Diseases

An overview of the types and causes of Edema

Over accumulation of fluid in the interstitial space is generally bad and it affects the proper function of the tissue. This is because the formation of oedema increases the diffusion distance of oxygen and other nutrients. And for the same reason it reduces the diffusional removal of potentially toxic substances of cellular metabolism. This is especially important in the lungs where pulmonary oedema can greatly affect exchange of gasses. Also, certain anatomical structures limit tissue expansion in response to oedema. For example, the kidneys, brain, and the skeletal muscles (Scallan et al., 2010a). This means that small incremental changes in transcapillary fluid filtration will induce a large increase in interstitial fluid pressure.

This is a condition that arises when there is too much fluid in the tissue spaces or cavities. In inflammation, fluid accumulation is normal, this is part of the process where the fluid that is rich in protein floods the area. This is different from non- inflammatory oedema, where the fluid accumulation is not rich in protein. This is due to the osmotic and hydrostatic pressures between the blood vessels, and tissue not functioning properly.  Intravascular hydrostatic forces and interstitial osmotic forces will move fluid in and out of the blood vessels. Opposite to this is the osmotic pressure which pushes or pulls fluid in and out of vessels. The two types of oedema include, generalised, which is when swelling is throughout the body, and localised oedema, when parts of the body are affected (Scallan et al., 2010a).

Over accumulation of fluid in the interstitial space is generally bad and it affects the proper function of the tissue. This is because the formation of oedema increases the diffusion distance of oxygen and other nutrients. And for the same reason it reduces the diffusional removal of potentially toxic substances of cellular metabolism. This is especially important in the lungs where pulmonary oedema can greatly affect exchange of gasses. Also, certain anatomical structures limit tissue expansion in response to oedema. For example, the kidneys, brain, and the skeletal muscles (Scallan et al., 2010a). This means that small incremental changes in transcapillary fluid filtration will induce a large increase in interstitial fluid pressure.

Oedema will happen when 

  • There is an increase in intravascular pressure, pushing the fluid out of the vessels into the interstitial area. This can be caused by poor venous flow especially in the lower limbs due to either a deep vein thrombosis. Also, increased venous pressure caused by congestive heart failure (right ventricle), this also causes a reduction in blood flow to the kidney. This then leads to retention of sodium and water, which then leads to the increase in blood volume.
  • There is a decrease in osmotic plasma pressure set by albumin which is produced by the liver. This is mainly caused by Kidney disease where albumin is excreted, meaning there is a reduction of flow through the kidney. Another disease that affects Osmotic pressure is Liver disease.  
  • There is blockage of the lymph flow retention of salt and water. Oedema is usually localized and because of an inflammatory response, either a neoplasm or obstruction (Scallan et al., 2010b).

Clinical note;

Acute Pulmonary Oedema 

This is a medical emergency resulting from ventricular failure. The blood returning to the heart from the lungs is slowed leading to a backup of blood back in the lungs, which results in congestion. This causes pressure in the capillaries to increase, due to increased blood volume. This then causes bleeding into the alveolar spaces. In pulmonary oedema the outlook is dependent on whether the treatment was immediate and the underlying cause. There are several conditions that contribute to heart-related pulmonary oedema. These include, pulmonary artery disease, unmanaged hypertension, congestive heart failure, some medications, kidney failure, and major injuries (Murray, 2011).

Left ventricular failure happens when there is dysfunction in the left ventricle causing insufficient delivery of oxygen to vital organs. The most common cause of left heart failure are coronary diseases and hypertension. Hypertension can cause left heart failure through left ventricular hypertrophy. Uncontrolled high blood pressure causes increased afterload which therefore increases cardiac workload. The hypertrophy seen in uncontrolled hypertension initially serves as a compensatory mechanism and can maintain cardiac output. But long term it can inhibit heart muscle relaxation leading to impaired cardiac filling. Which then reduces the cardiac output.  Hypertension also serves as a risk factors for coronary artery diseases. Other risk factors include; sedentary lifestyle, obesity, males are more at risk, and chronic anabolic steroid users. These risk factors are largely preventable hence risk factor control remains the most powerful way of preventing heart failure (Chahine & Alvey, 2020).

Cirrhosis of the liver is where healthy cells are replaced by scar tissue. The liver is then unable to perform vital functions of metabolism, production of proteins like albumin, blood clotting factors and filtering of toxins. Cirrhosis affects the normal flow of blood through the liver. This causes an increased pressure in the vein that brings blood to the liver from the intestines and the spleen. The increased pressure in the portal vein causes an accumulation of fluid in the legs and the abdomen. Portal hypertension can also cause blood to be redirected to the smaller veins. When these small veins are strained by pressure, they can burst leading to bleeding.   An increase in portal hypertension leads to the elevation of hydrostatic pressure. This causes the fluid to leak out into the interstitial spaces, this then leads to a decrease in plasma volume. The result is reduced kidney perfusion (Cirrhosis – Symptoms and Causes, 2019).

Management of Oedema

Treatment and management of fluid retention is dependent on the underlying cause. Management of oedema includes, a low salt diet, and adopting lifestyle changes in response to the underlying condition. For example, reducing alcohol intake and managing hypertension. Doctors can also use pharmacological therapies like diuretics and non-pharmacological interventions like compression stockings. Individuals can help themselves by exercising and eating healthy. This generally means making sure majority of your diet is fruits/vegetables and staying away from highly processed simple carbohydrates. Signs and symptoms of oedema include; a sudden unexplained weight gain, swollen stretched and shiny skin, puffiness of the ankles, face and eyes, tachycardia and blood pressure (Wu et al., 2017).


References

MacIver, D. H., & Clark, A. L. (2015). The vital role of the right ventricle in the pathogenesis of acute pulmonary oedema. The American journal of cardiology115(7), 992-1000.

Wilkins, M. R., Ghofrani, H. A., Weissmann, N., Aldashev, A., & Zhao, L. (2015). Pathophysiology and treatment of high-altitude pulmonary vascular disease. Circulation131(6), 582-590.

Welbourn, C. R. B., Goldman, G., Paterson, I. S., Valeri, C. R., Shepro, D., & Hechtman, H. B. (1991). Pathophysiology of ischaemia reperfusion injury: central role of the neutrophil. British Journal of Surgery78(6), 651-655.

Cadnapaphornchai, M. A., Tkachenko, O., Shchekochikhin, D., & Schrier, R. W. (2014). The nephrotic syndrome: pathogenesis and treatment of edema formation and secondary complications. Pediatric nephrology29(7), 1159-1167.

Choi, Y., Ju, S., & Chang, H. (2015). Food allergy knowledge, perception of food allergy labeling, and level of dietary practice: A comparison between children with and without food allergy experience. Nutrition research and practice9(1), 92-98.

Chahine, J., & Alvey, H. (2020). Left Ventricular Failure. In StatPearls. StatPearls Publishing. http://www.ncbi.nlm.nih.gov/books/NBK537098/

Cirrhosis—Symptoms and causes. (n.d.). Mayo Clinic. Retrieved May 29, 2020, from https://www.mayoclinic.org/diseases-conditions/cirrhosis/symptoms-causes/syc-20351487

Murray, J. F. (2011). Pulmonary edema: Pathophysiology and diagnosis. The International Journal of Tuberculosis and Lung Disease: The Official Journal of the International Union Against Tuberculosis and Lung Disease, 15(2), 155–160, i.

Scallan, J., Huxley, V. H., & Korthuis, R. J. (2010a). Pathophysiology of Edema Formation. In Capillary Fluid Exchange: Regulation, Functions, and Pathology. Morgan & Claypool Life Sciences. https://www.ncbi.nlm.nih.gov/books/NBK53445/

Scallan, J., Huxley, V. H., & Korthuis, R. J. (2010b). Pathophysiology of Edema Formation. In Capillary Fluid Exchange: Regulation, Functions, and Pathology. Morgan & Claypool Life Sciences. https://www.ncbi.nlm.nih.gov/books/NBK53445/

Wu, S. C., Crews, R. T., Skratsky, M., Overstreet, J., Yalla, S. V., Winder, M., Ortiz, J., & Andersen, C. A. (2017). Control of Lower Extremity Edema in Patients with Diabetes: Double Blind Randomized Controlled Trial Assessing the Efficacy of Mild Compression Diabetic Socks. Diabetes Research and Clinical Practice, 127, 35–43. https://doi.org/10.1016/j.diabres.2017.02.025

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