Acute limb ischemia in a morbidly obese diabetic patient with obstructive sleep apnea

INTRODUCTION

Obstructive sleep apnea (OSA) is a common sleep-related breathing disorder characterized by recurrent episodes of upper airway obstruction during sleep, resulting in intermittent hypoxia and sleep fragmentation. It affects nearly 1 billion people globally, with increasing prevalence due to rising obesity rates.^[1] OSA is associated with a range of cardiovascular complications, including systemic hypertension, coronary artery disease, heart failure, and stroke.^[2] Thepathophysiology involves sympathetic overactivity, oxidative stress, systemic inflammation, and endothelial dysfunction.^[3] These changes create a prothrombotic milieu, predisposing patients to both arterial and venous thromboembolic events.^[4] Although cardiovascular risks of OSA are well-documented, its role in peripheral arterial disease and acute limb ischemia (ALI) is less frequently described in the literature.^[5]

ALI is a vascular emergency defined as a sudden decrease in arterial perfusion to a limb, threatening tissue viability.^[6] It commonly results from embolic events, in situ thrombosis, or trauma.^[7] Prompt recognition and intervention are critical to prevent irreversible tissue damage and limb loss. Traditional risk factors for ALI include atrial fibrillation, atherosclerosis, smoking, and hypercoagulable states. OSA, especially when poorly managed, may represent an underrecognized contributor to this condition. Chronic intermittent hypoxia in OSA patients leads to increased erythropoietin production and elevated hemoglobin levels, contributing to blood viscosity and thrombosis. Moreover, metabolic comorbidities such as diabetes mellitus and obesity, which often coexist with OSA, further exacerbate vascular dysfunction. Inflammatory cytokines and activated platelets also contribute to a prothrombotic state in these patients. Despite these theoretical links, there are limited case reports or series directly connecting OSA with ALI.^[8] Here, we present the case of a morbidly obese diabetic patient with known OSA who developed ALI of the right lower limb, requiring urgent surgical intervention.

CASE REPORT

A man in his 50s presented to the emergency department with sudden, severe pain in the right lower limb for 4 h, associated with numbness and pallor. He denied trauma, recent surgery, or prolonged immobility. He had difficulty ambulating and had noticed coolness and loss of sensation below the knee.

Imaging

Computed tomography angiogram of the lower limbs revealed no flow beyond the right common femoral artery, consistent with acute arterial occlusion [Figure 1]. There was no evidence of thrombus proximally in the vascular tree.

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Figure 1:

Computed tomography angiogram image showing contrast only up to the right common femoral artery (yellow dot), with absent flow distally.

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Treatment and outcome

He was taken for urgent transfemoral embolectomy under general anesthesia. Intraoperatively, long-segment thrombi were extracted from the superficial femoral and popliteal arteries [Figure 2]. Postoperatively, perfusion improved, the limb became warm within 24 h, and sensory/motor function began to recover.

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Figure 2:

Arteriotomy over the right common femoral artery to retrieve blood clots (green arrow) using Fogarty catheter.

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The patient was started on low molecular weight heparin, transitioned to warfarin, and advised on strict CPAP adherence and diabetic control. He was discharged on postoperative day 5 with a vascular follow-up plan.

DISCUSSION

This case illustrates a rare but clinically important presentation of ALI in a patient with OSA, morbid obesity, and poorly controlled diabetes mellitus. OSA has been strongly associated with cardiovascular complications, but its link to peripheral arterial thrombotic events is less well established. The underlying pathophysiology of OSA includes intermittent hypoxia, oxidative stress, systemic inflammation, and endothelial dysfunction, all of which contribute to a hypercoagulable state.^[4] In this patient, chronic intermittent hypoxia likely stimulated erythropoietin production, leading to polycythemia, as evidenced by an elevated hemoglobin level of 18 g/dL. Increased blood viscosity and reduced nitric oxide availability may have further predisposed the patient to thrombosis. Obesity and diabetes, both independently prothrombotic conditions, may have compounded the vascular risk profile. Notably, there was no history of peripheral arterial disease or atrial fibrillation, and echocardiography did not reveal a cardiac thrombus, supporting a likely in situ thrombotic event. The long-segment clot removed during transfemoral embolectomy suggests an extensive thrombotic process rather than a small embolus. Literature directly linking OSA with ALI is limited, but this case adds to a growing body of evidence suggesting that OSA can have systemic vascular consequences beyond the coronary and cerebral circulation. In addition to the mechanical burden of upper airway obstruction, OSA causes metabolic disturbances and hormonal imbalances that further disrupt vascular homeostasis. Studies have shown that CPAP therapy can reverse endothelial dysfunction and reduce thrombotic markers, highlighting the importance of adherence to treatment.^[8] Unfortunately, our patient was non-compliant with CPAP, possibly contributing to the severity of his presentation. Prompt diagnosis and surgical intervention in ALI are critical for limb salvage and functional recovery. This case emphasizes the importance of considering OSA as a risk factor in patients presenting with thrombotic vascular events. Multidisciplinary management addressing OSA, metabolic comorbidities, and secondary prevention is essential to reduce recurrence risk and improve outcomes.

CONCLUSION

ALI can be a rare but serious vascular complication in patients with OSA, especially when compounded by obesity, diabetes, and polycythemia. This case highlights the potential systemic thrombotic risks associated with untreated or poorly managed OSA. Early recognition and prompt surgical intervention were critical in preserving limb viability. Clinicians should maintain a high index of suspicion for arterial thrombosis in high-risk OSA patients presenting with acute limb symptoms. Optimal management of OSA and its comorbidities may help prevent such life- and limb-threatening events.