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Pathophysiologic mechanisms of brain-body associations in ruptured brain aneurysms: A systematic review.

Lo BW, Fukuda H, Nishimura Y, Macdonald RL, Farrokhyar F, Thabane L, Levine MA - Surg Neurol Int (2015)

Bottom Line: Clinical results were described in sufficient detail and were applicable to aneurysmal subarachnoid hemorrhage patients in clinical practice.Limitations included small sample sizes and between-study differences in diagnostic tests and clinical outcome endpoints.Subsequent neuro-cardio-endocrine responses then interact with other body systems as part of the secondary responses to primary injury.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology and Neurosurgery, Montreal Neurological Institute and Hospital, McGill University, Montreal, Quebec, Canada.

ABSTRACT

Background: Patients with ruptured brain aneurysms and aneurysmal subarachnoid hemorrhage suffer neurological damage from primary injury of the aneurysm rupture itself, as well as a number of secondary injurious processes that can further worsen the affected individual's neurological state. In addition, other body systems can be affected in a number of brain-body associations.

Methods: This systematic review synthesizes prospective and retrospective cohort studies that investigate brain-body associations in patients with ruptured brain aneurysms. The methodologic quality of these studies will be appraised.

Results: Six cohort studies were included in this systemic review. The methodologic quality of each study was assessed. They had representative patient populations, clear selection criteria and clear descriptions of study designs. Reproducible study protocols with ethics board approval were present. Clinical results were described in sufficient detail and were applicable to aneurysmal subarachnoid hemorrhage patients in clinical practice. There were few withdrawals from the study. Limitations included small sample sizes and between-study differences in diagnostic tests and clinical outcome endpoints. Several pathophysiologic mechanisms of brain-body associations in ruptured brain aneurysms were clarified through this systematic review. Sympathetic activation of the cardiovascular system in aneurysmal subarachnoid hemorrhage not only triggers the release of atrial and brain natriuretic peptides it can also lead to increased pulmonary venous pressures and permeability causing hydrostatic pulmonary edema. Natriuretic states can herald the onset or worsening of clinical vasospasm as the renin-angiotensin-aldosterone system is activated in a delayed manner.

Conclusions: This systematic review synthesizes the most current evidence of underlying mechanisms of brain related associations with body systems in aneurysmal subarachnoid hemorrhage. Results gained from these studies are clinically useful and shed light on how ruptured brain aneurysms affect the cardiopulmonary system. Subsequent neuro-cardio-endocrine responses then interact with other body systems as part of the secondary responses to primary injury.

No MeSH data available.


Related in: MedlinePlus

Pathophysiologic mechanisms of brain-body associations after aneurysmal subarachnoid hemorrhage and delayed activation of the renin-angiotensin-aldosterone system
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Figure 3: Pathophysiologic mechanisms of brain-body associations after aneurysmal subarachnoid hemorrhage and delayed activation of the renin-angiotensin-aldosterone system

Mentions: Together, atrial and brain natriuretic peptides then act on renal tubules triggering sodium and volume loss. Without appropriate resuscitation, plasma sodium levels can fall drastically by postrupture day 4–6.[1011] This drop can be attenuated with preemptive judicious volume and salt replacement. With this treatment, the incidence of severe clinical vasospasm can be lowered.[1] Natriuretic and diuretic states in aneurysmal subarachnoid hemorrhage often herald the onset of clinical vasospasm. Between days 4 and 6, the renin-angiotensin-aldosterone system is activated.[1345678910111314] Figure 3 shows pathophysiologic mechanisms of brain-body associations after aneurysmal subarachnoid hemorrhage, as well as interrelationships, between the neuro-cardio-endocrine systems and the renin-angiotensin-aldosterone system. This system is activated in a delayed manner as a compensatory mechanism for prior sodium and water loss. Waiting for this mechanism alone to compensate for sodium and water balance in the aneurysmal subarachnoid hemorrhage patient will have severe negative consequences because the onset of vasospasm can lead to delayed strokes and further secondary neurological damage.


Pathophysiologic mechanisms of brain-body associations in ruptured brain aneurysms: A systematic review.

Lo BW, Fukuda H, Nishimura Y, Macdonald RL, Farrokhyar F, Thabane L, Levine MA - Surg Neurol Int (2015)

Pathophysiologic mechanisms of brain-body associations after aneurysmal subarachnoid hemorrhage and delayed activation of the renin-angiotensin-aldosterone system
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4544125&req=5

Figure 3: Pathophysiologic mechanisms of brain-body associations after aneurysmal subarachnoid hemorrhage and delayed activation of the renin-angiotensin-aldosterone system
Mentions: Together, atrial and brain natriuretic peptides then act on renal tubules triggering sodium and volume loss. Without appropriate resuscitation, plasma sodium levels can fall drastically by postrupture day 4–6.[1011] This drop can be attenuated with preemptive judicious volume and salt replacement. With this treatment, the incidence of severe clinical vasospasm can be lowered.[1] Natriuretic and diuretic states in aneurysmal subarachnoid hemorrhage often herald the onset of clinical vasospasm. Between days 4 and 6, the renin-angiotensin-aldosterone system is activated.[1345678910111314] Figure 3 shows pathophysiologic mechanisms of brain-body associations after aneurysmal subarachnoid hemorrhage, as well as interrelationships, between the neuro-cardio-endocrine systems and the renin-angiotensin-aldosterone system. This system is activated in a delayed manner as a compensatory mechanism for prior sodium and water loss. Waiting for this mechanism alone to compensate for sodium and water balance in the aneurysmal subarachnoid hemorrhage patient will have severe negative consequences because the onset of vasospasm can lead to delayed strokes and further secondary neurological damage.

Bottom Line: Clinical results were described in sufficient detail and were applicable to aneurysmal subarachnoid hemorrhage patients in clinical practice.Limitations included small sample sizes and between-study differences in diagnostic tests and clinical outcome endpoints.Subsequent neuro-cardio-endocrine responses then interact with other body systems as part of the secondary responses to primary injury.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology and Neurosurgery, Montreal Neurological Institute and Hospital, McGill University, Montreal, Quebec, Canada.

ABSTRACT

Background: Patients with ruptured brain aneurysms and aneurysmal subarachnoid hemorrhage suffer neurological damage from primary injury of the aneurysm rupture itself, as well as a number of secondary injurious processes that can further worsen the affected individual's neurological state. In addition, other body systems can be affected in a number of brain-body associations.

Methods: This systematic review synthesizes prospective and retrospective cohort studies that investigate brain-body associations in patients with ruptured brain aneurysms. The methodologic quality of these studies will be appraised.

Results: Six cohort studies were included in this systemic review. The methodologic quality of each study was assessed. They had representative patient populations, clear selection criteria and clear descriptions of study designs. Reproducible study protocols with ethics board approval were present. Clinical results were described in sufficient detail and were applicable to aneurysmal subarachnoid hemorrhage patients in clinical practice. There were few withdrawals from the study. Limitations included small sample sizes and between-study differences in diagnostic tests and clinical outcome endpoints. Several pathophysiologic mechanisms of brain-body associations in ruptured brain aneurysms were clarified through this systematic review. Sympathetic activation of the cardiovascular system in aneurysmal subarachnoid hemorrhage not only triggers the release of atrial and brain natriuretic peptides it can also lead to increased pulmonary venous pressures and permeability causing hydrostatic pulmonary edema. Natriuretic states can herald the onset or worsening of clinical vasospasm as the renin-angiotensin-aldosterone system is activated in a delayed manner.

Conclusions: This systematic review synthesizes the most current evidence of underlying mechanisms of brain related associations with body systems in aneurysmal subarachnoid hemorrhage. Results gained from these studies are clinically useful and shed light on how ruptured brain aneurysms affect the cardiopulmonary system. Subsequent neuro-cardio-endocrine responses then interact with other body systems as part of the secondary responses to primary injury.

No MeSH data available.


Related in: MedlinePlus