Both DM and other disorders of glucose metabolism are risk factors for CVD. In diabetic patients with pervasive insulin resistance, the development of CVD is characterized by early endothelial dysfunction and vascular inflammation, leading to mononuclear cell recruitment, foam cell formation, and subsequent development of fat striations. More than half the mortality and a vast amount of morbidity in people with DM is related to CVD .
The causes of myocardial infarction in diabetic patients may be multifactorial. Coronary artery embolism (CE), in which obstructive material enters the coronary artery, block its blood flow, and cause ischemia, is an uncommon cause of AMI. Patients with CE represent a high-risk subgroup of patients with AMI . The shedding of cardiogenic embolus can theoretically lead to embolization of lower extremity arteries, but spontaneous co-occurrence of acute embolization of the coronary arteries and the great arteries of the lower limbs is very rare.
Previous study reported that atrial fibrillation (AF) is the most frequent cause of CE . DM is frequent in patients with AF. Community studies demonstrated the presence of DM in 13% of patients with AF . However, DM is not necessarily an independent risk factor for AF. The patient in this case did not have AF. In the follow-up of the medical history, the patients diagnosed with type 1 diabetes did not control or monitor his blood glucose in any way. Due to the difficulty in using insulin to control blood glucose during hospitalization, we suspected that the patient's blood glucose level before admission was not well controlled. Therefore, he was at high risk of developing CVD due to long-term hyperglycemia. We speculated that the most likely cause of AMI in this patient was shedding of embolus in coronary artery or changes in coronary blood flow under stress state after lower limb artery occlusion.
In addition to cardiovascular disease, DM is also considered as an established risk factor for cerebrovascular and peripheral vascular diseases including stroke and peripheral artery disease (PAD) . A proinflammatory state in diabetic patients was considered as a possible reason that increased the levels of some clotting factors and impaired the fibrinolytic system leading to a hypercoagulable state. But the association between DM and venous thromboembolism (VTE) was not seemed to be confirmed by studies [5, 6]. Recently study reported that type 1 DM appeared to be an independent risk factor for VTE development . We know that the clinical characteristics between arterial and venous embolic diseases are different. The symptoms and signs of PAD are variable. Arterial ischemia is often characterized by low skin temperature, pain, or intermittent claudication. However, studies have demonstrated that the majority of patients with confirmed PAD do not have typical claudication . Acute limb ischemia (ALI) is one of the most treatable and potentially devastating presentations of PAD. This present case patient presented with an acute embolism of the lower extremity arteries, without any other PAD related symptoms before admission. Long-term abnormal blood glucose level in this patient may be a potential cause of lower extremity arterial disease (LEAD).
LEAD is particularly frequent in DM patients with worse outcomes, especially the risk of lower limb amputation (LLA), compared with non-diabetic subjects [9–11]. The pathogenesis of LEAD in individuals with diabetes included endothelial dysfunction and increased arterial wall stiffness, which may promote the process of atherosclerosis [12, 13]. Treatment strategies for LEAD patients include drug therapy and surgical or endovascular revascularization. However, in patients with ALEAE, the earlier the embolus is removed, the better the chance of preserving the lower extremity function. According to the guideline suggestion that if expertise of treatment for acute ischemia is not locally or rapidly available, there should be strong consideration of transfer of the patient to a facility with such resources .
Lower extremity symptoms in ALI can include both pain and loss of function. The longer these symptoms are present, the less likely the possibility of limb salvage [15, 16]. The duration of skeletal muscle tolerance to ischemia is roughly 4–6 hours . Systemic anticoagulation with heparin should be administered in patients with ALI unless contraindicated. For threatened limbs, revascularization should be performed emergently within 6 hours. For viable limbs revascularization should be performed within 6–24 hours. In the setting of prolonged ischemia (> 6 to 8 hours) are unlikely to save the limb, and the reperfusion and circulation of ischemic metabolites can result in multiorgan failure and cardiovascular collapse.
In this present case, the patient underwent amputation under general anesthesia during the stage of AMI. Preoperative multidisciplinary consultation provided adequate treatment preparation for patient. We used glucocorticoids intraoperatively to prevent the release of ischemic metabolites that cause inflammation during amputation. Protective lung ventilation strategies improved patients' OI. Although studies  have reported that regional anesthesia alone may be safer for amputations in critically ill patients, we consider that stress response under regional anesthesia may increase the risk of cardiac ischemia. Appropriate hemodynamic support and ventilation strategies under general anesthesia may reduce organ response to tissue necrosis metabolites.