Lymph Formation PDF

LYMPH FORMATION Vascular Pathology and Physiotherapy: Unit 4 UNIT 4 LEARNING OBJECTIVES  To be able to describe lymph and it’s contents  To understand how lymph is formed- Starling’s Principle  To understand what oedema is  To be able to describe mechanical and dynamic oedema  To be able to...

LYMPH FORMATION Vascular Pathology and Physiotherapy: Unit 4 UNIT 4 LEARNING OBJECTIVES  To be able to describe lymph and it’s contents  To understand how lymph is formed- Starling’s Principle  To understand what oedema is  To be able to describe mechanical and dynamic oedema  To be able to describe potential causes of dynamic oedema  To be able to describe causes of mechanical lymphoedema  To be able to describe the classifications of lymphoedema, and sub classifications of primary lymphoedema  To be able to describe the potential causes of secondary lymphoedema  To be aware of lymphangitis and it’s pathophysiology LYMPH What do you remember about lymph? LYMPH Lymph is the fluid contained in the lymphatic vessels Typically, it is transparent or slightly yellow in colour, or white within the specialist lacteal vessels The contents of lymph: • Water (90% of its content) • Electrolytes • White Blood Cells • Protein molecules • Cell debris • Bacteria & Viruses • Lipids (chyle in lacteals) BUT HOW IS LYMPH FORMED?  Unlike the cardio vascular (CV) system, the lymphatic system is closed-ended, rather than circulating  So how is the lymphatic fluid formed?  The English Physiologist Starling investigated the forces causing fluid to filter from the arterial ends of CV capillaries, and be reabsorbed at the venous ends  Remaining fluid in the interstitial spaces is what enters the lymphatic capillaries to form lymph  But what were Starling’s findings and why is there an excess of fluid? KEY POINTS: Hydrostatic pressure Filtration Reabsorption Oncotic pressure STARLING’S PRINCIPLE- HYDROSTATIC PRESSURE Hydrostatic pressure= pressure exerted by fluid against membrane • Blood against capillary membrane • Generated by heart pumping blood, blood volume, arterial constriction/dilation • Highest at arteriole end of CV capillary • Much lower at venule end Arteriole end Venule end CV Capillary bed Opposing hydrostatic pressure also acts from interstitial fluid to capillary wall, but this is very small in measure and due to lymphatic uptake and skin extensibility, remains equal STARLING’S PRINCIPLE- ONCOTIC PRESSURE Oncotic pressure= type of osmotic pressure= Pressure drawing water towards solutes.  Larger protein molecules remain in CV capillaries e.g. albumin.  Oncotic pressure draws water into the capillaries, towards the larger molecules.  The concentration of larger molecules remains equal along the capillary bed, therefore the oncotic pressure remains equal Opposing oncotic pressure is also present in the interstitial fluid, but as the number of solutes is so small, it measures very small STARLING’S PRINCIPLE- NET MOVEMENT OF FLUID The pressures can be measured in mmHg, if we therefore add some figures to our pressure flows we can determine the net movement of fluid between CV capillaries and interstitial space 32mmHg 14mmHg 25mmHg 2mmHg Filtration V absorption 5mmHg 25mmHg 2mmHg 5mmHg STARLING’S PRINCIPLE- MOVEMENT OF FLUID AT ARTERIOLE END Filtration or absorption? Movement of fluid at arteriole end of capillary bed Movement into interstitial space= 32+5= 37mmHg Movement into CV capillary= 25+2= 27mmHg Difference= 10mmHg into the interstitial space = movement of fluid into interstitial space STARLING’S PRINCIPLE- MOVEMENT OF FLUID AT VENULE END Filtration or absorption? Movement of fluid at venule end of capillary bed Movement into interstitial space= 14+5= 19mmHg Movement into CV capillary= 25+2= 27mmHg Difference= 8mmHg into CV capillary =movement of fluid into CV capillary STARLING’S PRINCIPLE- NET MOVEMENT OF FLUID Pressure difference = 10mmHg into interstitial space Filtration > Reabsorption Pressure difference = 8mmHg into capillary Differences in pressures at arteriole end compared to venule end correlates to more fluid being filtrated than what is reabsorbed Arteriole end CV capillary bed Therefore, in normal circumstances, the fluid that is not reabsorbed is taken up by the lymphatic system This is approximately 3L of fluid per day Venule end The difference in filtration pressure compared to reabsorption pressure under normal circumstances is due to the hydrostatic pressure remaining higher than oncotic pressure for more than half the length of the capillary bed. So proportionately more fluid filters out of the CV capillary for longer than when proportionately more fluid reabsorbs in OTHER FACTORS AFFECTING MOVEMENT AND QUANTITY In the absence of pathology, movement and amount is also determined by: Extension of Starling’s Principle also highlights the impact of small molecules continuing to travel across the membrane. This leads to sustained oncotic movement preventing the pressures from ever being fully balanced. The quantity of fluid filtration is additionally affected by two factors: 1) The fluid permeability of the membrane 2) The solute permeability of the membrane So we have established that under normal conditions there is an excess of fluid that remains in the interstitial spaces following the process of filtration and reabsorption. So how does this excess fluid then enter the lymphatic system? THE UPTAKE OF FLUID INTO THE LYMPHATIC SYSTEM THE UPTAKE OF FLUID INTO THE LYMPHATIC SYSTEM The filaments attached to the edges of the capillary endothelial cells are tensioned when there is increased fluid in the interstitial spaces OEDEMA OEDEMA  In a normal situation, the net movement of fluid is into the interstitial spaces, which is then taken into the lymphatic system  However, disruption to this process leads to an excess of fluid in the interstitial spaces This is oedema TYPES OF OEDEMA Oedemas can be divided into one of two types Dynamic Insufficiency Mechanical Insufficiency DYNAMIC INSUFFICIENCY  Amount of fluid in interstitial spaces exceeds lymphatic transport capacity  Therefore, no pathology with lymphatic system  But pathology causing increase in fluid filtration and/or decrease in reabsorption  These causes can be acute or chronic  Chronicity may cause permanent changes to the normal transport system of fluid HIGH CAPILLARY PRESSURE 32 mmHg 30 mmHg High capillary pressure means hydrostatic pressure remains high throughout the capillary, so there is increased filtration at the venule end compared to normal Causes of high capillary pressure:  Right ventricular failure  Chronic venous insufficiency Normal values approx. 32mmHg 14mmHg  Deep vein thrombosis DECREASED PLASMA ONCOTIC PRESSURE Low oncotic pressure means there is less pull of fluid into the capillaries, meaning reabsorption is lower then normal Causes of decreased plasma oncotic pressure include: 15 mmHg 15 mmHg  Dietary deficiencies  Liver disease (causing decreased protein synthesis)  Kidney disease (causing nephrotic syndrome- proteins leaked into urine) Normal values approx. 25mmHg INCREASE IN CAPILLARY PERMEABILITY AND INCREASED INTERSTITIAL ONCOTIC PRESSURE Increased permeability of capillaries means larger solutes are able to leave the capillaries and enter the interstitial spaces. 15 mmHg 15 mmHg Causes of increased permeability are:  Trauma  Allergy  Acute infection  Lipoedema (increased tissue compliance) Normal values approx. 5mmHg  Pregnancy  Menstruation Levick JR. Revision of the Starling principle: new views of tissue fluid balance. J Physiol. 2004;557(Pt 3):704. doi:10.1113/jphysiol.2004.066118 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1665155/ TO BE CONTINUED.. https://www.lymphcareusa.com/professional/lymph-a-what/what-is-lymphedema/what-causeslymphedema.html https://emedicine.medscape.com/article/1087313-overview#a4 https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/starling-equation