Cardiogenic shock associated with stress-induced cardiomyopathy in the setting of diabetic ketoacidosis initially suspected to be septic shock: a case report

Introduction

Shock associated with diabetic ketoacidosis (DKA) is typically hypovolemic due to volume depletion from DKA itself, or distributive, commonly triggered by sepsis (1). However, in rare cases, DKA can precipitate stress-induced cardiomyopathy, which may lead to cardiogenic shock (2,3).

DKA is also associated with significant metabolic derangements, including severe acidosis and electrolyte abnormalities, which can contribute to additional cardiac complications such as life-threatening arrhythmias and hypotension (4). Therefore, shock in the setting of DKA may involve complex and overlapping mechanisms, and early recognition of cardiac involvement is essential for appropriate management.

We report a case of cardiogenic shock due to DKA-triggered stress-induced cardiomyopathy, which was initially suspected to be septic shock given the presence of fever, but was subsequently identified as cardiogenic shock. Through this case, we emphasize that in patients with DKA and persistent shock, clinicians should promptly consider cardiogenic shock. We present this article in accordance with the CARE reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-2026-0100/rc).

Case presentation

A 30-year-old woman with no known past medical history presented to the emergency department (ED) with fever and altered mental status after four days of generalized fatigue. Her height was 157.5 cm, body weight was 78.8 kg, and body mass index was 31.8 kg/m². Vital signs showed heart rate of 148 bpm, blood pressure of 113/55 mmHg, respiratory rate of 33 breaths/min, and temperature of 38.8 ℃. Physical examination was notable for restlessness, confusion, and cold extremities. Cardiopulmonary examination revealed no cardiac murmurs or lung crackles, and there was no jugular venous distension or peripheral edema. Laboratory evaluation demonstrated marked hyperglycemia of 1,480 mg/dL (normal, 70–100 mg/dL), anion-gap metabolic acidosis with an anion gap of 31 (normal, 8–12), bicarbonate of 17 mmol/L (normal, 22–28 mmol/L), and pH of 7.28. Beta-hydroxybutyrate was elevated at 3.6 mmol/L (normal, <0.4 mmol/L), serum osmolality was elevated at 370 mOsm/kg (normal, 275–295 mOsm/kg), and lactate was severely elevated at 10.2 mmol/L (normal, <2.0 mmol/L). Hemoglobin A1c was 13.0% (normal, <5.6%). Complete blood count showed white blood cell count 15.9×10³/µL (normal, 4–10 ×10³/µL) with 86% neutrophils (normal, 40–70%). Polymerase chain reaction testing for influenza and coronavirus disease 2019 was negative. Chest radiography and computed tomography of the head, chest, and abdomen without contrast were unremarkable. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and the video. A copy of the written consent is available for review by the editorial office of this journal.

In the ED, diabetic ketoacidosis and hyperosmolar hyperglycemic state (DKA/HHS) overlap was diagnosed, and standard management was immediately initiated, including intravenous fluid resuscitation, continuous intravenous insulin infusion, and close monitoring of glucose, venous pH, beta-hydroxybutyrate, serum osmolality, and electrolytes. Sepsis was suspected given fever and Sequential Organ Failure Assessment score ≥2, and was considered a potential precipitating factor of her DKA/HHS. However, no clear source of infection was identified. The markedly elevated lactate level was considered multifactorial, reflecting possible tissue hypoperfusion from shock, severe metabolic derangements associated with DKA/HHS, and sepsis. Despite aggressive fluid resuscitation and empiric antibiotic therapy with cefepime, the patient required high-dose vasopressor support with norepinephrine and vasopressin. The patient was admitted to intensive care unit.

On hospital day 1, cardiac telemetry showed new ST-segment changes, and electrocardiography (ECG) demonstrated diffuse ST-segment elevations in leads I, II, aVL, and V2–V6 (Figure 1), accompanied by elevated troponin T levels (193 ng/L). Transthoracic echocardiography revealed a left ventricular ejection fraction (LVEF) of 30–35% with mid-distal anteroseptal and apical hypokinesis, as well as mild right ventricular dilation with reduced systolic function (Video 1). Coronary angiography demonstrated no obstructive coronary artery disease. Hemodynamic assessment by right and left heart catheterization demonstrated severe low-output cardiogenic shock with biventricular failure, characterized by markedly elevated right- and left-sided filling pressures, reduced cardiac index, low mixed venous oxygen saturation, and severely impaired right ventricular function despite high-dose vasopressor support (Table 1). An Impella CP device was initially placed; however, recurrent suction alarms occurred, likely due to a small left ventricular cavity, raising concern for inadequate hemodynamic support from reduced pump flow. Therefore, mechanical circulatory support (MCS) was transitioned to an intra-aortic balloon pump (IABP). The patient achieved hemodynamic stability with IABP support and vasopressors. Diuretics and continuous renal replacement therapy were initiated for volume overload.

Figure 1 Electrocardiography showing diffuse ST-segment elevations in leads I, II, aVL, and V2–V6.

In parallel with hemodynamic stabilization, treatment for DKA/HHS was continued, and resolution of DKA/HHS was achieved by hospital day 2. Electrolytes (potassium, phosphate, and magnesium) were repeatedly monitored and corrected.

On hospital day 3, hemodynamics improved and vasopressor requirements decreased. Serial echocardiography demonstrated gradual recovery of the LVEF to 45–50%. The IABP was successfully weaned off on hospital day 4. Follow-up echocardiography showed a normalized LVEF of 55–60% on hospital day 6, supporting a diagnosis of stress-induced cardiomyopathy. Cardiac magnetic resonance (CMR) and endomyocardial biopsy were not performed because of the rapid improvement in LVEF.

No life-threatening arrhythmias were observed during the course of treatment. An infectious workup, including blood, urine, and sputum cultures, was ultimately negative.

Discussion

In hyperglycemic crisis, hypovolemic shock resulting from osmotic diuresis due to hyperglycemia and hyperketonemia, as well as distributive shock secondary to infection-related sepsis, are the most commonly recognized causes of shock (1,5). In this case, although septic and hypovolemic shock were initially suspected, the markedly elevated lactate level raised concern for other etiologies, including tissue hypoperfusion. Persistent shock despite initial management prompted cardiac evaluation, which led to the timely identification of cardiogenic shock.

An association between DKA and stress-induced cardiomyopathy has been previously reported (3). Stress-induced cardiomyopathy can lead to cardiogenic shock due to catecholamine-mediated left ventricular dysfunction and is associated with high mortality (6). In the present case, early initiation of MCS immediately after the diagnosis achieved rapid hemodynamic stabilization and contributed to the favorable clinical outcome.

Several alternative diagnoses were carefully considered in this case. Although coronary angiography excluded obstructive coronary artery disease, the presence of ST-segment elevations, troponin elevation, fever, and biventricular dysfunction warranted careful consideration of alternative diagnoses. The differential diagnosis included myocarditis, myocardial infarction with non-obstructive coronary arteries (MINOCA), and septic cardiomyopathy (7-9). Acute myocarditis was an important differential in this case. Although right ventricular involvement can occur in stress-induced cardiomyopathy, prominent biventricular failure should prompt consideration of acute myocarditis (6). CMR was not performed; therefore, acute myocarditis and MINOCA could not be fully excluded. In addition, the ECG obtained at the time of recognition of myocardial dysfunction showed diffuse anterolateral ST-segment elevations, which were compatible with stress-induced cardiomyopathy (10). However, serial ECGs did not show the typical temporal evolution described in stress-induced cardiomyopathy, such as progressive T-wave inversion and QT prolongation after the acute phase (10). This represents an important diagnostic limitation. Despite these diagnostic limitations, the rapid recovery of LVEF favored stress-induced cardiomyopathy (11). Septic cardiomyopathy was considered less likely given the negative infectious workup (9). Overall, the clinical course was most consistent with stress-induced cardiomyopathy.

Several mechanisms may explain the development of stress-induced cardiomyopathy in the setting of DKA. Excessive catecholamine release during DKA may exert negative inotropic effects, and this process may be further amplified by ketoacidosis, hyperglycemic toxicity, and electrolyte abnormalities, leading to transient myocardial dysfunction associated with stress-induced cardiomyopathy (12,13). Ketosis and acidosis may disrupt excitation-contraction coupling and increase arrhythmogenicity (4). Hyperglycemia may impair myocardial blood flow and promote endothelial dysfunction through increased reactive oxygen species (14). Hypokalemia is associated with an increased risk of ventricular tachycardia and ventricular fibrillation (14). Hypophosphatemia may lead to impaired myocardial contractility, cardiomyopathy, and ventricular arrhythmias (15). These abnormalities are reversible with correction of DKA and electrolyte disturbances, which contributes to recovery of cardiac function in stress-induced cardiomyopathy (13). Therefore, prompt treatment of DKA itself with rigorous electrolyte correction is essential to prevent further cardiac complications (15).

In our case, prompt correction of electrolyte abnormalities together with rapid resolution of hyperglycemia and ketoacidosis likely helped prevent further cardiac complications and may also have contributed to the rapid recovery of stress-induced cardiomyopathy (13,16).

This case highlights the importance of considering cardiogenic shock as a potential cause of shock in patients with DKA. Early cardiac workup and hemodynamic evaluation can facilitate accurate identification of the underlying shock etiology and enable timely consideration of MCS. In addition, prompt treatment of DKA itself and concomitant electrolyte disturbance are essential for the management of stress-induced cardiomyopathy and for reducing cardiac complications. As a single case report, this study cannot inform specific recommendations regarding the timing or routine use of early cardiac evaluation in all patients with DKA; however, it underscores the importance of considering cardiogenic shock in all such cases.

Conclusions

Shock in the setting of DKA is not always attributable to hypovolemic or distributive shock. In cases of persistent shock in DKA, clinicians should promptly pursue early cardiac evaluation and consider MCS for possible cardiogenic shock due to stress-induced cardiomyopathy. Early hemodynamic stabilization alongside rigorous treatment of DKA is essential for favorable outcomes.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://acr.amegroups.com/article/view/10.21037/acr-2026-0100/rc

Peer Review File: Available at https://acr.amegroups.com/article/view/10.21037/acr-2026-0100/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://acr.amegroups.com/article/view/10.21037/acr-2026-0100/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and the video. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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