End organ damage
End organ damage usually refers to damage occurring in major organs fed by the circulatory system (heart, kidneys, brain, eyes) which can sustain damage due to uncontrolled hypertension, hypotension, or hypovolemia.
Evidence of hypertensive damage[]
In the context of hypertension, features include:[1]
- Heart - evidence on electrocardiogram screening[1] of the heart muscle thickening (but may also be seen on chest X-ray) suggesting left ventricular hypertrophy) or by echocardiography of less efficient function (left ventricular failure).
- Brain- hypertensive encephalopathy, hemorrhagic stroke, subarachnoid hemorrhage, confusion, loss of consciousness, eclampsia, seizures, or transient ischemic attack.
- Kidney - leakage of protein into the urine (albuminuria or proteinuria), or reduced renal function,[1] hypertensive nephropathy, acute renal failure, or glomerulonephritis.
- Eye - evidence upon fundoscopic examination of hypertensive retinopathy,[1] retinal hemorrhage, papilledema and blindness.
- Peripheral arteries - peripheral vascular disease and chronic lower limb ischemia.
Evidence of shock (poor end organ perfusion)[]
- Kidney - poor urine output (less than 0.5 mL/kg), low glomerular filtration rate.
- Skin - pallor or mottled appearance, capillary refill > 2 secs, cool limbs.
- Brain - orientation to time, person, and place. The Glasgow Coma Scale may be used to quantify altered consciousness.
References[]
- ^ a b c d "CG34 Hypertension - quick reference guide" (PDF). National Institute for Health and Clinical Excellence. 28 June 2006. Archived from the original (PDF) on 2009-03-13. Retrieved 2009-03-04.
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