Wu Chaoneng, Kambhatla Sujata, Zazaian Andrew, Jaber Ali, Brenner Barry, Saad Chadi
Internal Medicine Department, Garden City Hospital, Michigan State University, USA.
Emergency Department, Garden City Hospital, Michigan State University, USA.
Clin Med Insights Endocrinol Diabetes. 2025 Jun 13;18:11795514251341383. doi: 10.1177/11795514251341383. eCollection 2025.
Hyperglycemic crises, including diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS), significantly affect clinical outcomes and impose a heavy economic burden. Among the steadily increased recreational drug abuse, cocaine has become the most frequently misused substance. However, there is limited understanding of the relationship between cocaine use and hyperglycemic crises. We report 4 cases retrospectively to examine the relationship between cocaine abuse and DKA/HHS. In Case 1, a patient with Type 1 diabetes mellitus (T1DM) presented with altered mental status and a combination of DKA and HHS, where cocaine use led to missed insulin doses, resulting in the crisis. Case 2 involved the same patient who later developed DKA due to cavitary pneumonia and sepsis, requiring mechanical ventilation, vasopressors, and renal replacement therapy. Cocaine inhalation caused pulmonary damage that triggered DKA. Case 3 involved a patient with Type 2 diabetes mellitus (T2DM) who abused cocaine intravenously, leading to DKA-HHS and necrotizing fasciitis that required emergency surgery. Case 4 was a patient with obesity, insulin resistance, and T2DM on oral medications, where cocaine likely exacerbated insulin resistance and triggered DKA. In all 4 cases, treatment focused on aggressive rehydration, insulin infusion, electrolyte correction, and addressing underlying causes. The hyperglycemic crises resolved within 12 to 24 hours. However, managing cocaine-related complications proved difficult, leading to high morbidity and mortality rates, including altered mental status with airway issues, kidney failure, rhabdomyolysis, and infections that could result in septic shock or death. In Case 4, cocaine use significantly worsened insulin resistance and T2DM, contributing to DKA. In conclusion, cocaine abuse has multiple effects and can act as an unusual trigger for hyperglycemic crises by causing missed insulin doses, dehydration, infections, and chronic worsening of insulin resistance. Cocaine abuse can trigger and/or worsen hyperglycemic crises through various mechanisms, such as damage to the cardiopulmonary and renal systems, psychosocial changes, weakened immunity and infections, and alterations in hormones and metabolism (Figure 3). We suggest incorporating questions about substance abuse into routine patient history assessment and performing toxicology screenings, particularly for individuals who have frequent admissions for DKA/HHS. Additionally, we share our expertise in managing this specific group of patients.
高血糖危象，包括糖尿病酮症酸中毒（DKA）和高血糖高渗状态（HHS），会显著影响临床结局并带来沉重的经济负担。在不断增加的娱乐性药物滥用中，可卡因已成为最常被滥用的物质。然而，人们对可卡因使用与高血糖危象之间的关系了解有限。我们回顾性报告4例病例，以研究可卡因滥用与DKA/HHS之间的关系。病例1中，一名1型糖尿病（T1DM）患者出现精神状态改变，同时合并DKA和HHS，可卡因使用导致胰岛素剂量漏用，从而引发了危象。病例2涉及同一名患者，该患者后来因空洞性肺炎和脓毒症发展为DKA，需要机械通气、血管升压药和肾脏替代治疗。吸入可卡因导致肺部损伤，进而引发DKA。病例3涉及一名2型糖尿病（T2DM）患者，该患者静脉滥用可卡因，导致DKA-HHS和坏死性筋膜炎，需要进行急诊手术。病例4是一名肥胖、胰岛素抵抗且正在服用口服药物的T2DM患者，可卡因可能加剧了胰岛素抵抗并引发了DKA。在所有4例病例中，治疗重点是积极补液、胰岛素输注、电解质纠正以及解决潜在病因。高血糖危象在12至24小时内得到缓解。然而，处理与可卡因相关的并发症被证明很困难，导致高发病率和死亡率，包括伴有气道问题的精神状态改变、肾衰竭、横纹肌溶解以及可能导致感染性休克或死亡的感染。在病例4中，可卡因使用显著恶化了胰岛素抵抗和T2DM，导致了DKA。总之，可卡因滥用具有多种影响，可通过导致胰岛素剂量漏用、脱水、感染以及胰岛素抵抗的慢性恶化，成为高血糖危象的异常触发因素。可卡因滥用可通过多种机制触发和/或加重高血糖危象，如对心肺和肾脏系统的损害、心理社会变化、免疫力减弱和感染以及激素和代谢改变（图3）。我们建议将关于药物滥用的问题纳入常规患者病史评估，并进行毒理学筛查，特别是对于那些因DKA/HHS频繁入院的个体。此外，我们分享了管理这一特定患者群体的专业知识。
