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Lymphatic System Response to Trauma

Ask just about anyone with lymphedema about the relationship between trauma injury and the lymphatics and they will be quick to tell you that trauma causes edema and that sometimes the edema becomes permanent, which means lymphedema.

As one person recently wrote to me “…However, we already know that any traumatic injury to tissue containing lymphatics (including the lymphatics in bone marrow and possibly the Haversian canals of the bony formations themselves) will likely result in some kind of edemic response. There is almost always some kind of edema associated with the healing response (or Stage 1 Inflammatory response) which subsides on its own in time.”

But, why trauma causes lymphedema in some patients while not in others is an important question and consideration. Research being done today has focused on this in seeking an answer. The consensus that is emerging is that some individuals are born with an “at risk” lymphatic system.

Which means they may actually be genetically programmed for susceptibility towards lymphedema. All that is needed is the triggering event. When the individual with an at risk lymph system experiences trauma, the system becomes overloaded in its ability to cope with the additional fluids that are rushed to the injury site.

It is also important to have an understanding of the actuals mechanics of (and within) the lymph system as it responds to a trauma injury.


The pathomechanism of posttraumatic edema of lower limbs: I. The effect of extravasated blood, bone marrow cells, and bacterial colonization on tissues, lymphatics, and lymph nodes.

J Trauma. 2002 Feb

Szczesny G, Olszewski WL. Department of Surgical Research & Transplantology, Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.

BACKGROUND: The mechanical injury of soft tissues and bones of lower extremities is frequently followed by long-lasting edema at the site of trauma and distally. The pathomechanism of this complication remains unclear. Venous thrombosis and interruption of lymphatics are considered to be the main etiologic factors.

We propose a concept that protracted healing of injured tissues and bones with involvement of the regional lymphatic system (lymphatics and nodes) is responsible for persistence of edema. The events affecting the first (scavenging) phase of healing of traumatized tissues, such as hematoma, translocation of bone marrow cells to soft tissues, and colonization by microorganisms, and in particular their effects on lymphatics and lymph nodes, were studied.

METHODS: Mongrel dogs weighing 15-20 kg were used. Fresh blood or bone marrow cell (BMC) suspension was injected subcutaneously or intralymphatically into the paw. Strains of saprophyte bacteria residing on the skin surface were cultured and injected intradermally. Oil-contrast lymphography was performed before and after injections to evaluate the changes in lymphatics and nodes. Biopsy samples of paw skin, subcutaneous tissue, and regional lymph nodes (LN) were taken. The responsiveness of LN lymphocytes was studied in autologous mixed cultures with peripheral blood lymphocytes (PBL), BMC, and cultured bacteria.

RESULTS: The PBL from subcutaneously injected blood were evacuated by the lymphatic route at a rate of 1-3%/6 hr. There was no thrombosis of lymphatic vessels or obstruction of LN sinusoids. The BMC evoked major inflammatory changes in both the skin and the LN. Bacteria caused local inflammation, dilatation of lymphatics, and destruction of node parenchyma. Autologous BMC and PBL stimulated LN lymphocytes in a 6-day culture. The responsiveness of lymph node lymphocytes to previously subcutaneously injected bacterial antigens was increased.

CONCLUSION: The extravasated blood did not produce changes in skin, subcutaneous tissue, and lymphatics; however, it stimulated LN lymphocytes. The BMC and saprophyte bacteria caused major local and lymph node inflammatory response. All these factors may contribute to the local edema in the initial phases of healing of traumatized tissues.

Journal of Trauma

The pathomechanism of posttraumatic edema of the lower limbs: II--Changes in the lymphatic system.

J Trauma. 2003 Aug

Szczesny G, Olszewski WL. Department of Surgical Research and Transplantology, Medical Research Center, Polish Academy of Sciences, Warsaw, Poland.

BACKGROUND: The peripheral lymphatic system reacts to penetrating microorganisms and self-antigens released from tissues and cells damaged by trauma or intracellular pathogens. The response of regional lymph nodes to tissue trauma has not been thoroughly studied. We investigated the changes in lower limb lymphatics and nodes after fractures and soft tissue injuries. This type of injury is frequently complicated by limb edema. Posttraumatic edema of lower limbs is characterized by long-lasting swelling of the limb, erythema, and increased skin temperature at the site of injury. This suggests that a local inflammatory process is proceeding, even though the process of bone or soft tissue healing is considered to be completed.

METHODS: Twenty-one patients with closed lower limb bone fractures and soft tissues injuries were studied by means of isotope lymphography.

RESULTS: Dilated lymphatics of the entire limb were found in all patients, and 62% of them showed enlarged inguinal lymph nodes. Venous thrombosis was found in 24% of cases. There was no correlation between the degree of lymphatic dilatation, lymph node enlargement, and bone fracture or soft tissue injury or venous thrombosis. Surgical intervention was not an independent factor for lymph node enlargement.

CONCLUSION: This study has shown that although the fracture or injured tissues are clinically healed, local inflammatory reaction at the site of injury persists and cytokine signals are sent to the regional lymph nodes.

Journal of Trauma Injury, Infection and Critical Care

Post-traumatic lymphatic and venous drainage changes in persistent edema of lower extremities

Chir Narzadow Ruchu Ortop Pol. 2000

Szczesny G, Olszewski WL, Deszczyński J.

Oddział Ortopedyczno-Urazowy, Szpital Czerniakowski w Warszawie.

Mechanical injury of soft tissues and bones of the lower extremity is followed by chronic edema at the site of trauma and distally to it. This complication affects almost every patient with a fracture of the lower limb. The question is whether posttraumatic edema is due to lymphatic obstruction, venous thrombosis or both, or a local cytokine and growth factor hyperactivity at the fracture site. The aim of study was to assess the venous and lymph outflow in patient with chronic postraumatic edema of the lower limbs. A group of 19 patients with chronic edema lasting for more than 3 months was evaluated. Limb circumference, tissue tone measurements, skin temperature and Doppler enhanced ultrasonography were all taken down for the 19 patients in the evaluated group. Limb circumference was measured at the following level: foot, ankle, calf and thigh. Results showed an increase of circumference in comparison with the healthy extremity at each evaluated level of: 1.20 +/- 1.65 cm, 1.63 +/- 1.41 cm, 1.40 +/- 1.72 cm and 0.30 +/- 1.90 cm. Local temperature increase compared to the healthy extremity was also noted (0.93 +/- 0.81 degree C and 0.37 +/- 0.21 degree C measured at ankle and calf level). Tissue tone measurements and tone index (a quotient of tone measurement values in the extremity with edema and in the healthy extremity) were also increased by 0.86 +/- 0.57, 0.85 +/- 0.34 and 0.86 +/- 0.28, when measured with 40 g, 110 g and 180 g weights respectively. In 17 cases (89.5%) lymphoscintigraphy demonstrated an increased lymphatic outflow compared to the contralateral extremity. A marked increase in the inguinal lymph nodes was also noted. In the remaining 2 cases (10.5%) extravasation of the contrast medium into the skin indicated lymph outflow disorders. Only in 5 cases (26.3%) ultrasonography indicated deep vein thrombosis. The obtained results indicate that the pathophysiology of chronic postraumatic edema is linked with an inflammatory and restorative reaction at the fracture site. Only in a limited number of cases deep vein thrombosis and damaged lymphatic vessels are responsible for postraumatic edema.


Changes in the local blood and lymph microcirculation in response to direct mechanical trauma applied to leg: in vivo study in an animal model.

J Trauma. 2001 Sep

Szczesny G, Veihelmann A, Nolte D, Messmer K. Institute for Surgical Research, Department of Orthopedics, Klinikum Grosshadern, Ludwig-Maximilians-University, Munich, Germany.

BACKGROUND: The aim of this study was to investigate changes in the blood microcirculation of skin, subcutaneous tissue, and striated muscle, and the venous and lymphatic outflow from hind limb, after a standardized mechanical trauma.

METHODS: Trauma, defined as 50% of the minimal energy needed for tibia fracture (3.7 J/g), was applied to the leg of hairless mice. Intravenously injected fluorescein isothiocyanate-dextran 150 kDa and Rhodamine-6G were used for intra-vital fluorescence microscopy of blood vessels. Lymphatics were stained with fluorescein isothiocyanate-dextran injected into the footpad. A computer-assisted analysis system allowed measurement of the functional capillary density (FCD), vessel diameters, velocity of blood flow, and edema value expressed as extravasation index (EV). The percentage of slowly rolling and sticking leukocytes in postcapillary venules was estimated.

RESULTS: At the site of injury, trauma resulted in significant reduction of FCD in skin, subcutaneous tissue, and striated muscle. There were no significant differences in the vessel diameter (skin subcutaneous and muscle arterioles and venules, and superficial saphenous artery and vein) or velocity of blood flow (subcutaneous tissue and muscle venules). The EV increased significantly in muscle venules and was higher in muscles, subcutaneous tissue, and superficial saphenous veins than in controls (nonsignificantly). An increased percentage of slowly rolling and sticking leukocytes was noted in the superficial saphenous vein at the site of injury and proximal to it. The lymphatics remained patent, with faster visualization and increased summarized cross-sectional areas in traumatized extremities.

CONCLUSION: Early changes occurring in soft tissues in response to mechanical injury were characterized by reduction in FCD of skin and muscles, and less in subcutis; increased EV, reflecting leakage of macromolecules; increased percentage of slowly rolling and sticking leukocytes; maintenance of lymphatic vessel continuity; and increased lymph formation and flow rate.

Journal of Trauma Injury, Infection and Critical Care

Lymphoscintigraphic monitoring of the lower limb lymphatic system response to bone fracture and healing.

Lymphat Res Biol. 2005

Szczesny G, Olszewski WL, Gorecki A. Department of Surgical Research, Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.

Closed bone fractures, and torn muscles and tendons are “internal wounds”. What kind of reaction do they evoke in the local and systemic immune system? Cellular debris of damaged tissue and extravasated blood cells are removed by scavenger cells. They are transported via lymphatics to the lymph nodes. There elimination of self antigens takes place. Clinically, no enlargement of lymph nodes is observed after closed fractures and soft tissue damage. The question arises whether there is really no enlargement of regional lymph nodes, in other words, no reaction to damaged cell antigens. This question was studied by using lymphoscintigraphy to visualize lymphatics and lymph nodes draining the site of closed bone fracture. The lymphoscintigraphic pictures of two groups of patients, those with a rapid noncomplicated healing of leg fractures, and those with protracted healing and undergoing surgical reconstructions, were evaluated. The surface area of lymphatic pathways and inguinal lymph nodes on the injured and contralateral normal limb were measured. Enlarged superficial lymphatics and inguinal lymph nodes were found in limbs with healed bone fractures, and decreased inguinal lymph nodes and visualization of deep lymphatics and popliteal nodes in the majority of patients with nonhealing fractures. There was a lack of correlation between age of patients, duration of healing, and surgical interventions and the lymphoscintigraphic changes.

Mary Ann Liebert Inc

Related External Links

The role of lymph factors in lung injury, bone marrow suppression, and endothelial cell dysfunction in a primate model of trauma-hemorrhagic shock.

Gut-lymph hypothesis of systemic inflammatory response syndrome/multiple-organ dysfunction syndrome: validating studies in a porcine model.

A study of the biologic activity of trauma-hemorrhagic shock mesenteric lymph over time and the relative role of cytokines.

Trauma/hemorrhagic shock mesenteric lymph upregulates adhesion molecule expression and IL-6 production in human umbilical vein endothelial cells.

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