Politt Katharina, Gaik Christine, Wiesmann Thomas
Klinik für Anästhesie und Intensivmedizin, Universitätsklinikum Gießen und Marburg, Philipps-Universität Marburg, Baldingerstraße, 35033, Marburg, Deutschland.
Klinik für Anästhesiologie, operative Intensivmedizin und Schmerztherapie, Diak Klinikum Landkreis Schwäbisch Hall gGmbH, Diakoniestraße 10, 74523, Schwäbisch Hall, Deutschland.
Med Klin Intensivmed Notfmed. 2025 Mar 21. doi: 10.1007/s00063-025-01259-8.
Hypercalcemic crisis is a rare but life-threatening complication of severe hypercalcemia. In most cases (> 90%), primary hyperparathyroidism or malignancy are the causes of a hypercalcemic crisis. Prodromes are often nonspecific and can present as nausea, vomiting, or a lack of concentration. The transition from hypercalcemia to a hypercalcemic crisis is often caused by a dysregulated volume status. As rapid treatment is essential, differential diagnostics should not delay treatment. In the human body, there is a complex system that keeps the extracellular calcium concentration within a narrow range (total calcium level: 2.1-2.5 mmol/L), whereby only about 50% of the total extracellular calcium is ionized and, therefore, biologically active. The remaining 50% is mostly bound to albumin and globulins. A hypercalcemic crisis is defined as a (albumin-corrected) total calcium over 3.5 mmol/L with accompanying severe symptoms. In addition to the measurement of the albumin-corrected total calcium concentration and ionized calcium, measuring the (intact) parathyroid hormone level is also crucial, as the causes of the hypercalcemic crisis can be roughly divided into parathyroid hormone (PTH)-dependent and PTH-independent causes. Initially, treatment is primarily symptomatic; in patients with a hypercalcemic crisis, the focus is on evaluation and appropriate emergency treatment according to the ABCDE scheme (e.g., securing the airway). At the same time, the calcium level should be lowered as quickly as possible in a controlled manner. Therefore, differentiated volume therapy is recommended. In addition, treatment with loop diuretics such as furosemide can be considered (after correcting hypovolemia). If therapy is not successful quickly or if there are contraindications to increased fluid administration (e.g., cardiac or renal insufficiency), the start of (calcium-free) dialysis is usually unavoidable. Calcitonin can be used to rapidly reduce calcium levels. Depending on the clinical cause of the severe hypercalcemia, cinacalcet, bisphosphonates, and denosumab are also drugs that can effectively reduce calcium levels within 2-3 days. The long-term prognosis depends on the underlying disease. A cohort of patients with primary hyperparathyroidism showed a 3-year survival rate of 80%.
高钙血症危象是严重高钙血症的一种罕见但危及生命的并发症。在大多数情况下（>90%），原发性甲状旁腺功能亢进或恶性肿瘤是高钙血症危象的病因。前驱症状通常不具有特异性，可表现为恶心、呕吐或注意力不集中。从高钙血症转变为高钙血症危象通常是由容量状态失调引起的。由于快速治疗至关重要，鉴别诊断不应延误治疗。在人体中，存在一个复杂的系统，可将细胞外钙浓度维持在狭窄范围内（总钙水平：2.1 - 2.5 mmol/L），其中细胞外总钙中只有约50%是离子化的，因此具有生物活性。其余50%大多与白蛋白和球蛋白结合。高钙血症危象定义为（经白蛋白校正的）总钙超过3.5 mmol/L并伴有严重症状。除了测量经白蛋白校正的总钙浓度和离子钙外，测量（完整的）甲状旁腺激素水平也至关重要，因为高钙血症危象的病因大致可分为甲状旁腺激素（PTH）依赖性和PTH非依赖性病因。最初，治疗主要是对症治疗；对于高钙血症危象患者，重点是根据ABCDE方案进行评估和适当的紧急治疗（例如确保气道通畅）。同时，应尽快以可控方式降低钙水平。因此，推荐进行有差别的容量治疗。此外，可考虑使用呋塞米等袢利尿剂进行治疗（纠正低血容量后）。如果治疗不能迅速成功或存在增加液体输注的禁忌证（如心功能不全或肾功能不全），通常不可避免地要开始（无钙）透析。降钙素可用于快速降低钙水平。根据严重高钙血症的临床病因，西那卡塞、双膦酸盐和地诺单抗也是可在2 - 3天内有效降低钙水平的药物。长期预后取决于基础疾病。一组原发性甲状旁腺功能亢进患者的3年生存率为80%。
