Subarachnoid hemorrhage (SAH), most frequently caused by intracranial aneurysmal rupture, is a prevalent condition that results in high morbidity and mortality in the ICU. While the central nervous system is the primary affected organ, SAH triggers a complex response in different organs, particularly the immune, cardiovascular, respiratory, and endocrine systems. The immune cascade in response to SAH comprises both cellular and humoral responses and leads to blood-brain barrier damage and neuroinflammation. Cardiovascular complications of SAH may range from mild electrocardiographic changes to Takotsubo cardiomyopathy or neurogenic pulmonary edema, hence the need for strict hemodynamic monitoring and early treatment in patients with SAH. The endocrine system, more specifically the hypothalamus-pituitary and the adrenal axes, can be transiently or persistently compromised after SAH; therefore, entities such as syndrome of inappropriate antidiuretic hormone secretion (SIADH), central diabetes insipidus, or adrenal insufficiency should be actively screened. Understanding the crosstalk among these systems is key to advancing our comprehension of the mechanisms that perpetuate damage in SAH, and may provide novel therapeutic alternatives for these patients.

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Subarachnoid Hemorrhage and System Crosstalk

  • Nekane Romero-García,
  • A. Devís-Peiró,
  • Berta Monleón López,
  • Rafael Badenes

摘要

Subarachnoid hemorrhage (SAH), most frequently caused by intracranial aneurysmal rupture, is a prevalent condition that results in high morbidity and mortality in the ICU. While the central nervous system is the primary affected organ, SAH triggers a complex response in different organs, particularly the immune, cardiovascular, respiratory, and endocrine systems. The immune cascade in response to SAH comprises both cellular and humoral responses and leads to blood-brain barrier damage and neuroinflammation. Cardiovascular complications of SAH may range from mild electrocardiographic changes to Takotsubo cardiomyopathy or neurogenic pulmonary edema, hence the need for strict hemodynamic monitoring and early treatment in patients with SAH. The endocrine system, more specifically the hypothalamus-pituitary and the adrenal axes, can be transiently or persistently compromised after SAH; therefore, entities such as syndrome of inappropriate antidiuretic hormone secretion (SIADH), central diabetes insipidus, or adrenal insufficiency should be actively screened. Understanding the crosstalk among these systems is key to advancing our comprehension of the mechanisms that perpetuate damage in SAH, and may provide novel therapeutic alternatives for these patients.