impaired glucose tolerance, which was identified during health screening, although he had not been receiving regular medical follow-ups. He had been experiencing malaise for 3 days before presentation to the hospital. On the day of admission, family members discovered him unconscious at home.

Upon arrival at the Emergency Department, the patient presented with a Glasgow Coma Scale score of E1V1M5, body surface temperature below 30°C, and blood pressure of 48/27 mmHg. Shortly after arrival, he developed seizures, which were followed by ventricular fibrillation. Cardiopulmonary resuscitation achieved return of spontaneous circulation within 2 min.

Post-resuscitation arterial blood gas analysis showed a blood glucose concentration of 58.8 mmol/L and severe acidosis (pH: 6.853, base excess: −31.2 mmol/L, HCO3−: 8.1 mmol/L), which indicated DKA. Laboratory findings demonstrated severe metabolic derangement and underlying diabetes mellitus (Table 1), including marked hyperosmolality (calculated serum osmolality: 392 mmol/kg; reference range: 275–295 mmol/kg), acute kidney injury (creatinine concentration: 681 μmol/L; reference ranges: 57–95 μmol/L), and an elevated lactate concentration (5.6 mmol/L). The serum sodium concentration was 139 mmol/L. However, when corrected for hyperglycemia, the corrected sodium concentration was 159 mmol/L, which indicated severe hypernatremia and profound hypertonic dehydration. Immediate resuscitative measures were initiated, including rapid infusion of warm bicarbonate solution (1000 mL), insulin therapy (8 units intravenous bolus followed by continuous infusion at 10 U/h), and continuous noradrenaline infusion for hemodynamic support. Despite the return of spontaneous circulation and these interventions, the patient remained hemodynamically unstable with refractory shock and required repeated boluses of adrenaline (0.25 mg) to maintain minimal blood pressure. VA-ECMO was initiated to provide circulatory support because of the refractory cardiogenic shock unresponsive to maximal medical therapy.

Head CT following the implementation of VA-ECMO showed mild effacement of cortical sulci suggestive of mild cerebral edema (Figure 1). These findings may have been related to the hypoxic-ischemic injury or DKA-associated cerebral edema. Based on the patient’s core temperature of 31°C, targeted temperature management (TTM) was initiated at 32°C for neuroprotection, maintained for 24 h, and followed by controlled rewarming at 0.1°C/h. The actual temperature course showed successful adherence to the protocol (Figure 2). Continuous renal replacement therapy (CRRT) was used for metabolic correction. Intensive glucose management was implemented with continuous insulin infusion, with initial infusion at 12.5 U/h, and it was titrated according to the glycemic response (Figure 3). Blood glucose concentrations decreased from 52.2 to 12.1 mmol/L within 72 h, while serum osmolality improved from 392 to 327 mmol/kg over the same period (Figure 3).

The acidosis resolved rapidly, and vasopressor requirements decreased correspondingly. Fluid management consisted predominantly of crystalloid solutions (lactated Ringer’s solution) for resuscitation and maintenance. Transfusion support was required (red blood cell concentrate: 2 units, fresh frozen plasma: 20 units) because of bleeding from catheter insertion sites and coagulopathy. CRRT was performed without ultrafiltration and was exclusively used for metabolic correction. A progressive improvement in urine output was observed from day 2, with net fluid balance becoming negative by day 3, which indicated restoration of renal function (Figure 4). Hemodynamic stability allowed weaning from VA-ECMO on hospital day 4 and extubation on hospital day 8. Brain MRI on intensive care unit day 6 showed no major hypoxic-ischemic injury. The patient was transferred from the intensive care unit on day 12, underwent management of diabetes and rehabilitation, and was discharged home on hospital day 97 with good functional recovery.

The patient expressed gratitude for the care received during his hospitalization. Written informed consent was obtained from the patient for publication of this case report and accompanying figures.

Discussion

This case highlights the life-saving potential of VA-ECMO in the rare and challenging clinical scenario of concurrent DKA, hypothermia, and cardiac arrest. The combination of DKA-induced shock and hypothermia-related circulatory instability can create refractory hemodynamic collapse that requires VA-ECMO as a life-saving intervention. Beyond providing circulatory support, VA-ECMO also offers precise temperature control capabilities that enable optimal TTM [6], contributing to favorable neurological recovery following cardiac arrest.

The pathophysiological basis of this case involves a cascade from metabolic decompensation to cardiovascular failure. The etiology was ultimately determined to be type 2 diabetes with severe glucotoxicity rather than fulminant type 1 diabetes. Following the resolution of hyperglycemia, insulin requirements progressively decreased, and glycemic control was achieved with oral hypoglycemic agents alone at discharge, which indicated preserved pancreatic β-cell function. The patient’s history of frequent consumption of high-sugar energy drinks before admission likely contributed to the acute metabolic decompensation. Hyperglycemia-induced osmotic diuresis resulted in severe hypovolemia and hypertonic dehydration (corrected sodium concentration: 159 mmol/L), while ketoacidosis caused profound acidemia (pH: 6.85), which can directly impair myocardial contractility and blunt catecholamine responsiveness [8].

The addition of profound hypothermia to this metabolic crisis created a particularly dangerous synergy that amplified the hemodynamic instability. DKA-associated hypothermia results from insulin deficiency-induced impairment of cellular glucose uptake, causing substrate deficiency for thermogenesis [2]. Previous studies identified DKA as the underlying cause in 12% of hypothermia cases, highlighting this important association [9]. The profound hypothermia (body surface temperature: <30°C) in this case resulted from DKA-related thermogenic impairment and prolonged environmental exposure in a cold home during winter. When the core temperature falls to 32°C, cardiac arrest can occur, and temperatures below 28°C considerably increase the risk of ventricular fibrillation from minor stimuli [3]. In our case, hypothermia further compromised cardiovascular function by triggering ventricular fibrillation and reducing cardiac output. This case exemplifies the vicious cycle created by DKA, severe acidemia, and profound hypothermia.

VA-ECMO played a crucial dual role in managing this life-threatening condition by providing circulatory support and controlled temperature management. Each condition exacerbates the other’s hemodynamic instability, necessitating mechanical circulatory support [5]. VA-ECMO serves as effective bridging therapy until metabolic abnormalities resolve [10], although adequate volume resuscitation is essential for circuit maintenance. Beyond hemodynamic support, VA-ECMO enables controlled rewarming through extracorporeal circulation [7], permitting management of potential complications, such as afterdrop [3], which can cause sudden cardiovascular collapse during conventional external warming methods.

Lin et al [7] previously reported a similar case of VA-ECMO resuscitation in a 25-year-old woman with insulin-dependent diabetes mellitus and hypothermic cardiocirculatory instability (tympanic temperature: 29°C, pH: 6.63), in whom rapid rewarming was performed with ECMO set at 37°C, achieving a rectal temperature of 36.5°C within 4 h with full neurological recovery. In contrast, our patient developed ventricular fibrillation requiring CPR, raising additional concern for hypoxic-ischemic brain injury. DKA also carries a risk of cerebral edema because of rapid osmotic changes during treatment [4], and head CT showed mild effacement of cortical sulci in our patient. Given these dual risks, we employed TTM at 32°C for 24 h followed by controlled slow rewarming at 0.1°C/h, rather than rapid rewarming as in the Lin et al case. While current guidelines recommend actively preventing fever (target of 37.5°C) as suggested by the TTM2 trial [11], patient-specific factors may favor hypothermia therapy. Studies in animal models and cardiac surgery data suggest that hypothermia provides neuroprotection through improved ischemic tolerance [12,13], and some case reports have suggested a possible neuroprotective role in DKA [2]. Our patient achieved favorable neurological recovery, suggesting that slow controlled rewarming with TTM may offer neuroprotective benefits in cases of DKA-associated hypothermia complicated by cardiac arrest, although further case reports are needed to confirm this approach [14].

Conclusions

This case highlights the dual role of VA-ECMO as circulatory support and a precise temperature control platform in DKA-related hypothermia and cardiac arrest. In cases complicated by cardiac arrest, slow controlled rewarming with TTM may offer additional neuroprotective benefits. These findings demonstrate the value of VA-ECMO beyond traditional cardiogenic shock applications.