British Journal of Anaesthesia 91 (2): 265±72 (2003)

DOI: 10.1093/bja/aeg155

Disorders of the lymph circulation: their relevance to anaesthesia

and intensive care
A. Mallick and A. R. Bodenham*

Department of Anaesthesia, Leeds General In®rmary, United Leeds Teaching Hospitals, Leeds LS1 3EX, UK
*Corresponding author. E-mail: andy.bodenham@leedsth.nhs.uk

The lymphatic system is known to perform three major functions in the body: drainage of
excess interstitial ¯uid and proteins back to the systemic circulation; regulation of immune
responses by both cellular and humoral mechanisms; and absorption of lipids from the intes-
tine. 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 dis®guration. Many lymphatic disorders are encoun-
tered 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.
Br J Anaesth 2003; 91: 265±72
Keywords: anaesthesia; anatomy, lymphatic system; chylothorax, chylous ascites;
chylothorax, lymphoedema; critical care

Exchange of ¯uid and movement of macromolecules across Applied anatomy

the systemic capillaries are governed by Starling forces and
capillary permeability. In healthy tissues, small volumes of
¯uid are ®ltered continuously into the interstitial tissues.
The lymphatic circulation forms an accessory pathway to
return this excess ¯uid and proteins from the tissue spaces
back to the blood stream. This ¯uid 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 ¯uid ®ltered 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.66 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, malig-
nancy, 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 capillar-
ies. 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 ¯uid circulation, in the form of the
cerebrospinal ¯uid, aqueous and vitreous humour, and the
synovial ¯uid 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 ¯ows through the
thoracic duct while that from the right upper quadrant drains
into the right lymphatic duct.
Dynamics of lymph ¯ow
The lymphatic circulation is devoid of any central pump.
Lymph ¯ow 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 ¯ow in lymphatic vessels.
Conversely, if the interstitial tissue pressure is greater than
2 mm Hg above atmospheric pressure, then lymph ¯ow may

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 Mallick and Bodenham
Table 1 Features of chyle
Characteristics
Milky appearance
Alkaline pH: 7.4±7.8
Speci®c gravity: 1012±1025
Sterile
Fat globules
Lymphocytes, principally T cells: 400±7000 mm±3
Composition
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
decrease as a result of compression of the lymphatic vessels.
The anterograde ¯ow of lymph is further facilitated by the
presence of numerous microscopic and macroscopic bi-
lea¯et valves, which exist at least every few millimetres to
prevent retrograde ¯ow. 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 succes-
sive 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,42
including alpha and beta agonists, appear to mediate
lymphatic truncal contraction, as do the by-products of
arachidonic acid including thromboxane and prostaglan-
dins.30 There is evidence for the presence of G proteins,
adenyl cyclase, and phospholipase C activities in lymphatic
smooth muscle cell membranes.31 Lymphatic endothelial
cells produce nitric oxide,48 that in turn relaxes lymphatic
smooth muscles, via accumulation of guanosine 3¢, 5¢ cyclic
monophosphate. Angiotensin II65 appears to increase lymph
¯ow by a direct effect on lymphatic vessels, while
5-hydroxytryptamine43 has an opposite action by inhibiting
spontaneous contractility.
The contractility of the mesenteric lymphatics is sup-
pressed in a dose-dependent manner by halothane.17 57 The
effects of other anaesthetic agents are not known.
Stimulation of the greater splanchnic nerve (sympathetic)
appears to increase lymphangion contractility and lymph
¯ow.62 It has been shown that increased sympathetic
activity gives rise to peripheral lymphoedema, which
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shows improvement after sympathectomy. This has been
proposed to be one mechanism for re¯ex sympathetic
dystrophy and its treatment.28
In the thoracic duct, lymph ¯ow 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 inter-
actions have not been studied in any detail, compared with
the large amount of work on ventilatory/circulatory inter-
actions in venous and arterial systems. PEEP and positive
pressure ventilation appear to increase lymph ¯ow through
the thoracic duct. Conversely, excessively high intrathoracic
pressure and a high PEEP can impede the thoracic duct ¯ow
both by direct pressure on the duct and venous hyperten-
sion.24
Lymphatic out¯ow and pumping have been shown to
increase in the setting of hypovolaemic shock in order to
restore the blood volume.38 After major burn injury, lymph
¯ow from the injured area increases and transports a large
amount of hyaluronan, a connective tissue component of the
interstitial matrix.49 Clinical and radiological studies have
demonstrated markedly raised thoracic duct ¯ow, 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
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 1.59 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.
Normal chyle ¯ow 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 ¯ow in the thoracic duct in a resting adult.
Varying the pressure within the thoracic duct can alter each
organ's contribution to thoracic duct ¯ow and thereby affect
the composition of chyle. A raised pressure in the thoracic
duct can decrease the lymph ¯ow out of the gut without
much effect on the hepatic lymph ¯ow.
Formation of oedema
Oedema results when tissue ¯uid accumulates faster than
the lymphatic system can remove it. Ascites, pleural, and
 Disorders of the lymph circulation
Fig 1 Chyle in a bottle from a pleural drain, in the patient whose chest
x-ray is shown in Figure 4. This ¯uid was photographed 5 days after
injury, when the patient was receiving nasogastric feed. The ¯uid shows
three distinct layers on standing.
pericardial effusions are localized ¯uid 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 dif®culties in meas-
uring lymph ¯ow. Pulmonary lymph ¯ow 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
in¯ammatory process, and histology of lungs from patients
with ARDS has shown a marked disruption of lymphatic as
well as pulmonary capillaries.63 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
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Fig 2 An adult male with congenital bilateral lower limb lymphoedema,
referred because he required bilateral knee replacement. The left side
only has been treated by compression bandage therapy (see bandage
marks on left lower leg), with impressive reduction in the lymphoedema.
Photograph, with patient permission, courtesy of lymphoedema service,
Cookridge Hospital, Leeds.
role of the lymphatics is uncertain. A signi®cantly raised
intrathoracic pressure in mechanically ventilated critically
ill patients can increase the impedance to lymph ¯ow 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
Lymphoedema is de®ned as accumulation of lymph in the
extracellular space as a result of lymphatic block or
dysfunction. Many cases follow chronic lymphatic obstruc-
tion but it can develop acutely in any organ following
surgery. The early oedema seen in surgically transposed free
¯aps, 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.55 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
 Mallick and Bodenham
Fig 3 Late trophic changes in a leg following longstanding
lymphoedema. So called `Elephantiasis'. Photograph, with patient
permission, courtesy of lymphoedema service, Cookridge Hospital,
Leeds.
myocardial function and cause pulmonary hypertension as a
result of perivascular oedema.12 37 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, ®lariasis, 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 in¯ammatory state develops with collagen
deposition and soft tissue overgrowth. At this stage, the
tissue becomes less pitting, more ®rm or brawny, and
elevation of the limb no longer results in reduction of the
oedema.10 Superimposed occult or overt infection (lym-
phangitis) commonly contributes to progressive limb
deformity and elephantiasis (Fig. 3).
Early diagnosis is essential to prevent worsening of the
condition and to help relieve the psychological impact of the
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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.10
Prevention of acute in¯ammation 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.
Drug absorption
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.9 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.50 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 infesta-
tions including ®lariasis.
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.58 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.29 Firm pressure
bandaging is an effective means of restricting the lymphatic
transport of toxins, provided the bandage is applied within a
de®ned pressure range of 5±9 kPa. Strict limb immobiliza-
tion is necessary to minimize lymphatic ¯ow, and walking
after upper or lower limb envenomation will inevitably
result in systemic envenomation despite other ®rst-aid
measures.29
Mesenteric lymph and organ dysfunction
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
 Disorders of the lymph circulation
Fig 4 Chest x-ray from an adult male with blunt chest trauma following
severe deceleration injury in a road traf®c accident. Multiple ribs
fractures are seen on the left side (arrows). There are signs of left lung
contusion and a left sided chest drain has been inserted to remove pleural
¯uid. A left thoracotomy and thoracic duct ligation was carried out after
10 days, when chyle loss was persistently greater than 3 litre day±1. This
procedure cured his chyle leak.
description of bacterial translocation. Bacterial trans-
location has been shown to occur in animal models but
data from human studies are less convincing.13 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.36 47 54
New reports suggest that mesenteric lymph has a
signi®cant role in the generation of remote organ injury in
the presence of dysfunctional gut.13 46 Shock, trauma or
sepsis-induced gut injury can result in the generation of
cytokines and other pro-in¯ammatory mediators in the
gut.39 Mesenteric lymph appears to be the route of delivery
of in¯ammatory mediators from the gut to remote
organs.38 45 These toxic mediators have been demonstrated
in mesenteric lymph,45 but not in the systemic or portal
circulation. Acute lung injury,33 endothelial damage,63
haemopoietic failure,3 and activation of white
cells,2 22 64 68 69 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 recruit-
ment.1 14 53
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.16 This may be because the lung is the ®rst organ
exposed to mesenteric lymph. Further work needs to be
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performed in this area before recommending this approach
for clinical use.
Sentinel node biopsy
Sentinel node biopsy is increasingly performed to decide
whether a patient requires a regional lymph node clearance
following removal of breast or other cancers.5 The sentinel
node is the ®rst node to receive lymph from a primary
tumour and therefore the most likely to have metastatic
cells.4 A blue dye or a radioactive compound is injected
around the primary tumour and becomes concentrated in the
sentinel node to help in its identi®cation.
Anaesthetists should be aware of some practical impli-
cations of this procedure.8 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.52 This decrease in
SpO2 reading can occur between 30 s to 20 min following
injection, and can last several hours.8 52 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;67 discolouration
of urine; and tattooing of skin around the injection site.8
Other lymphatic disorders
Disorders associated with the lymphatic system are princi-
pally seen in relation to congenital malformations, the
spread of infection or invasion by tumour cells, and the
effects of lymphatic obstruction or leak.
Airway compromise
Many lymphatic tumours including lymphomas progres-
sively enlarge without any pain or tenderness and are often
noticed ®rst in the neck. They can present as symptomatic or
asymptomatic mediastinal masses. They can result in upper
and lower airway compression,25 26 as well as superior vena
caval obstruction. The anaesthetic implications of these
conditions have been reviewed.15 Induction of anaesthesia
can result in the `cannot intubate, cannot ventilate' situation
or complete loss of the airway.60 Some slow growing
lymphatic tumours including lymphangiomas can involve
several organs in the neck and the mediastinum and can
present with acute airway obstruction because of encroach-
ment on the tongue base, parapharyngeal space, or the
larynx.26 Cystic hygroma is a lymphatic tumour seen in
infants and children, and airway management remains a
challenge during induction of anaesthesia.32
 Mallick and Bodenham
Chylothorax
Chylothorax is de®ned as an accumulation of chyle within a
pleural cavity. A milky appearance of pleural ¯uid is
considered typical. The condition results from either
obstruction or damage of the central lymphatics, including
the thoracic duct or cisterna chyli. Such damage can result
from trauma, or surgery involving the oesophagus, thoracic
spine, and aorta. Traumatic chylothorax is seen after blunt
or penetrating chest injuries (Fig. 4). A signi®cant number
of such cases can be associated with a fracture dislocation of
the thoracic spine.56 Sudden hyperextension of the spine has
been suggested as the cause of thoracic duct injury in this
setting. Spontaneous chylothorax has been reported after
minor trauma such as coughing or stretching following
ingestion of a fatty meal.
Chylothorax, right, left, or bilateral, is a recognized
complication of central venous cannulation,7 34 and stellate
ganglion,61 and coeliac plexus blocks.20 This may result
from direct damage to the thoracic duct or thrombosis of the
superior vena cava, innominate, or subclavian veins.
The clinical presentation of a chylothorax may be delayed
from the time of injury if the patient is not receiving enteral
feeding or is receiving continuous gastric suction. The
probability of chylothorax is increased if the effusion
increases in size with resumption of enteral feeding. The
diagnosis can be con®rmed by demonstrating a typical
chylous composition (Table 1).
The principles of management include: (i) pleural
drainage with appropriate ¯uid and nutritional replacement;
(ii) measures to reduce the production of chyle; (iii)
treatment of the underlying cause; and (iv) obliteration of
the pleural space or ligation of a demonstrated thoracic duct
leak.18 Conservative therapy is usually tried ®rst for 2±3
weeks, after which surgical/radiological intervention is
considered.
Decompression of the pleural space by continuous tube
drainage relieves symptoms and accurately monitors chyle
loss. Fibrin clots can block the chest drains. Occasionally
multiple chest drains are required, if there are multiple
loculations and re-accumulation. Placement of a chest drain
may be dif®cult in the presence of a ¯ail segment in patients
with multiple trauma. Ultrasound or CT guided insertion of
chest drains is helpful in these situations.
Replacement of daily losses of ¯uid, calories, proteins
and electrolytes is essential to avoid severe hypovolaemia,
hypoalbuminaemia, and malnutrition. Continuous loss of
lymphocytes leads to immunosuppression and an increased
susceptibility to infections. Chyle has been re-transfused
into patients to prevent the loss of lymphocytes and proteins,
but this procedure has inherent technical dif®culties.44 Oral
or enteral nutrition may increase lymph ¯ow and therefore is
not generally encouraged. Commercially available enteral
feeds with a fat content less than 1 g litre±1, which are rich in
medium chain triglycerides, may be suitable for some
patients. Total parenteral nutrition at the outset is now
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considered to be the optimal approach in critically ill
patients.
In isolated case reports, chylothorax has been success-
fully treated with octreotide,40 and etilefrine.23 The exact
mechanism of the action of octreotide is not clear.
Octreotide is used in patients with high output gastro-
intestinal ®stulae because of its inhibitory effect on gastric
and pancreatic secretion. If gastrointestinal volume and
enzymes are reduced by octreotide, it may subsequently
decrease chyle ¯ow in the thoracic duct. Etilefrine23 is a
sympathomimetic agent used in the management of postural
hypotension. It is thought to cause smooth muscle contrac-
tion of the thoracic duct and may thereby reduce the leak.
There have been case reports in children where persistent
thoracic duct leaks have been reduced by the application of
very high intrathoracic pressures over a number of days.19
Also, the reduction of venous hypertension, secondary to
pulmonary arterial hypertension, by inhaled nitric oxide has
been found to be helpful in such cases.41 51
It may take several weeks for a chylothorax to resolve. A
high volume chyle output predicts failure of continuing
conservative management. The decision to abandon con-
servative management is frequently dif®cult. However, an
operative intervention is usually indicated if the average
daily chyle loss exceeds 1500 ml in adults, or chyle drainage
is unchanged after 2 weeks of conservative management.
The thoracic duct can be tied off surgically to prevent
leakage of chyle into the body cavities.6 21 Interventions
including videoassisted thoracoscopy, thoracotomy, or
pleurectomy have to be individualized depending on the
primary cause.56 It may be helpful to administer nasogastric
olive oil or cream before surgery in order to increase chyle
¯ow and help identify the site of the leak. Alternatively
methylene blue, injected between the toes, helps outline the
thoracic duct. Percutaneous transabdominal catheterization
of the cisterna chyli or thoracic duct has been used to
embolize chylous ®stulae.11 21 27 Following such interven-
tions, lymph is thought to return to the venous circulation
via collateral channels.
Although the mortality from chylothorax is decreasing,
signi®cant morbidity continues as a result of lymphopenia,
hypoalbuminaemia, malnutrition, and prolonged hospitali-
zation. Prolonged central venous catheterization, total
parenteral nutrition, multiple chest drain insertions, and
additional surgical procedures contribute to the risk.
Chylous ascites
In chylous ascites, chyle accumulates in the peritoneal
cavity. It results from an obstruction or leak in either the
cisterna chyli or its large afferent lymphatics. It has a similar
aetiology to chylothorax. Lymphomas account for more
than half of the cases. Abdominal and retroperitoneal
surgical procedures can damage the lymphatics. In post-
surgical cases, the diagnosis is often delayed because the
 Disorders of the lymph circulation
peritoneal ¯uid is initially serous until enteral feeding is
reintroduced.35
The diagnosis of chylous ascites is based on the chemical
content of the peritoneal ¯uid. Peritoneal ¯uid in this
condition is very rich in proteins, usually 50% greater than
that of plasma. Management of chylous ascites is similar to
that of chylothorax. Repeated paracentesis is performed for
patient comfort and to minimize the risk of development of
the abdominal compartment syndrome.35 Persistent chylous
ascites following several weeks of conservative treatment
warrants a more aggressive approach including insertion of
a peritoneovenous shunt, percutaneous embolization,27 or
direct surgical repair of the cisterna chili.35
Chylopericardium
Chylopericardium is a rare disorder in which chyle accu-
mulates in the pericardial cavity. It can be congenital or
secondary to pericarditis, pancreatitis, cardiac or thoracic
surgery, or malignancies. Chylopericardium is seen in
children undergoing cardiac surgery with development of
cardiac tamponade. The principles of management include:
pericardial drainage, a low lipid diet, and surgery in
persistent cases.
Conclusions
The lymphatic circulation is important in health and disease
but its functions are poorly understood and often over-
looked. Clinicians need to be aware of lymphatic disorders,
which have direct relevance to anaesthesia and intensive
care medicine. It is likely that future research will uncover
other functions for the lymphatic circulation.
References
1 Adams CA jr, 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±31
2 Adams JM, Hauser CJ, Adams CA jr, et al. Entry of gut lymph into
the circulation primes rat neutrophil respiratory burst in
hemorrhagic shock. Crit Care Med 2001; 29: 2194±8
3 Anjaria DJ, Rameshwar P, Deitch EA, et al. Haematopoietic
failure after hemorrhagic shock is mediated partially through
mesenteric lymph. Crit Care Med 2001; 29; 1780±5
4 Allan R. Sentinel nodal localization: do or dye alone? Br J Radiol
2001; 74: 475±7
5 Bass 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±94
6 Buchan KG, Hosseinpour AR, Ritchie AJ. Thoracoscopic thoracic
duct ligation for traumatic chylothorax. Ann Thorac Surg 2001;
72: 1366±7
7 Campistol JM, Cases A. Lopez-Pedret J, Revert L. Thoracic duct
injury: an unusual complication following subclavian
catheterization for hemodialysis. Nephron 1987; 46: 390±1
271
Downloaded from https://academic.oup.com/bja/article-abstract/91/2/265/371142
by guest
on 24 May 2018
8 Cashman JN. Sentinel lymph node biopsy: anaesthetic
implications. Eur J Anaesthesiol 2001; 18: 273±5
9 Charman SA, McLennan DN, Edwards GA, Porter CJ. Lymphatic
absorption is a signi®cant contributor to the subcutaneous
bioavailability of insulin in a sheep model. Pharm Res 2001; 18:
1620±6
10 Cohen SR, Payne DK, Tunkel RS. Lymphedema: strategies for
management. Cancer 2001; 92: 980±7
11 Cope C. Diagnosis and treatment of postoperative chyle leakage
via percutaneous transabdominal catheterization of the cisterna
chyli; a preliminary study. J Vasc Interv Radiol 1998; 9: 727±34
12 Cui Y, Urschel JD, Petrelli NJ. The effect of cardiopulmonary
lymphatic obstruction on heart and lung function. Thorac
Cardiovasc Surg 2001; 49: 35±40
13 Deitch EA. Role of the gut lymphatic system in multiple organ
failure. Curr Opin Crit Care 2001; 7: 92±8
14 Deitch 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±47
15 Dilworth KE, Mchugh K, Stacey S, Howard RF. Mediastinal mass
obscured by a large pericardial effusion in a child: a potential
cause of serious anaesthetic morbidity. Paediatr Anaesth 2001;
11: 479±82
16 Dugernier 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±8
17 Elk JR, Adair T, Drake RE, Gabel JC. The effect of anaesthesia and
surgery on diaphragmatic lymph vessel ¯ow after endotoxin in
sheep. Lymphology 1990; 23: 145±8
18 Fahimi H, Cassleman FP, Mariani MA, et al. Current management
of postoperative chylothorax. Ann Thorac Surg 2001; 71: 448±51
19 Fernandez ME, Vazquez MG, Cardenas A, et al. Ventilation with
positive end-expiratory pressure reduces extravascular lung
water and increases lymphatic ¯ow in hydrostatic pulmonary
edema. Crit Care Med 1996; 24: 1562±7
20 Fine PG, Bubela C. Chylothorax following celiac plexus block.
Anesthesiology 1985; 63: 454±6
21 Fishman SJ, Burrows PE, Upton J, Hendren WH. Life-threatening
anomalies of the thoracic duct: anatomic delineation dictates
management. J Pediatr Surg 2001; 36: 1269±72
22 Ganzalez RJ, Moore EE, Ciesla DJ, et al. Mesenteric lymph is
responsible for post-hemorrhagic shock systemic neutrophil
priming. J Trauma 2001; 51: 1069±72
23 Guillem P, Billert V, Houcke ML, Triboulet JP. Successful
management of post-esophagectomy chylothorax and
chyloperitoneum by etilefrine. Dis Esophagus 1999; 12: 155±6
24 Haider M, Schad H, Mendler N. Thoracic duct lymph and PEEP
studies in anaesthetized dogs. I. Lymph formation and the effect
of a thoracic duct ®stula on lymph ¯ow. Intensive Care Med 1987;
13: 183±91
25 Hammer GB, Cao S, Boltz MG, Messner A. Post-transplant
lymphoproliferative disease may present with severe airway
obstruction. Anesthesiology 1998; 89: 263±5
26 Hartl DM, Roger G, Denoyelle F, et al. Extensive lymphangioma
presenting with upper airway obstruction. Arch Otolaryngol Head
Neck Surg 2000; 126: 1378±82
27 Hoffer EK, Bloch RD, Mulligan MS, Borsa JJ, Fontaine AB.
Treatment of chylothorax: percutaneous catheterization and
embolization of the thoracic duct. Am J Roentgenol 2001; 176:
1040±2
28 Howarth D, Burstal R, Hayes C, Lan L, Lantry G. Autonomic
 Mallick and Bodenham
regulation of lymphatic ¯ow in the lower extremity
demonstrated on lymphoscintigraphy in patients with re¯ex
symphathetic dystrophy. Clin Nuclear Med 1999; 24: 383±7
29 Howarth DM, Southee AE, Whyte IM. Lymphatic ¯ow rates and
®rst-aid in simulated peripheral snake or spider envenomation.
Med J Aust 1994; 161: 695±700
30 Johnston MG, Gordon JL. Regulation of lymphatic contractility by
arachidonate metabolites. Nature 1981; 293: 294±7
31 Kelly 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±32
32 Kennedy TL, Whitaker M, Pellitteri P, Wood WE. Cystic
hygroma/lymphangioma: a rational approach to management.
Laryngoscope 2001; 111: 1929±37
33 Koike K, Moore EE, Moore FA, et al. Gut ischemia/reperfusion
produces lung injury independent of endotoxin. Crit Care Med
1994; 22: 1438±44
34 Kurukei E, Kaye R, Koehler M. Chylothorax and
chylopericardium: a complication of a central venous catheter.
J Pediatr 1998; 132: 1064±6
35 Leibovitch I, Mor Y, Golomb J, Ramon J. The diagnosis and
management of postoperative chylous ascites. J Urol 2002; 167:
449±57
36 Lemaire 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±36
37 Ludwig LL, Schertel ER, Pratt JW, et al. Impairment of left
ventricular function by acute cardiac lymphatic obstruction.
Cardiovasc Res 1997; 33: 164±71
38 Magnotti 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±27
39 Magnotti LJ, Xu DZ, Lu Q, et al. Gut-derived mesenteric lymph: a
link between burn and lung injury. Arch Surg 1999; 143: 1333±41
40 Markham KM, Glover JL, Welsh RJ, Lucas RJ, Bendick PJ.
Octreotide in the treatment of thoracic duct injuries. Am Surg
2000; 66: 1165±7
41 Mavroudis C. Management of postoperative chylothorax with
nitric oxide. Crit Care Med 1999; 27: 877
42 McHale NG, Roddie IC. The effects of intravenous adrenaline
and noradrenaline infusion on peripheral lymph ¯ow in the
sheep. J Physiol 1983; 341: 517±26
43 McHale NG, Thornbury KD, Hollywood MA. 5HT inhibits
spontaneous contractility of isolated sheep mesenteric
lymphatics via activation of 5HT4 receptors. Microvasc Res
2000; 60: 261±8
44 Montebugnoli M, Borghi B, Bugamelli B, et al. Salvage and
reinfusion of chyle in closed chest injury. Int J Artif Organs 1998;
21: 235±9
45 Montravers 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±33
46 Moore EE. Mesenteric lymph: the critical bridge between
dysfunctional gut and multiple organ failure. Shock 1998; 10:
415±6
47 Moore 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±38
48 Ohhashi T, Takahashi N. Acetylcholine-induced release of
endothelium-derived relaxing factor from lymphatic endothelial
cells. Am J Physiol 1991; 260: H1172±8
272
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on 24 May 2018
49 Onarheim H, Brofeldt BT, Gunther RA. Markedly increased
lymphatic removal of hyaluronan from skin after major thermal
injury. Burns 1996; 22: 212±6
50 Oussoren C, Storm G. Liposomes to target the lymphatics by
subcutaneous administration. Adv Drug Deliv Rev 2001; 23:
143±56
51 Ragosta KG, Al®eris G. Chylothorax: a novel therapy. Crit Care
Med 2000; 28: 1208±9
52 Saito S, Fukura H, Shimada H, Fujita T. Prolonged interference of
patent blue with pulse oximeter readings. Acta Anaesthesiol Scand
1995; 39: 268±69
53 Sambol 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±20
54 Sanchez-Garcia M, Prieto A, Tejedor A, et al. Characteristics of
thoracic duct lymph in multiple organ dysfunction syndrome.
Arch Surg 1997; 132: 13±8
55 Schmid T, Korozsi G, Klima G, Oberhuber G, Margreiter R.
Regeneration of lymph drainage following transplantation of
small intestine. Langenbecks Archiv Chirurgie 1989; 374: 299±322
56 Silen ML, Weber TR. Management of thoracic duct injury
associated with fracture-dislocation of the spine following blunt
trauma. J Trauma 1995; 39: 1185±7
57 Takeshita T, Morio M, Kawahara M, Fujii K. Halothane-induced
changes in contractions of mesenteric lymphatics of the rat.
Lymphology 1988; 21: 128±30
58 Taylor MD, Kim SS, Vaias LJ. Therapeutic digoxin level in chylous
drainage with no detectable plasma digoxin level. Chest 1998;
114: 1482±4
59 Teba L, Dedhia HV, Bowen R, Alexander JC. Chylothorax
review. Crit Care Med 1985; 13: 49±52
60 Theaker NJ, Brady PW, Fisher MM. Postesophagectomy
mediastinal chylothorax causing upper airway obstruction
misdiagnosed as asthma: a report of two cases. Chest 1997;
111: 1126±8
61 Thompson KJ, Melding P, Hatangdi VS. Pneumochylothorax: a
rare complication of stellate ganglion block. Anesthesiology1981;
55: 589±91
62 Thornbury KD, Harty HR, McGeown JG, McHale NG.
Mesenteric lymph ¯ow response to splanchnic nerve
stimulation in sheep. Am J Physiol 1993; 264: H604±10
63 Tomashefski JF jr, 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±26
64 Upperman 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±14
65 Valenzuela GJ, Hewitt CW, Graham AD. Angiotensin II infusion
increases thoracic duct lymph ¯ow in chronically catheterized
sheep. Am J Physiol 1987; 252: R853±8
66 Witte CL, Witte MH, Unger EC, et al. Advances in imaging of
lymph ¯ow disorders. Radiographics 2000; 20: 1697±719
67 Woltsche-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±4
68 Zallen G, Moore EE, Ciesla DJ, et al. Lipids from post-shock
mesenteric lymph are responsible for systemic neutrophil
priming. Surg Forum 1999; 50: 240±2
69 Zallen 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±8