End organ damage

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End organ damage is severe impairment of major body organs due to systemic disease. Commonly this is referred to in diabetes, high blood pressure, or states of low blood pressure or low blood volume. [1] This can present as a heart attack or heart failure, pulmonary edema, neurologic deficits including a stroke, or acute kidney failure. [2]

Contents

Pathophysiology

End organ damage typically occurs where systemic disease causes cell death in most or all organs.

Hypertensive

When blood pressures are critically high (>180/120 mm Hg) or the rate of rise in blood pressure is rapid, a large volume of blood circulating in a small space creates turbulence and can damage the inner lining of blood vessels. The body’s repair systems are activated by damage and circulating blood components, like platelets, work on repair. The deposition of platelets can clutter the vessel space and impair the body’s natural ability to produce nitrous oxide, which would dilate blood vessels and help lower blood pressure. When high pressure is pushing on the walls of narrowed blood vessels, fluid leaves the inside of blood vessels and moves to the space just outside. This impairs necessary blood flow and cuts off circulating oxygen, which can lead to tissue death and permanent damage to the brain, heart, arteries, and kidneys. This may occur as a result of chronic or poorly controlled hypertension, illicit drug use, or as a complication of pregnancy. [3] Recent studies have shown that activation of the immune system may also be closely involved with the development of end organ damage in hypertensive states. [4]

Shock

Shock is when the body does not have adequate circulation to provide oxygen to body tissues. Hypovolemic shock occurs due to low circulating volume of fluids in the blood vessels. Distributive shock, which can occur due to anaphylaxis or sepsis, results in widespread dilation of blood vessels in the body resulting in lower blood pressure. In cases of extremely low circulating volume or inability to maintain an adequate blood pressure, body tissues do not receive enough oxygen and nutrients. [5] When tissues lack oxygen and adequate circulation, organs can fail. [6]

Diabetes

In diabetes, the dysregulation of insulin and blood glucose levels damages end organ cells and as the body compensates through regulating fluid volume to adjust glucose concentration, it also incurs collateral damage to organs. Microvascular and macrovascular complications include nephropathy, retinopathy, neuropathy, and ASCVD events. [7] In diabetic neuropathy, glucose promotes oxidative stress leading to nerve damage. [8] Chronically high insulin levels are also associated with early development of atherosclerotic plaques inside blood vessel walls. [9]

Clinical presentation

Hypertensive

Important definitions

Presentation

Source: [3]

Shock

Important definitions

  • Systemic Inflammatory Response Syndrome (SIRS) meets any two criteria: [10]
    • Body temperature >38 or <36 degrees Celsius
    • Heart rate >90 beats per minute
    • Respiratory rate >20 breaths per minute or partial pressure CO2 <32 mm Hg
    • White blood cell count >12000 or <4000 per microliter or >10% immature forms or bands
  • qSOFA score helps predict organ dysfunction outside of the intensive care unit by assessing 3 components: [10]
    • Systolic blood pressure <100 mm Hg
    • Maximum respiratory rate >21 breaths per minute
    • Decreased Glasgow coma score <15

Presentation

Source: [11]

  • Altered mental status - person may not be oriented to person, place, or time
  • Delayed capillary refill - skin may be pale or mottled, limbs may be cool
  • Little or no urine output - poor urine output
  • Absent bowel sounds

Diabetes

End organ damage can occur at any diagnostic stage of diabetes, including pre-diabetes. [12]

Presentation

Source: [13]

Evaluation and work-up

Physical examination

Labs

Imaging

Management

Hypertensive

When there is concern for the presence or development of end organ damage, blood pressure should be lowered emergently with intravenous antihypertensive medications. Patients should be admitted to the hospital to be closely monitored for complications of end organ damage, notably strokes. Blood pressure should be lowered a maximum of 10% over the first hour and 25% over the first two hours as rapid lowering of blood pressure can lead to decreased blood flow in the brain and cause the development of an ischemic stroke. Once blood pressure is stabilized, patients can be changed from intravenous medications to oral. [3]

For patients with long-standing hypertension, patient education on the importance of consistently taking prescribed medications and keeping blood pressure well-controlled is critical. [2] Additionally, future treatments may focus not only on blood pressure control but also the reduction of local inflammation that can lead to end organ damage. [4]

In pregnant patients where there is concern for pre-eclampsia, patients should be given magnesium sulfate and admitted. Urine output, breathing, and reflexes should be monitored closely with concern for the development of worsening kidney function and magnesium toxicity. Systolic blood pressure should be treated with antihypertensive medications only if it is higher than 160 mm Hg. [2]

Shock

When a patient is in shock, the development of end organ damage is typically due to circulating blood volume or blood pressure that is not high enough to maintain oxygen and nutrient supply to vital organs. Initial treatment is focused on stabilizing the patient. Fluids are given to increase circulating blood volume. Vasopressors, medications that constrict blood vessels, can also be given in order to maintain a higher blood pressure and help vital organs receive enough oxygen and nutrients. High-dose steroids, like hydrocortisone, may also help maintain blood pressures in patients. Close monitoring in the critical care unit is often necessary to measure blood pressures. [10]

The next step in treating end organ damage due to septic shock is to identify the source of the infection and treat it. Broad-spectrum antibiotics can be started that will treat many potential bacteria before cultures grow the specific bacteria that is causing the infection. Once cultures identify the culprit of the infection, the antibiotic therapy can be changed so that it is only covering what needs to be treated. Treatment of the source of infection should resolve low blood pressures that compromise vital organ function. Complications, including acute respiratory distress syndrome, acute kidney injury, and electrolyte abnormalities, can be treated proactively and managed on an individual basis. [10]

Diabetes

Lifelong treatment and monitoring is often necessary for glucose control. Glucose levels should be maintained at 90 to 130 mg/dL and HbA1c at less than 7%. [7] Medical treatment includes use of insulin and/or other medications to control glucose levels. Monitoring for end organ damage complications is recommended on guidelines by different regional medical bodies. [7]

Related Research Articles

<span class="mw-page-title-main">Blood vessel</span> Tubular structure of circulatory system

Blood vessels are the structures of the circulatory system that transport blood throughout the human body. These vessels transport blood cells, nutrients, and oxygen to the tissues of the body. They also take waste and carbon dioxide away from the tissues. Blood vessels are needed to sustain life, because all of the body's tissues rely on their functionality.

The following is a glossary of diabetes which explains terms connected with diabetes.

<span class="mw-page-title-main">Hypertension</span> Long-term high blood pressure in the arteries

Hypertension, also known as high blood pressure, is a long-term medical condition in which the blood pressure in the arteries is persistently elevated. High blood pressure usually does not cause symptoms itself. It is, however, a major risk factor for stroke, coronary artery disease, heart failure, atrial fibrillation, peripheral arterial disease, vision loss, chronic kidney disease, and dementia. Hypertension is a major cause of premature death worldwide.

<span class="mw-page-title-main">Hyperglycemia</span> Too much blood sugar, usually because of diabetes

Hyperglycemia is a condition in which an excessive amount of glucose circulates in the blood plasma. This is generally a blood sugar level higher than 11.1 mmol/L (200 mg/dL), but symptoms may not start to become noticeable until even higher values such as 13.9–16.7 mmol/L (~250–300 mg/dL). A subject with a consistent fasting blood glucose range between ~5.6 and ~7 mmol/L is considered slightly hyperglycemic, and above 7 mmol/L is generally held to have diabetes. For diabetics, glucose levels that are considered to be too hyperglycemic can vary from person to person, mainly due to the person's renal threshold of glucose and overall glucose tolerance. On average, however, chronic levels above 10–12 mmol/L (180–216 mg/dL) can produce noticeable organ damage over time.

<span class="mw-page-title-main">Shock (circulatory)</span> Medical condition of insufficient blood flow

Shock is the state of insufficient blood flow to the tissues of the body as a result of problems with the circulatory system. Initial symptoms of shock may include weakness, fast heart rate, fast breathing, sweating, anxiety, and increased thirst. This may be followed by confusion, unconsciousness, or cardiac arrest, as complications worsen.

A hypertensive urgency is a clinical situation in which blood pressure is very high with minimal or no symptoms, and no signs or symptoms indicating acute organ damage. This contrasts with a hypertensive emergency where severely high blood pressure is accompanied by evidence of progressive organ or system damage.

<span class="mw-page-title-main">Vasodilation</span> Widening of blood vessels

Vasodilation, also known as vasorelaxation, is the widening of blood vessels. It results from relaxation of smooth muscle cells within the vessel walls, in particular in the large veins, large arteries, and smaller arterioles. Blood vessel walls are composed of endothelial tissue and a basal membrane lining the lumen of the vessel, concentric smooth muscle layers on top of endothelial tissue, and an adventitia over the smooth muscle layers. Relaxation of the smooth muscle layer allows the blood vessel to dilate, as it is held in a semi-constricted state by sympathetic nervous system activity. Vasodilation is the opposite of vasoconstriction, which is the narrowing of blood vessels.

<span class="mw-page-title-main">Hypotension</span> Abnormally low blood pressure

Hypotension, also known as low blood pressure, is a cardiovascular condition characterized by abnormally reduced blood pressure. Blood pressure is the force of blood pushing against the walls of the arteries as the heart pumps out blood and is indicated by two numbers, the systolic blood pressure and the diastolic blood pressure, which are the maximum and minimum blood pressures within the cardiac cycle, respectively. A systolic blood pressure of less than 90 millimeters of mercury (mmHg) or diastolic of less than 60 mmHg is generally considered to be hypotension. Different numbers apply to children. However, in practice, blood pressure is considered too low only if noticeable symptoms are present.

<span class="mw-page-title-main">Hypovolemia</span> Low blood volume

Hypovolemia, also known as volume depletion or volume contraction, is a state of abnormally low extracellular fluid in the body. This may be due to either a loss of both salt and water or a decrease in blood volume. Hypovolemia refers to the loss of extracellular fluid and should not be confused with dehydration.

<span class="mw-page-title-main">Pulse pressure</span> Difference between systolic and diastolic blood pressure

Pulse pressure is the difference between systolic and diastolic blood pressure. It is measured in millimeters of mercury (mmHg). It represents the force that the heart generates each time it contracts. Healthy pulse pressure is around 40 mmHg. A pulse pressure that is consistently 60 mmHg or greater is likely to be associated with disease, and a pulse pressure of 50 mmHg or more increases the risk of cardiovascular disease. Pulse pressure is considered low if it is less than 25% of the systolic. A very low pulse pressure can be a symptom of disorders such as congestive heart failure.

Antihypertensives are a class of drugs that are used to treat hypertension. Antihypertensive therapy seeks to prevent the complications of high blood pressure, such as stroke, heart failure, kidney failure and myocardial infarction. Evidence suggests that reduction of the blood pressure by 5 mmHg can decrease the risk of stroke by 34% and of ischaemic heart disease by 21%, and can reduce the likelihood of dementia, heart failure, and mortality from cardiovascular disease. There are many classes of antihypertensives, which lower blood pressure by different means. Among the most important and most widely used medications are thiazide diuretics, calcium channel blockers, ACE inhibitors, angiotensin II receptor antagonists (ARBs), and beta blockers.

<span class="mw-page-title-main">Hypovolemic shock</span> Medical condition

Hypovolemic shock is a form of shock caused by severe hypovolemia. It can be caused by severe dehydration or blood loss. Hypovolemic shock is a medical emergency; if left untreated, the insufficient blood flow can cause damage to organs, leading to multiple organ failure.

A complication in medicine, or medical complication, is an unfavorable result of a disease, health condition, or treatment. Complications may adversely affect the prognosis, or outcome, of a disease. Complications generally involve a worsening in the severity of the disease or the development of new signs, symptoms, or pathological changes that may become widespread throughout the body and affect other organ systems. Thus, complications may lead to the development of new diseases resulting from previously existing diseases. Complications may also arise as a result of various treatments.

<span class="mw-page-title-main">Hypertensive kidney disease</span> Medical condition

Hypertensive kidney disease is a medical condition referring to damage to the kidney due to chronic high blood pressure. It manifests as hypertensive nephrosclerosis. It should be distinguished from renovascular hypertension, which is a form of secondary hypertension, and thus has opposite direction of causation.

<span class="mw-page-title-main">Hypertensive emergency</span> Very high blood pressure and signs of organ damage

A hypertensive emergency is very high blood pressure with potentially life-threatening symptoms and signs of acute damage to one or more organ systems. It is different from a hypertensive urgency by this additional evidence for impending irreversible hypertension-mediated organ damage (HMOD). Blood pressure is often above 200/120 mmHg, however there are no universally accepted cutoff values.

<span class="mw-page-title-main">Complications of hypertension</span>

Complications of hypertension are clinical outcomes that result from persistent elevation of blood pressure. Hypertension is a risk factor for all clinical manifestations of atherosclerosis since it is a risk factor for atherosclerosis itself. It is an independent predisposing factor for heart failure, coronary artery disease, stroke, kidney disease, and peripheral arterial disease. It is the most important risk factor for cardiovascular morbidity and mortality, in industrialized countries.

Complications of diabetes are secondary diseases that are a result of elevated blood glucose levels that occur in diabetic patients. These complications can be divided into two types: acute and chronic. Acute complications are complications that develop rapidly and can be exemplified as diabetic ketoacidosis (DKA), hyperglycemic hyperosmolar state (HHS), lactic acidosis (LA), and hypoglycemia. Chronic complications develop over time and are generally classified in two categories: microvascular and macrovascular. Microvascular complications include neuropathy, nephropathy, and retinopathy; while cardiovascular disease, stroke, and peripheral vascular disease are included in the macrovascular complications.

Hypertensive disease of pregnancy, also known as maternal hypertensive disorder, is a group of high blood pressure disorders that include preeclampsia, preeclampsia superimposed on chronic hypertension, gestational hypertension, and chronic hypertension.

<span class="mw-page-title-main">Labile hypertension</span> Medical condition

Labile hypertension occurs when there are unexpected changes in blood pressure. The term can be used to describe when people have blood pressure measurements that abruptly fluctuate from being abnormally high, approximately 140/90mm Hg or over and returns to its normal range.

<span class="mw-page-title-main">Hypertension and the brain</span>

Hypertension is a condition characterized by an elevated blood pressure in which the long term consequences include cardiovascular disease, kidney disease, adrenal gland tumors, vision impairment, memory loss, metabolic syndrome, stroke and dementia. It affects nearly 1 in 2 Americans and remains as a contributing cause of death in the United States. There are many genetic and environmental factors involved with the development of hypertension including genetics, diet, and stress.

References

  1. ↑ Kyada P, Jadhav K, Biswas TK, Mehta V, Zaman SB (June 2017). "End organ damage in hypertensive geriatric age group: a cross sectional study". Journal of Medical Research and Innovation. 1 (3): 10–16. doi:10.5281/zenodo.808966.
  2. 1 2 3 Alley WD, Schick MA (July 2023). "Hypertensive Emergency". StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. PMID   29261994.
  3. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 Brathwaite L, Reif M (August 2019). "Hypertensive Emergencies: A Review of Common Presentations and Treatment Options". Cardiology Clinics. 37 (3): 275–286. doi:10.1016/j.ccl.2019.04.003. PMID   31279421. S2CID   181625435.
  4. 1 2 Wenzel UO, Kemper C, Bode M (July 2021). "The role of complement in arterial hypertension and hypertensive end organ damage". British Journal of Pharmacology. 178 (14): 2849–2862. doi: 10.1111/bph.15171 . PMC   10725187 . PMID   32585035. S2CID   220079482.
  5. ↑ Kislitsina ON, Rich JD, Wilcox JE, Pham DT, Churyla A, Vorovich EB, et al. (2019-03-12). "Shock - Classification and Pathophysiological Principles of Therapeutics". Current Cardiology Reviews. 15 (2): 102–113. doi:10.2174/1573403X15666181212125024. PMC   6520577 . PMID   30543176.
  6. ↑ Blumlein D, Griffiths I (April 2022). "Shock: aetiology, pathophysiology and management". British Journal of Nursing. 31 (8): 422–428. doi:10.12968/bjon.2022.31.8.422. PMID   35439071.
  7. 1 2 3 Sapra, Amit; Bhandari, Priyanka (2024), "Diabetes", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID   31855345 , retrieved 2024-06-15
  8. ↑ Bodman, Myron A.; Dreyer, Mark A.; Varacallo, Matthew (2024), "Diabetic Peripheral Neuropathy", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID   28723038 , retrieved 2024-06-15
  9. ↑ Poznyak, Anastasia; Grechko, Andrey V.; Poggio, Paolo; Myasoedova, Veronika A.; Alfieri, Valentina; Orekhov, Alexander N. (2020-03-06). "The Diabetes Mellitus–Atherosclerosis Connection: The Role of Lipid and Glucose Metabolism and Chronic Inflammation". International Journal of Molecular Sciences. 21 (5): 1835. doi: 10.3390/ijms21051835 . ISSN   1422-0067. PMC   7084712 . PMID   32155866.
  10. 1 2 3 4 Chakraborty RK, Burns B (May 2023). "Systemic Inflammatory Response Syndrome.". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID   31613449.
  11. 1 2 3 4 5 6 7 "Bacterial Sepsis Clinical Presentation: History, History and Physical Examination, Physical Examination". emedicine.medscape.com. Retrieved 2023-11-10.
  12. 1 2 3 "Diabetes Diagnosis & Tests | ADA". diabetes.org. Retrieved 2024-06-15.
  13. ↑ "Diabetes Signs and Symptoms | ADA". diabetes.org. Retrieved 2024-06-15.
  14. 1 2 3 "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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