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• W1998004700 abstract "The lymphatic system is known to perform three major functions in the body: drainage of excess interstitial fluid and proteins back to the systemic circulation; regulation of immune responses by both cellular and humoral mechanisms; and absorption of lipids from the intestine. Lymphatic disorders are seen following malignancy, congenital malformations, thoracic and abdominal surgery, trauma, and infectious diseases. They can occasionally cause mortality, and frequently morbidity and cosmetic disfiguration. Many lymphatic disorders are encountered in the operating theatre and critical care settings. Disorders of the lymphatic circulation relevant to anaesthesia and intensive care medicine are discussed in this review. The lymphatic system is known to perform three major functions in the body: drainage of excess interstitial fluid and proteins back to the systemic circulation; regulation of immune responses by both cellular and humoral mechanisms; and absorption of lipids from the intestine. Lymphatic disorders are seen following malignancy, congenital malformations, thoracic and abdominal surgery, trauma, and infectious diseases. They can occasionally cause mortality, and frequently morbidity and cosmetic disfiguration. Many lymphatic disorders are encountered in the operating theatre and critical care settings. Disorders of the lymphatic circulation relevant to anaesthesia and intensive care medicine are discussed in this review. Exchange of fluid and movement of macromolecules across the systemic capillaries are governed by Starling forces and capillary permeability. In healthy tissues, small volumes of fluid are filtered continuously into the interstitial tissues. The lymphatic circulation forms an accessory pathway to return this excess fluid and proteins from the tissue spaces back to the blood stream. This fluid is called lymph. Lymph contains a large number of lymphocytes, macrophages, and small amounts of plasma proteins including coagulation factors. The lymphatic circulation starts from blind-ended lymphatic capillaries and ends at the subclavian veins. In disease states with altered Starling forces and increased capillary permeability, the amount of fluid filtered out of the systemic capillaries may greatly increase in volume and overwhelm this system to produce oedema. Disturbances of the lymph circulation are less well recognized than those of the arterial and venous circulation. The lymphatic vessels, unlike the arteries and veins, are not easily seen during dissection or surgery.66Witte CL Witte MH Unger EC et al.Advances in imaging of lymph flow disorders.Radiographics. 2000; 20: 1697-1719Crossref PubMed Scopus (137) Google Scholar Damage to the lymphatics is generally not followed by any obvious immediate consequences and it is often believed that they are expendable in surgical practice. In the clinical setting, lymphatic pathways can be disrupted by many different causes including congenital anomalies, infection, malignancy, radiation, surgery, and trauma. The effects of blockage/leakage become problematic when the usual compensatory mechanisms are overwhelmed. In the human body the lymphatic system is organized in the form of lymphatic vessels, lymph nodules, and nodes. The lymphatic vessels begin as blind-ended lymphatic capillaries. They branch and interconnect freely and extend into almost all tissues in parallel with systemic capillaries, with the exception of the central nervous system, eyes, and certain cartilaginous structures. These anatomical areas have other forms of fluid circulation, in the form of the cerebrospinal fluid, aqueous and vitreous humour, and the synovial fluid of joints respectively. Lymphatic capillaries join to form lymph venules and veins that drain via regional lymph nodes into the thoracic duct on the left side or the right lymphatic duct. The lymph from the major portion of the body flows through the thoracic duct while that from the right upper quadrant drains into the right lymphatic duct. The lymphatic circulation is devoid of any central pump. Lymph flow depends, predominantly, on local pressure effects and intrinsic contraction of the larger lymphatics. Any factor that increases the interstitial tissue pressure by 2 mm Hg tends to increase lymph flow in lymphatic vessels. Conversely, if the interstitial tissue pressure is greater than 2 mm Hg above atmospheric pressure, then lymph flow may decrease as a result of compression of the lymphatic vessels. The anterograde flow of lymph is further facilitated by the presence of numerous microscopic and macroscopic bi-leaflet valves, which exist at least every few millimetres to prevent retrograde flow. To achieve a continuous local lymph output, external intermittent compression of the lymphatics is essential from: (i) contraction of muscles; (ii) movement of body parts; (iii) arterial pulsations; and (iv) compression of the tissues by forces outside the body. Lymph veins have contractile smooth muscles and the segment of the vessel between successive valves is called a lymphangion. The lymphangion contracts when it is stretched with lymph and empties proximally into successive lymphangions. The contraction of a lymphangion can generate a pressure as high as 25 mm Hg. The exact mechanisms of lymphatic smooth muscle contractility are unclear. Sympathomimetic agents,42McHale NG Roddie IC The effects of intravenous adrenaline and noradrenaline infusion on peripheral lymph flow in the sheep.J Physiol. 1983; 341: 517-526Crossref PubMed Scopus (29) Google Scholar including alpha and beta agonists, appear to mediate lymphatic truncal contraction, as do the by-products of arachidonic acid including thromboxane and prostaglandins.30Johnston MG Gordon JL Regulation of lymphatic contractility by arachidonate metabolites.Nature. 1981; 293: 294-297Crossref PubMed Scopus (85) Google Scholar There is evidence for the presence of G proteins, adenyl cyclase, and phospholipase C activities in lymphatic smooth muscle cell membranes.31Kelly J Brazil D Clyne C et al.Evidence for the presence of G-proteins, adenyl cyclase and phospholipase C activities in lymphatic smooth muscle cell membrane.Cell Signal. 1996; 8: 425-432Crossref PubMed Scopus (4) Google Scholar Lymphatic endothelial cells produce nitric oxide,48Ohhashi T Takahashi N Acetylcholine-induced release of endothelium-derived relaxing factor from lymphatic endothelial cells.Am J Physiol. 1991; 260: H1172-H1178PubMed Google Scholar that in turn relaxes lymphatic smooth muscles, via accumulation of guanosine 3′, 5′ cyclic monophosphate. Angiotensin II65Valenzuela GJ Hewitt CW Graham AD Angiotensin II infusion increases thoracic duct lymph flow in chronically catheterized sheep.Am J Physiol. 1987; 252: R853-R858PubMed Google Scholar appears to increase lymph flow by a direct effect on lymphatic vessels, while 5-hydroxytryptamine43McHale NG Thornbury KD Hollywood MA 5HT inhibits spontaneous contractility of isolated sheep mesenteric lymphatics via activation of 5HT4 receptors.Microvasc Res. 2000; 60: 261-268Crossref PubMed Scopus (17) Google Scholar has an opposite action by inhibiting spontaneous contractility. The contractility of the mesenteric lymphatics is suppressed in a dose-dependent manner by halothane.17Elk JR Adair T Drake RE Gabel JC The effect of anaesthesia and surgery on diaphragmatic lymph vessel flow after endotoxin in sheep.Lymphology. 1990; 23: 145-148PubMed Google Scholar 57Takeshita T Morio M Kawahara M Fujii K Halothane-induced changes in contractions of mesenteric lymphatics of the rat.Lymphology. 1988; 21: 128-130PubMed Google Scholar The effects of other anaesthetic agents are not known. Stimulation of the greater splanchnic nerve (sympathetic) appears to increase lymphangion contractility and lymph flow.62Thornbury KD Harty HR McGeown JG McHale NG Mesenteric lymph flow response to splanchnic nerve stimulation in sheep.Am J Physiol. 1993; 264: H604-H610PubMed Google Scholar It has been shown that increased sympathetic activity gives rise to peripheral lymphoedema, which shows improvement after sympathectomy. This has been proposed to be one mechanism for reflex sympathetic dystrophy and its treatment.28Howarth D Burstal R Hayes C Lan L Lantry G Autonomic regulation of lymphatic flow in the lower extremity demonstrated on lymphoscintigraphy in patients with reflex symphathetic dystrophy.Clin Nuclear Med. 1999; 24: 383-387Crossref PubMed Scopus (34) Google Scholar In the thoracic duct, lymph flow is dependent on: (i) pressure gradients generated by contractile elements in the lymphatics; (ii) the intrathoracic pressure; and (iii) the venous backpressure in the subclavian vein. These interactions have not been studied in any detail, compared with the large amount of work on ventilatory/circulatory interactions in venous and arterial systems. PEEP and positive pressure ventilation appear to increase lymph flow through the thoracic duct. Conversely, excessively high intrathoracic pressure and a high PEEP can impede the thoracic duct flow both by direct pressure on the duct and venous hypertension.24Haider M Schad H Mendler N Thoracic duct lymph and PEEP studies in anaesthetized dogs. I. Lymph formation and the effect of a thoracic duct fistula on lymph flow.Intensive Care Med. 1987; 13: 183-191Crossref PubMed Scopus (9) Google Scholar Lymphatic outflow and pumping have been shown to increase in the setting of hypovolaemic shock in order to restore the blood volume.38Magnotti LJ Upperman JS Xu DZ Lu Q Deitch EA Gut-derived mesenteric lymph but not portal blood increases endothelial cell permeability and potentiates lung injury following hemorrhagic shock.Ann Surg. 1998; 228: 518-527Crossref PubMed Scopus (371) Google Scholar After major burn injury, lymph flow from the injured area increases and transports a large amount of hyaluronan, a connective tissue component of the interstitial matrix.49Onarheim H Brofeldt BT Gunther RA Markedly increased lymphatic removal of hyaluronan from skin after major thermal injury.Burns. 1996; 22: 212-216Abstract Full Text PDF PubMed Scopus (9) Google Scholar Clinical and radiological studies have demonstrated markedly raised thoracic duct flow, with gross dilatation and increased pressures, in patients with cirrhosis. It is not understood whether such changes are a cause or secondary effect of the underlying pathology. Chyle is a mixture of lymph and chylomicrons from intestinal lymphatics. It is normally found in the mesenteric lymphatics, the cisterna chili, and the thoracic duct. The presence of chylomicrons gives chyle its milky white colour. Its characteristics and composition are shown in Table 1.59Teba L Dedhia HV Bowen R Alexander JC Chylothorax review.Crit Care Med. 1985; 13: 49-52Crossref PubMed Scopus (72) Google Scholar Chyle normally forms three layers on standing: a creamy top layer, a milky middle layer, and cellular sediment (Fig. 1). It may clot over time. Chyle is strongly bacteriostatic and rarely becomes infected. It contains a large number of lymphocytes without any leukocytes.Table 1Features of chyleCharacteristics Milky appearance Alkaline pH: 7.4–7.8 Specific gravity: 1012–1025 Sterile Fat globules Lymphocytes, principally T cells: 400–7000 mm−3Composition Total protein: 20–40 g litre−1 Albumin: 10–30 g litre−1 Globulin: 10–15 g litre−1 Fibrinogen: 150–250 mg litre−1 Total fat: 10–60 g litre−1 Triglycerides > plasma level (pleural: plasma ratio >1) Cholesterol < plasma values (pleural:plasma ratio <1) Chylomicrons (lipoprotein electrophoresis) Cholesterol/triglyceride ratio <1 Glucose: 2–11 mmol litre−1 Urea: 1–3 mmol litre−1 Electrolytes = plasma values, except low calcium content Presence of pancreatic exocrine enzymes Open table in a new tab Normal chyle flow in the thoracic duct of an adult is about 1500–2500 ml day−1. Daily chyle output varies with the level of activity, bowel function, and the fat content of the diet. It can be as low as 10–15 ml h−1 during periods of immobility, starvation, and continuous nasogastric suction, but it can markedly increase after a meal rich in long chain triglycerides. Normally, the liver contributes one-third of the lymph flow in the thoracic duct in a resting adult. Varying the pressure within the thoracic duct can alter each organ's contribution to thoracic duct flow and thereby affect the composition of chyle. A raised pressure in the thoracic duct can decrease the lymph flow out of the gut without much effect on the hepatic lymph flow. Oedema results when tissue fluid accumulates faster than the lymphatic system can remove it. Ascites, pleural, and pericardial effusions are localized fluid collections formed by similar mechanisms. Most clinical presentations of oedema are thought to be due, primarily, to disturbances in the arterial or venous circulation, for example the pulmonary oedema seen in heart failure or ARDS. The role of the lymphatics in such disorders has not been well studied clinically because of inherent difficulties in measuring lymph flow. Pulmonary lymph flow has been shown to increase in animal models of ARDS, and has been used as an index of alveolar-capillary membrane permeability. Lymphatic endothelial cells appear to be affected by the inflammatory process, and histology of lungs from patients with ARDS has shown a marked disruption of lymphatic as well as pulmonary capillaries.63Tomashefski jr, JF Davies P Boggis C Greene R Zapol WM Reid LM The pulmonary vascular lesions of the adult respiratory distress syndrome.Am J Pathol. 1983; 112: 112-126PubMed Google Scholar Lymphatic damage may therefore have a role in the pathogenesis of the interstitial oedema of ARDS. Widespread tissue oedema is common in critically ill patients. Multiple factors are involved including increased systemic capillary permeability, alterations in plasma oncotic forces, and altered lymphatic transport. The exact role of the lymphatics is uncertain. A significantly raised intrathoracic pressure in mechanically ventilated critically ill patients can increase the impedance to lymph flow in the thoracic duct and other larger lymphatics. In addition, alterations in lymphangion contractility and lymphatic capillary permeability may be important in critically ill patients. Lymphoedema is defined as accumulation of lymph in the extracellular space as a result of lymphatic block or dysfunction. Many cases follow chronic lymphatic obstruction but it can develop acutely in any organ following surgery. The early oedema seen in surgically transposed free flaps, or transplanted visceral organs, for example bowel, lungs, and heart, is in part a result of accumulation of lymph as a result of transected lymphatics.55Schmid T Korozsi G Klima G Oberhuber G Margreiter R Regeneration of lymph drainage following transplantation of small intestine.Langenbecks Archiv Chirurgie. 1989; 374: 299-322Crossref PubMed Scopus (4) Google Scholar Surgeons usually make no attempt to anastomose lymphatic vessels during such procedures. Acute lymphoedema has been shown to affect the heart and lungs following thoracic surgery. It can depress myocardial function and cause pulmonary hypertension as a result of perivascular oedema.12Cui Y Urschel JD Petrelli NJ The effect of cardiopulmonary lymphatic obstruction on heart and lung function.Thorac Cardiovasc Surg. 2001; 49: 35-40Crossref PubMed Scopus (26) Google Scholar 37Ludwig LL Schertel ER Pratt JW et al.Impairment of left ventricular function by acute cardiac lymphatic obstruction.Cardiovasc Res. 1997; 33: 164-171Crossref PubMed Scopus (42) Google Scholar Acute lymphoedema typically settles over a few days and studies have shown early restoration of lymphatic collaterals. Chronic lymphoedema is usually seen as a complication of radical cancer surgery or radiotherapy in the Western world. In tropical and subtropical countries, filariasis, a parasitic infection, is responsible for lymphoedema in more than 90 million people. Lymph slowly accumulates in the tissues distal to the site of damage over weeks, months or years. In the initial stage the oedema is soft, pitting and temporarily reduced by elevation and a compression bandage (Fig. 2). Pain may occur from stretching of soft tissues and be related to conditions such as infection, thrombosis, and nerve entrapment syndromes. If left untreated, an inflammatory state develops with collagen deposition and soft tissue overgrowth. At this stage, the tissue becomes less pitting, more firm or brawny, and elevation of the limb no longer results in reduction of the oedema.10Cohen SR Payne DK Tunkel RS Lymphedema: strategies for management.Cancer. 2001; 92: 980-987Crossref PubMed Google Scholar Superimposed occult or overt infection (lymphangitis) commonly contributes to progressive limb deformity and elephantiasis (Fig. 3).Fig 3Late trophic changes in a leg following longstanding lymphoedema. So called ‘Elephantiasis’. Photograph, with patient permission, courtesy of lymphoedema service, Cookridge Hospital, Leeds.View Large Image Figure ViewerDownload (PPT) Early diagnosis is essential to prevent worsening of the condition and to help relieve the psychological impact of the disease. There is no effective drug treatment. Current options include education of patients in prevention of infection, limb positioning, exercise, compression garments and bandages, pneumatic pumps, and lymphatic massage.10Cohen SR Payne DK Tunkel RS Lymphedema: strategies for management.Cancer. 2001; 92: 980-987Crossref PubMed Google Scholar Prevention of acute inflammation including lymphangitis and cellulitis is crucial as the swelling tends to worsen after each episode. Surgery is occasionally undertaken to de-bulk excessive tissue or to bypass local lymphatic defects by lympho-venous anastomosis, in patients with severe deformity. During anaesthesia, neither arterial nor venous cannulation should be attempted in the lymphoedematous limbs. Non-invasive measurement of arterial pressure is often not possible. Protein-based drugs are broken down when administered by the enteral route and therefore have poor bioavailabilty. Therefore, the s.c. or i.m. route is widely used for delivery of protein drugs. The lymphatics are responsible for the absorption of subcutaneously or intramuscularly injected protein drugs including certain vaccines, human growth hormone and insulin.9Charman SA McLennan DN Edwards GA Porter CJ Lymphatic absorption is a significant contributor to the subcutaneous bioavailability of insulin in a sheep model.Pharm Res. 2001; 18: 1620-1626Crossref PubMed Scopus (59) Google Scholar These drugs are not absorbed by the systemic capillaries because of their large molecular size. Liposomes, injected subcutaneously, can potentially act as carriers for the delivery of therapeutic and diagnostic agents for lymphatic disorders.50Oussoren C Storm G Liposomes to target the lymphatics by subcutaneous administration.Adv Drug Deliv Rev. 2001; 23: 143-156Crossref Scopus (290) Google Scholar Liposomes, on reaching the lymph nodes, will be phagocytosed by the macrophages, releasing the drugs to be concentrated in the lymph nodes. This route of administration may prove useful in the treatment of metastatic malignancies and parasitic infestations including filariasis. Some oral medications including digoxin may also be absorbed by the mesenteric lymphatics. In a recent case report, a patient who was receiving oral digoxin developed an unrelated chylothorax. The patient's plasma digoxin concentration was measured as near to zero, but that in chyle, collected from the chylothorax, was at therapeutic levels.58Taylor MD Kim SS Vaias LJ Therapeutic digoxin level in chylous drainage with no detectable plasma digoxin level.Chest. 1998; 114: 1482-1484Abstract Full Text Full Text PDF PubMed Scopus (6) Google Scholar It is not known which other medications are absorbed via the mesenteric lymphatics into the systemic circulation. Lymphatics play a major role in systemic dissemination of toxins in cases of snake and spider bites.29Howarth DM Southee AE Whyte IM Lymphatic flow rates and first-aid in simulated peripheral snake or spider envenomation.Med J Aust. 1994; 161: 695-700PubMed Google Scholar Firm pressure bandaging is an effective means of restricting the lymphatic transport of toxins, provided the bandage is applied within a defined pressure range of 5–9 kPa. Strict limb immobilization is necessary to minimize lymphatic flow, and walking after upper or lower limb envenomation will inevitably result in systemic envenomation despite other first-aid measures.29Howarth DM Southee AE Whyte IM Lymphatic flow rates and first-aid in simulated peripheral snake or spider envenomation.Med J Aust. 1994; 161: 695-700PubMed Google Scholar Recently, there has been an increase in the understanding of the gut mucosal barrier, and the pathophysiology of sepsis and multiple organ dysfunction, beyond the original description of bacterial translocation. Bacterial translocation has been shown to occur in animal models but data from human studies are less convincing.13Deitch EA Role of the gut lymphatic system in multiple organ failure.Curr Opin Crit Care. 2001; 7: 92-98Crossref PubMed Scopus (222) Google Scholar Recent work failed to demonstrate any bacteria or endotoxin in the portal blood, mesenteric lymph, and chyle in patients with multiple organ dysfunction secondary to sepsis or multiple trauma.36Lemaire JC van Lanschot JB Stoutenbeck CP et al.Thoracic duct in patients with multiple organ failure: no major route of bacterial translocation.Ann Surg. 1999; 229: 128-136Crossref PubMed Scopus (66) Google Scholar 47Moore FA Moore EE Pogetti R et al.Gut bacterial translocation via the portal vein: a clinical perspective with major torso trauma.J Trauma. 1991; 31: 629-638Crossref PubMed Scopus (447) Google Scholar 54Sanchez-Garcia M Prieto A Tejedor A et al.Characteristics of thoracic duct lymph in multiple organ dysfunction syndrome..Arch Surg. 1997; 132: 13-18Crossref PubMed Scopus (30) Google Scholar New reports suggest that mesenteric lymph has a significant role in the generation of remote organ injury in the presence of dysfunctional gut.13Deitch EA Role of the gut lymphatic system in multiple organ failure.Curr Opin Crit Care. 2001; 7: 92-98Crossref PubMed Scopus (222) Google Scholar 46Moore EE Mesenteric lymph: the critical bridge between dysfunctional gut and multiple organ failure.Shock. 1998; 10: 415-416Crossref PubMed Scopus (21) Google Scholar Shock, trauma or sepsis-induced gut injury can result in the generation of cytokines and other pro-inflammatory mediators in the gut.39Magnotti LJ Xu DZ Lu Q et al.Gut-derived mesenteric lymph: a link between burn and lung injury.Arch Surg. 1999; 143: 1333-1341Crossref Scopus (128) Google Scholar Mesenteric lymph appears to be the route of delivery of inflammatory mediators from the gut to remote organs.38Magnotti LJ Upperman JS Xu DZ Lu Q Deitch EA Gut-derived mesenteric lymph but not portal blood increases endothelial cell permeability and potentiates lung injury following hemorrhagic shock.Ann Surg. 1998; 228: 518-527Crossref PubMed Scopus (371) Google Scholar 45Montravers P Chollet-Martin S Marmuse JP Gougerot-Pocidalo MA Desmonts JM Lymphatic release of cytokines during acute lung injury complicating severe pancreatitis.Am J Respir Crit Care Med. 1995; 152: 1527-1533Crossref PubMed Scopus (86) Google Scholar These toxic mediators have been demonstrated in mesenteric lymph,45Montravers P Chollet-Martin S Marmuse JP Gougerot-Pocidalo MA Desmonts JM Lymphatic release of cytokines during acute lung injury complicating severe pancreatitis.Am J Respir Crit Care Med. 1995; 152: 1527-1533Crossref PubMed Scopus (86) Google Scholar but not in the systemic or portal circulation. Acute lung injury,33Koike K Moore EE Moore FA et al.Gut ischemia/reperfusion produces lung injury independent of endotoxin.Crit Care Med. 1994; 22: 1438-1444Crossref PubMed Scopus (128) Google Scholar endothelial damage,63Tomashefski jr, JF Davies P Boggis C Greene R Zapol WM Reid LM The pulmonary vascular lesions of the adult respiratory distress syndrome.Am J Pathol. 1983; 112: 112-126PubMed Google Scholar haemopoietic failure,3Anjaria DJ Rameshwar P Deitch EA et al.Haematopoietic failure after hemorrhagic shock is mediated partially through mesenteric lymph.Crit Care Med. 2001; 29: 1780-1785Crossref PubMed Scopus (40) Google Scholar and activation of white cells,2Adams JM Hauser CJ Adams jr, CA et al.Entry of gut lymph into the circulation primes rat neutrophil respiratory burst in hemorrhagic shock.Crit Care Med. 2001; 29: 2194-2198Crossref PubMed Scopus (66) Google Scholar 22Ganzalez RJ Moore EE Ciesla DJ et al.Mesenteric lymph is responsible for post-hemorrhagic shock systemic neutrophil priming.J Trauma. 2001; 51: 1069-1072PubMed Google Scholar 64Upperman JS Deitch EA Guo W Lu Q Xu D Post-hemorrhagic shock mesenteric lymph is cytotoxic to endothelial cells and activates neutrophils.Shock. 1998; 10: 407-414Crossref PubMed Scopus (98) Google Scholar 68Zallen G Moore EE Ciesla DJ et al.Lipids from post-shock mesenteric lymph are responsible for systemic neutrophil priming.Surg Forum. 1999; 50: 240-242Google Scholar 69Zallen G Moore EE Johnson JL et al.Post hemorrhagic shock mesenteric lymph primes circulating neutrophils and provokes gut injury.J Surg Res. 1999; 83: 83-88Abstract Full Text PDF PubMed Scopus (100) Google Scholar have been shown to be caused by these toxic products carried in mesenteric lymph. Division or ligation of lymphatics in the gut mesentery before induction of shock prevents the increase in lung permeability and limits shock-induced pulmonary neutrophil recruitment.1Adams jr, CA Sambol JT Xu DZ Lu Q Granger DN Deitch EA Hemorrhagic shock induced up-regulation of P-selectin expression is mediated by factors in mesenteric lymph and blunted by mesenteric duct interruption.J Trauma. 2001; 51: 625-631Crossref PubMed Scopus (41) Google Scholar 14Deitch EA Adams CA Lu Q Xu DZ A time course study of the protective effect of mesenteric lymph duct ligation on hemorrhagic shock-induced pulmonary injury and the toxic effects of lymph from shocked rats on endothelial cell monolayer permeability.Surgery. 2001; 129: 39-47Abstract Full Text Full Text PDF PubMed Scopus (127) Google Scholar 53Sambol JT Xu DZ Adams CA Magnotti LJ Deitch EA Mesenteric lymph duct ligation provides long term protection against hemorrhagic shock-induced lung injury.Shock. 2000; 14: 416-420Crossref PubMed Scopus (61) Google Scholar Thoracic duct drainage has been proposed as a means of removing these substances before they reach the pulmonary and systemic circulation. Preliminary trials in patients with pancreatitis were promising in reducing the severity of acute lung injury.16Dugernier T Reynaert MS Deby-Dupont G et al.Prospective evaluation of thoracic-duct drainage in the treatment of respiratory failure complicating severe acute pancreatitis.Intensive Care Med. 1989; 15: 372-378Crossref PubMed Scopus (45) Google Scholar This may be because the lung is the first organ exposed to mesenteric lymph. Further work needs to be performed in this area before recommending this approach for clinical use. Sentinel node biopsy is increasingly performed to decide whether a patient requires a regional lymph node clearance following removal of breast or other cancers.5Bass SS Cox CE Ku NN Berman C Reintgen DS The role of sentinel lymph node biopsy in breast cancer.J Am Coll Surg. 1999; 189: 183-194Abstract Full Text Full Text PDF PubMed Scopus (202) Google Scholar The sentinel node is the first node to receive lymph from a primary tumour and therefore the most likely to have metastatic cells.4Allan R Sentinel nodal localization: do or dye alone?.Br J Radiol. 2001; 74: 475-477Crossref PubMed Scopus (3) Google Scholar A blue dye or a radioactive compound is injected around the primary tumour and becomes concentrated in the sentinel node to help in its identification. Anaesthetists should be aware of some practical implications of this procedure.8Cashman JN Sentinel lymph node biopsy: anaesthetic implications.Eur J Anaesthesiol. 2001; 18: 273-275Crossref PubMed Google Scholar Patent V dye absorbs light wavelength at 640 nm, which corresponds to the wavelength of red light used in pulse oximeters. When this dye ultimately reaches blood, the percentage of deoxygenated haemoglobin is overestimated, that is the pulse oximeter reads a lower SpO2 than the actual value.52Saito S Fukura H Shimada H Fujita T Prolonged interference of patent blue with pulse oximeter readings.Acta Anaesthesiol Scand. 1995; 39: 268-269Crossref PubMed Scopus (31) Google Scholar This decrease in SpO2 reading can occur between 30 s to 20 min following injection, and can last several hours.8Cashman JN Sentinel lymph node biopsy: anaesthetic implications.Eur J Anaesthesiol. 2001; 18: 273-275Crossref PubMed Google Scholar 52Saito S Fukura H Shimada H Fujita T Prolonged interference of patent blue with pulse oximeter readings.Acta Anaesthesiol Scand. 1995; 39: 268-269Crossref PubMed Scopus (31) Google Scholar Arterial blood gas analysis is recommended during the procedure. There are reports of other adverse reactions to patent V dye including: anaphylactic and anaphylactoid reactions;67Woltsche-Kahr I Komericki P Kranke B et al.Anaphylactic shock following peritumoural injection of patent blue in sentinel node biopsy procedure.Eur J Surg Oncol. 2000; 26: 313-314Abstract Full Text PDF PubMed Scopus (53) Google Scholar discolouration of urine; and tattooing of skin around the injection site.8Cashman JN Sentinel lymph node biopsy: anaesthetic implications.Eur J Anaesthesiol. 2001; 18: 273-275Crossref PubMed Google Scholar Disorders associated with the lymphatic system are principally" @default.
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• W1998004700 title "Disorders of the lymph circulation: their relevance to anaesthesia and intensive care" @default.
• W1998004700 cites W1558643593 @default.
• W1998004700 cites W1965241527 @default.
• W1998004700 cites W1967776204 @default.
• W1998004700 cites W1969569886 @default.
• W1998004700 cites W1971773090 @default.
• W1998004700 cites W1975058996 @default.
• W1998004700 cites W1975165725 @default.
• W1998004700 cites W1982764059 @default.
• W1998004700 cites W1984345127 @default.
• W1998004700 cites W1985443137 @default.
• W1998004700 cites W1989432109 @default.
• W1998004700 cites W1991634495 @default.
• W1998004700 cites W1992444509 @default.
• W1998004700 cites W1993687308 @default.
• W1998004700 cites W1998058562 @default.
• W1998004700 cites W2003319473 @default.
• W1998004700 cites W2004549381 @default.
• W1998004700 cites W2007100753 @default.
• W1998004700 cites W2015575081 @default.
• W1998004700 cites W2018205808 @default.
• W1998004700 cites W2020173715 @default.
• W1998004700 cites W2020518984 @default.
• W1998004700 cites W2022632404 @default.
• W1998004700 cites W2027134056 @default.
• W1998004700 cites W2027556932 @default.
• W1998004700 cites W2028073449 @default.
• W1998004700 cites W2028898179 @default.
• W1998004700 cites W2034330198 @default.
• W1998004700 cites W2036053143 @default.
• W1998004700 cites W2036530108 @default.
• W1998004700 cites W2040527099 @default.
• W1998004700 cites W2041153276 @default.
• W1998004700 cites W2047317813 @default.
• W1998004700 cites W2053522978 @default.
• W1998004700 cites W2055465979 @default.
• W1998004700 cites W2059682888 @default.
• W1998004700 cites W2067107760 @default.
• W1998004700 cites W2072824771 @default.
• W1998004700 cites W2073744836 @default.
• W1998004700 cites W2074288792 @default.
• W1998004700 cites W2077287220 @default.
• W1998004700 cites W2081789917 @default.
• W1998004700 cites W2082140396 @default.
• W1998004700 cites W2085910914 @default.
• W1998004700 cites W2089538444 @default.
• W1998004700 cites W2104323690 @default.
• W1998004700 cites W2137193137 @default.
• W1998004700 cites W2156985039 @default.
• W1998004700 cites W2165407126 @default.
• W1998004700 cites W2187115695 @default.
• W1998004700 cites W2194461370 @default.
• W1998004700 cites W2292536157 @default.
• W1998004700 cites W2333191486 @default.
• W1998004700 cites W2335224921 @default.
• W1998004700 cites W2440183640 @default.
• W1998004700 cites W4242961528 @default.
• W1998004700 cites W4252705583 @default.
• W1998004700 cites W4256049365 @default.
• W1998004700 cites W4300835158 @default.
• W1998004700 cites W4322574841 @default.
• W1998004700 cites W61023349 @default.
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