End organ damage refers to damage affecting major organs fed by the circulatory system (typically the heart, kidneys, brain, and eyes) which can occur as a result of uncontrolled hypertension, hypotension, or hypovolemia 1. End organ damage can present as a heart attack or heart failure, pulmonary edema, acute kidney failure, or neurological deficits, including stroke 2. Understanding end organ injury is critical to minimizing its occurrence.

First, end organ damage can occur as a result of hypertension 3. When blood pressure is very high (>180/120 mmHg), or blood pressure is rising rapidly, a large volume of blood circulating through a small space may create turbulence which damages the inner linings of blood vessels. The body’s repair systems are activated, and platelets are deposited in the area. These can clutter the vessel and impair the body’s ability to generate nitrous oxide, whose job it is to dilate blood vessels and lower blood pressure. As a result of the pressure build up, fluid leaves blood vessels. This can impair blood flow and cut off circulating oxygen, leading to tissue death and damage to the brain, arteries, heart, and/or kidneys. This may occur in cases of chronic or uncontrolled hypertension, drug use, or as a complication of pregnancy 4. In addition, interestingly, recent studies have demonstrated that an activated immune system may also be linked to end organ damage in hypertension 5.

Second, end organ injury can occur as a result of shock. Shock occurs when the body’s blood circulation is insufficient to oxygenate the body’s tissues. Hypovolemic shock occurs as a result of a low circulating volume of fluids in blood vessels. In cases of extremely low circulating volume or an inadequate, low blood pressure, body tissues fail to receive sufficient oxygen and nutrients, which, too, can lead to end organ failure 6.

Evaluation and work-up protocols for end organ injury consists of a physical examination, labs, and imaging. In particular, for patients with end organ damage in hypertension,, a patient’s blood pressure should be lowered immediately using intravenous antihypertensive medications 7. Patients should be admitted to a hospital to be closely monitored for complications as well, including strokes. A patient’s blood pressure should be lowered a maximum of 10% over the first hour and 25% over the first two hours since a rapid lowering of blood pressure can result in an ischemic stroke. Once a patient’s blood pressure is stabilized, they can shift from an intravenous to an oral medication regimen 4.

For patients with end organ damage in shock, the development of end organ damage results from a low circulating blood volume or insufficient blood pressure to maintain oxygen and nutrient supply to vital organs. The initial treatment aims at stabilizing the patient. To this end, fluids are administered to increase the circulating blood volume, and vasopressors can also be administered in order to maintain a higher blood pressure. High-dose steroids like hydrocortisone may also help maintain a high enough blood pressure. Close monitoring in the critical care unit is often required as well in order to continuously monitor blood pressure 8. The next step in treating end organ damage is then to identify any source of infection and treat it, using targeted antibiotics.

End organ injury is not uncommon but with proper anticipation and management can be treated effectively. Research is still warranted in order to elaborate on and specify contemporary best practices.

References

1. Kyada, P., Jadhav, K., Biswas, T. K., Mehta, V. & Zaman, S. Bin. End Organ Damage in Hypertensive Geriatric Age Group: A Cross Sectional Study. J. Med. Res. Innov. 1, 10–16 (2017). DOI : 10.15419/jmri.75

2. End Organ Damage – an overview | ScienceDirect Topics. Available at: https://www.sciencedirect.com/topics/medicine-and-dentistry/end-organ-damage. (Accessed: 9th December 2023)

3. Schmieder, R. E. End Organ Damage In Hypertension. Dtsch. Arztebl. Int. 107, 866 (2010). doi: 10.3238/arztebl.2010.0866.

4. Brathwaite, L. & Reif, M. Hypertensive Emergencies: A Review of Common Presentations and Treatment Options. Cardiol. Clin. 37, 275–286 (2019). doi: 10.1016/j.ccl.2019.04.003.

5. Wenzel, U. O., Kemper, C. & Bode, M. The role of complement in arterial hypertension and hypertensive end organ damage. Br. J. Pharmacol. 178, 2849–2862 (2021). doi: 10.1111/bph.15171.

6. Blumlein, D. & Griffiths, I. Shock: aetiology, pathophysiology and management. https://doi.org/10.12968/bjon.2022.31.8.422 31, 422–428 (2022). doi: 10.12968/bjon.2022.31.8.422.

7. Assessment of end-organ damage in hypertension: rationale, indications and therapeutic implications. Available at: https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-3/Assessment-of-end-organ-damage-in-hypertension-Rationale-Indications-and-Thera. (Accessed: 9th December 2023)

8. Chakraborty, R. K. & Burns, B. Systemic Inflammatory Response Syndrome. StatPearls (2023).