Systemic lupus erythematosus (SLE) is a multiorgan system autoimmune disease with numerous immunological and clinical

manifestations. It is characterized by an autoantibody response to nuclear and cytoplasmic antigens. The disease mainly involves the
skin, joints, kidneys, blood cells, and nervous system. Diagnosing and managing SLE in the emergency department can be very
challenging if it is not considered in one's differential diagnosis. Also, the laboratory testing of SLE may be unavailable on an
emergent basis.
Pathophysiology
Systemic lupus erythematosus (SLE) is a multifactorial disease involving genetic, environmental, and hormonal factors. Its precise
pathogenesis is unclear. There is growing evidence in favor of a clearance deficiency of apoptotic cells as the core mechanism in the
pathogenesis of SLE.Defective clearance of apoptotic cells causes secondary necrosis with release of intracellular content and
inflammatory mediators. Macrophages respond and present self-antigens to T and B cells

Pathogenic autoantibodies are the primary cause of tissue damage in patients with lupus. The production of these antibodies arises by
means of complex mechanisms involving every key facet of the immune system.The abnormal cellular and humoral response to the
formation of these autoantibodies is modulated by genetic, environmental, and hormonal factors:

• Genetic factors
○ Genes of the MHC HLA-A1, B8, and DR3 have been linked to lupus.
○ Genetic deficiency of complement factors C1q, C2, or C4
• Environmental factors
○ Occupational exposure - Silica, pesticides, mercury
○ Drugs - Many drugs have been implicated in drug-induced lupus.
○ Sunlight
• Epstein-Barr virus (EBV) has also been identified as a possible factor in the development of lupus.

Classification
Lupus is a chronic autoimmune disease in which the body's own defense system attacks otherwise healthy tissue. Clinically, it can
affect multiple organ systems including the heart, skin, joints, kidneys and nervous system. There are several types of lupus; in
general, when the word lupus alone is used, reference is to systemic lupus erythematosus, as discussed in this article. Other types
include:Other types include:
• Chronic cutaneous lupus erythematosus
○ Discoid lupus erythematosus, a skin disorder that causes a red, raised rash on the face and
scalp. Discoid lupus occasionally (1–5%) develops into SLE.[7]
 Localized discoid lupus erythematosus
 Generalized discoid lupus erythematosus
 Childhood discoid lupus erythematosus
○ Chilblain lupus erythematosus (Hutchinson)
○ Lupus erythematosus-lichen planus overlap syndrome
○ Lupus erythematosus panniculitis (Lupus erythematosus profundus)
○ Subacute cutaneous lupus erythematosus, which causes nonscarring skin lesions on patches
of skin exposed to sunlight.[8]
○ Tumid lupus erythematosus
○ Verrucous lupus erythematosus (Hypertrophic lupus erythematosus)
• Neonatal lupus erythematosus, a rare disease affecting babies born to women with SLE, Sjögren's
syndrome, or sometimes no autoimmune disorder. It is theorized that maternal antibodies attack
the fetus, causing skin rash; liver problems; low blood counts, which gradually fade; and heart
block, leading to bradycardia.[8]
• Childhood systemic lupus erythematosus, the pediatric variant of systemic lupus erythematosus.
• Drug-induced lupus erythematosus, a drug-induced form of SLE; this type of lupus can occur
equally in either sex.
• Lupus nephritis, an inflammation of the kidneys caused by SLE.
 • Complement deficiency syndromes

Causes
Despite the dramatic rise in Lupus research in recent years, the exact cause of the disease remains unknown. Indeed, consensus is still
lacking on whether Lupus is a single condition or a group of related diseases. SLE is a chronic inflammatory disease believed to be a
type III hypersensitivity response with potential type II involvement,[9] characterized by the body's production of antibodies against the
nuclear components of its own cells. There are three mechanisms by which lupus is thought to develop: genetic predisposition,
environmental triggers and drug reaction (drug-induced lupus).
Genetics
The first mechanism may arise genetically. Research indicates that SLE may have a genetic link. Lupus does run in families, but no
single "lupus gene" has yet been identified. Instead, multiple genes appear to influence a person's chance of lupus developing when
triggered by environmental factors. The most important genes are located on chromosome 6, where mutations may occur randomly
(de novo) or be inherited. Additionally, people with SLE have an altered RUNX-1 binding site, which may be either cause or
contributor (or both) to the condition. Altered binding sites for RUNX-1 have also been found in people with psoriasis and rheumatoid
arthritis.
Environmental triggers
The second mechanism may be due to environmental factors. These factors may not only exacerbate existing lupus conditions, but
also trigger the initial onset. They include certain medications (such as some antidepressants and antibiotics), extreme stress, exposure
to sunlight, hormones, and infections. Some researchers have sought to find a connection between certain infectious agents (viruses
and bacteria), but no pathogen can be consistently linked to the disease. UV radiation has been shown to trigger the photosensitive
lupus rash, but some evidence also suggests that UV light is capable of altering the structure of the DNA, leading to the creation of
autoantibodies. Some researchers have found that women with silicone gel-filled breast implants have produced antibodies to their
own collagen, but it is not known how often these antibodies occur in the general population and there is no data that show these
antibodies cause connective tissue diseases such as lupus.
Drug reactions
Drug-induced lupus erythematosus is a reversible condition that usually occurs in patients being treated for a long-term illness. Drug-
induced lupus mimics systemic lupus. However, symptoms of drug-induced lupus generally disappear once a patient is taken off the
medication which triggered the episode. There are about 400 medications currently in use that can cause this condition, though the
most common drugs are procainamide, hydralazine and quinidine.
Non-SLE forms of lupus
Discoid (cutaneous) lupus is limited to skin symptoms and is diagnosed via biopsy of skin rash on the face, neck or scalp. Often an
anti-nuclear antibody (ANA) test for discoid patients is negative or a low-titre positive. About 10% of discoid lupus patients
eventually develop SLE.

Pathophysiology
Lupus is an example of pathophysiology, a disturbance of the normal functioning of the body. One manifestation of lupus is
abnormalities in apoptosis, a type of programmed cell death in which aging or damaged cells are neatly disposed of as a part of normal
growth or functioning.
Transmission
In SLE, the body's immune system produces antibodies against itself, particularly against proteins in the cell nucleus. SLE is triggered
by environmental factors that are unknown.
"All the key components of the immune system are involved in the underlying mechanisms" of SLE, according to Rahman, and SLE
is the prototypical autoimmune disease. The immune system must have a balance (homeostasis) between being sensitive enough to
protect against infection, and being too sensitive and attacking the body's own proteins (autoimmunity). From an evolutionary
perspective, according to Crow, the population must have enough genetic diversity to protect itself against a wide range of possible
infection; some genetic combination's result in autoimmunity. The likely environmental triggers include ultraviolet light, drugs, and
viruses. These stimuli cause the destruction of cells and expose their DNA, histones, and other proteins, particularly parts of the cell
nucleus. Because of genetic variations in different components of the immune system, in some people the immune system attacks
these nuclear-related proteins and produces antibodies against them. In the end, these antibody complexes damage blood vessels in
critical areas of the body, such as the glomeruli of the kidney; these antibody attacks are the cause of SLE. Researchers are now
identifying the individual genes, the proteins they produce, and their role in the immune system. Each protein is a link on the
autoimmune chain, and researchers are trying to find drugs to break each of those links. [10][11][12]
SLE is a chronic inflammatory disease believed to be a type III hypersensitivity response with potential type II involvement.[13]
Abnormalities in apoptosis
• Apoptosis is increased in monocytes and keratinocytes
• Expression of Fas by B cells and T cells is increased
 • There are correlations between the apoptotic rates of lymphocytes and disease activity
Tangible body macrophages (TBMs) are large phagocytic cells in the germinal centers of secondary lymph nodes. They express CD68
protein. These cells normally engulf B cells which have undergone apoptosis after somatic hypermutation. In some patients with SLE,
significantly fewer TBMs can be found, and these cells rarely contain material from apoptotic B cells. Also, uningested apoptotic
nuclei can be found outside of TBMs. This material may present a threat to the tolerization of B cells and T cells. Dendritic cells in the
germinal center may endocytose such antigenic material and present it to T cells, activating them. Also, apoptotic chromatin and
nuclei may attach to the surfaces of follicular dendritic cells and make this material available for activating other B cells which may
have randomly acquired self-specificity through somatic hypermutation.
Clearance deficiency
The exact mechanisms for the development of systemic lupus erythematosus (SLE) are still unclear since
the pathogenesis is a multifactorial event. Beside discussed causations, impaired clearance of dying cells
is a potential pathway for the development of this systemic autoimmune disease. This includes deficient
phagocytic activity, scant serum components in addition to increased apoptosis.

Monocytes isolated from whole blood of SLE patients show reduced expression of CD44 surface molecules involved in the uptake of
apoptotic cells. Most of the monocytes and tingible body macrophages (TBM), which are found in the germinal centres of lymph
nodes, even show a definitely different morphology in patients with SLE. They are smaller or scarce and die earlier. Serum
components like complement factors, CRP and some glycoproteins are furthermore decisively important for an efficiently operating
phagocytosis. In patients these components are often missing, diminished or inefficient.
The clearance of early apoptotic cells is an important function in multicellular organisms. It leads to a progression of the apoptosis
process and finally to secondary necrosis of the cells, if this ability is disturbed. Necrotic cells release nuclear fragments as potential
autoantigens as well as internal danger signals, inducing maturation of dendritic cells (DC), since they have lost their membranes
integrity. Increased appearance of apoptotic cells also is simulating inefficient clearance. That leads to maturation of DC and also to
the presentation of intracellular antigens of late apoptotic or secondary necrotic cells, via MHC molecules.
Autoimmunity possibly results by the extended exposure to nuclear and intracellular autoantigens derived from late apoptotic and
secondary necrotic cells. B and T cell tolerance for apoptotic cells is abrogated and the lymphocytes get activated by these
autoantigens; inflammation and the production of autoantibodies by plasma cells is initiated. A clearance deficiency in the skin for
apoptotic cells has also been observed in patients with cutaneous lupus erythematosus (CLE).
Germinal centres

In healthy conditions apoptotic lymphocytes are removed in germinal centres by specialised phagocytes, the tingible body
macrophages (TBM); that’s why no free apoptotic and potential autoantigenic material can bee seen.
In some patients with SLE accumulation of apoptotic debris can be observed in GC, because of an ineffective clearance of apoptotic
cells.
In close proximity to TBM, follicular dendritic cells (FDC) are localized in GC, which attach antigen material to their surface and in
contrast to bone marrow-derived DC, neither take it up nor present it via MHC molecules.
Autoreactive B cells can accidentally emerge during somatic hypermutation and migrate into the GC light zone. Autoreactive B cells,
maturated coincidently, normally don’t receive survival signals by antigen planted on follicular dendritic cells and perish by apoptosis.
In the case of clearance deficiency apoptotic nuclear debris accumulates in the light zone of GC and gets attached to FDC. This serves
as a germinal centre survival signal for autoreactive B-cells.
After migration into the mantle zone autoreactive B cells require further survival signals from autoreactive helper T cells, which
promote the maturation of autoantibody producing plasma cells and B memory cells.
In the presence of autoreactive T cells a chronic autoimmune disease may be the consequence.

Anti-nRNP autoimmunity
Autoantibodies to nRNP A and nRNP C initially targeted restricted, proline-rich motifs. Antibody binding subsequently spread to
other epitopes. The similarity and cross-reactivity between the initial targets of nRNP and Sm autoantibodies identifies a likely
commonality in cause and a focal point for intermolecular epitope spreading.[15]
Others
Elevated expression of HMGB1 was found in the sera of patients and mice with systemic lupus erythematosus, High Mobility Group
Box 1 (HMGB1) is a nuclear protein participating in chromatin architecture and transcriptional regulation. Recently, there is
increasing evidence that HMGB1 contributes to the pathogenesis of chronic inflammatory and autoimmune diseases due to its pro-
inflammatory and immunostimulatory properties.[16]
Signs and symptoms
SLE is one of several diseases known as the great imitator[17] because its symptoms vary so widely it often mimics or is mistaken for
other illnesses, and because the symptoms come and go unpredictably. Diagnosis can be elusive, with patients sometimes suffering
unexplained symptoms and untreated SLE for years. Common initial and chronic complaints are fever, malaise, joint pains, myalgias
and fatigue. Because they are so often seen with other diseases, these signs and symptoms are not part of the diagnostic criteria for
SLE. When occurring in conjunction with other signs and symptoms (below), however, they are considered suggestive.
Most Common Symptoms
1. Joint pain or joint swelling
2. Skin rash
3. Malaise or fatigue
Complete List of Signs and Symptoms
• Abdominal pain
• Discoid skin lesions
• Erythematous macules
• Fatigue
• Hemolytic anemia
• Interstitial lung disease
• Keratoconjunctivitis sicca
• Leukopenia
• Mucosal lesions
• Pericarditis
• Photo distributed rash
• Pleural effusion
• Pleuritic chest pain
• Pneumonitis
• Polyarthritis / polyarthralgia
• Raynaud phenomenon
• Renal disease
• Renal vasculitis
• Seizures
• Stroke
• Thrombocytopenia
• Weight loss

Diagnosis
Antinuclear antibody (ANA) testing and anti-extractable nuclear antigen (anti-ENA) form the mainstay of serologic testing for
SLE.Several techniques are used to detect ANAs.Clinically the most widely used method is indirect immunofluorescence.The pattern
of fluorescence suggests the type of antibody present in the patient's serum.
ANA screening yields positive results in many connective tissue disorders and other autoimmune diseases, and may occur in normal
individuals. Subtypes of antinuclear antibodies include anti-Smith and anti-double stranded DNA (dsDNA) antibodies (which are
linked to SLE) and anti-histone antibodies (which are linked to drug-induced lupus). Anti-dsDNA antibodies are highly specific for
SLE; they are present in 70% of cases, whereas they appear in only 0.5% of people without SLE.[10] The anti-dsDNA antibody titers
also tend to reflect disease activity, although not in all cases.[10] Other ANA that may occur in SLE sufferers are anti-U1 RNP (which
also appears in systemic sclerosis), SS-A (or anti-Ro) and SS-B (or anti-La; both of which are more common in Sjögren's syndrome).
SS-A and SS-B confer a specific risk for heart conduction block in neonatal lupus.[22]
Other tests routinely performed in suspected SLE are complement system levels (low levels suggest consumption by the immune
system), electrolytes and renal function (disturbed if the kidney is involved), liver enzymes, complete blood count and recently By
proteomics, we can directly detect proteins as gene products as well as their alterations by post-translational modification and internal
abscission which are characteristically observed in proteins.[23]
Previously, the lupus erythematosus (LE) cell test was not commonly used for diagnosis because those LE cells are only found in 50–
75% of SLE cases, and are also found in some people with rheumatoid arthritis, scleroderma, and drug sensitivities. Because of this,
the LE cell test is now performed only rarely and is mostly of historical significance.[24]
As a summary:
• Medical history
• Complete physical examination
• Laboratory tests:
• Complete blood count (CBC)
• Erythrocyte sedimentation rate (ESR)
• Urinalysis
• Blood chemistries
• Complement levels
• Antinuclear antibody test (ANA)
• Other autoantibody tests (anti-DNA, anti-Sm, anti-RNP, anti-Ro [SSA], anti-La [SSB])
• Anticardiolipin antibody test
• Skin biopsy
• Kidney biopsy
• Malar rash (rash on cheeks). sensitivity = 57%; specificity = 96%[28]
• Discoid lupus (red, scaly patches on skin which cause scarring) sensitivity = 18%; specificity = 99%[28]
• Photosensitivity (exposure to ultraviolet light causes rash). sensitivity = 43%; specificity = 96%[28]
• Oral ulcers: include oral or nasopharyngeal ulcers
• Arthritis: nonerosive arthritis of two or more peripheral joints, with tenderness, swelling or effusionsensitivity = 86%;
specificity = 37%[28]
• Renal disorder: More than 0.5 g per day protein in urine, or cellular casts seen in urine under a microscope.sensitivity = 51%;
specificity = 94%[28]
• Neurologic disorder: Seizures or psychosis. sensitivity = 20%; specificity = 98%[28]
• Serositis: Pleuritis (inflammation of the membrane around the lungs) or pericarditis (inflammation of the membrane around
the heart)sensitivity = 56%; specificity = 86% (pleural is more sensitive; cardiac is more specific)[28]
• Hematologic disorder: Hemolytic anemia (low red blood cell count) or leukopenia (white blood cell count<4000/ul),
lymphopenia ( <1500/ul ) or thrombocytopenia (<100000/uL) in the absence of offending drug.sensitivity = 59%; specificity
= 89%[28] Hypocomplementemia is also seen, due to either consumption of C3 and C4 by immune complex-induced
inflammation, or to congenitally complement deficiency, which may predispose to SLE.
• Anti-nuclear antibody test positive. sensitivity = 99%; specificity = 49%[28]
• Immunologic disorder: Positive anti-Sm, anti-ds DNA, anti-phospholipid antibody and/or false positive serological test for
syphilis. sensitivity = 85%; specificity = 93%[28]. Presence of anti-ss DNA in 70% of patients (though also positive in patients
with rheumatic disease and healthy persons[29])
Medications
Due to the variety of symptoms and organ system involvement with SLE, its severity in an individual must be assessed in order to
successfully treat SLE. Mild or remittant disease can sometimes be safely left untreated. If required, nonsteroidal anti-inflammatory
drugs and antimalarials may be used.

Disease-modifying antirheumatic drugs

Disease-modifying antirheumatic drugs (DMARDs) are used preventively to reduce the incidence of flares, the process of the disease,
and lower the need for steroid use; when flares occur, they are treated with corticosteroids. DMARDs commonly in use are
antimalarials such as plaquenil and immunosuppressants (e.g. methotrexate and azathioprine). Hydroxychloroquine is an FDA-
approved antimalarial used for constitutional, cutaneous, and articular manifestations. Hydroxychloroquine has relatively few side
effects, and there is evidence that it improves survival among people who have SLE.[56] Cyclophosphamide is used for severe
glomerulonephritis or other organ-damaging complications. Mycophenolic acid is also used for treatment of lupus nephritis, but it is
not FDA-approved for this indication, and FDA is investigating reports that it may be associated with birth defects when used by
pregnant women.[57]
Analgesia
Since a large percentage of people with SLE suffer from varying amounts of chronic pain, stronger prescription analgesics (pain
killers) may be used if over-the-counter drugs (mainly nonsteroidal anti-inflammatory drugs) do not provide effective relief. Potent
NSAIDs such as indomethacin and diclofenac are relatively contraindicated for patients with SLE because they increase the risk of
kidney failure and heart failure.[56]
Moderate pain is typically treated with mild prescription opiates such as dextropropoxyphene and co-codamol. Moderate to severe
chronic pain is treated with stronger opioids, such as hydrocodone or longer-acting continuous-release opioids, such as oxycodone,
MS Contin, or Methadone. The Fentanyl duragesic transdermal patch is also a widely-used treatment option for the chronic pain
caused by complications because of its long-acting timed release and ease of use. When opioids are used for prolonged periods, drug
tolerance, chemical dependency, and addiction may occur. Opiate addiction is not typically a concern, since the condition is not likely
to ever completely disappear. Thus, lifelong treatment with opioids is fairly common for chronic pain symptoms, accompanied by
periodic titration that is typical of any long-term opioid regimen.

Edema (American English) or oedema (British English; both words from the Greek οἴδημα),
formerly known as dropsy or hydropsy, is an abnormal accumulation of fluid beneath the skin
or in one or more cavities of the body. Generally, the amount of interstitial fluid is determined by
the balance of fluid homeostasis, and increased secretion of fluid into the interstitium or
impaired removal of this fluid may cause edema.

Formation
Five factors can contribute to the formation of edema:
1. It may be facilitated by increased hydrostatic pressure or,
2. reduced oncotic pressure within blood vessels;
3. by increased blood vessel wall permeability as in inflammation;
4. by obstruction of fluid clearance via the lymphatic; or,
5. by changes in the water retaining properties of the tissues themselves. Raised hydrostatic
pressure often reflects retention of water and sodium by the kidney.[1]

Mechanism
Generation of interstitial fluid is regulated by the forces of the Starling equation.[2] Hydrostatic pressure within blood
vessels tends to cause water to filter out into the tissue. This leads to a difference in protein concentration between blood
plasma and tissue. As a result the oncotic pressure of the higher level of protein in the plasma tends to suck water back
into the blood vessels from the tissue. Starling's equation states that the rate of leakage of fluid is determined by the
difference between the two forces and also by the permeability of the vessel wall to water, which determines the rate of
flow for a given force imbalance. Most water leakage occurs in capillaries or post capillary venules, which have a semi-
permeable membrane wall that allows water to pass more freely than protein. (The protein is said to be reflected and the
efficiency of reflection is given by a reflection constant of up to 1.) If the gaps between the cells of the vessel wall open
up then permeability to water is increased first, but as the gaps increase in size permeability to protein also increases with
a fall in reflection coefficient.
Changes in the variables in Starling's equation can contribute to the formation of edema either by an increase in
hydrostatic pressure within the blood vessel, a decrease in the oncotic pressure within the blood vessel or an increase in
vessel wall permeability. The latter has two effects. It allows water to flow more freely and it reduces the oncotic pressure
difference by allowing protein to leave the vessel more easily.

Organ-specific edema

Left and right ring fingers of the same individual. The distal phalanx of the finger on the right
exhibits edema due to acute paronychia.

Edema will occur in specific organs as part of inflammation, as in pharyngitis, tendonitis or pancreatitis, for instance.
Certain organs develop edema through tissue specific mechanisms.
Examples of edema in specific organs:
 • Cerebral edema is extracellular fluid accumulation in the brain. It can occur in toxic
or abnormal metabolic states and conditions such as systemic lupus. It causes
drowsiness or loss of consciousness.
• Pulmonary edema occurs when the pressure in blood vessels in the lung is raised
because of obstruction to removal of blood via the pulmonary veins. This is usually
due to failure of the left ventricle of the heart. It can also occur in altitude sickness
or on inhalation of toxic chemicals. Pulmonary edema produces shortness of breath.
Pleural effusions may occur when fluid also accumulates in the pleural cavity.
• Edema may also be found in the cornea of the eye with glaucoma, severe
conjunctivitis or keratitis or after surgery. It may produce coloured haloes around
bright lights.
• Edema surrounding the eyes is called periorbital edema or eye puffiness. The
periorbital tissues are most noticeably swollen immediately after waking, perhaps
due to the gravitational redistribution of fluid in the horizontal position.
• Common appearances of cutaneous edema are observed with mosquito bites,
spider bites, bee stings (wheal and flare), and skin contact with certain plants such
as Poison Ivy or Western Poison Oak,[5] the latter of which are termed contact
dermatitis.
• Another cutaneous form of edema is myxedema, which is caused by increased
deposition of connective tissue. In myxedema (and a variety of other rarer
conditions) edema is due to an increased tendency of the tissue to hold water within
its extracellular space. In myxedema this is because of an increase in hydrophilic
carbohydrate-rich molecules (perhaps mostly hyaluronan) deposited in the tissue
matrix. Edema forms more easily in dependent areas in the elderly (sitting in chairs
at home or on aeroplanes) and this is not well understood. Estrogens alter body
weight in part through changes in tissue water content. There may be a variety of
poorly understood situations in which transfer of water from tissue matrix to
lymphatics is impaired because of changes in the hydrophilicity of the tissue or
failure of the 'wicking' function of terminal lymphatic capillaries.
(Foot, c. 2 weeks post surgery because of compartment syndrome)

• In the case of human feet, the Starling forces are always a long way out of balance,
because the variation in hydrostatic pressure in the vessels in the feet as compared
to the face is about a metre of water. In severe heart failure the change in central
venous pressure is tiny in comparison and cannot explain why edema of the feet
develops simply through an effect on capillary leakage. Three other factors may be
involved. If the central venous pressure rises to equal that of the thoracic lymph
duct then clearance of fluid from the tissue will be impeded (see below). That is to
say the edema may actually be caused by a change in output of fluid from the
tissue, as much as input to the tissue. Secondly, severe heart failure is one of the
most exhausting conditions there is. The sufferers tend to spend what little effort
they can make trying to breathe with edematous lungs. They tend to sit up to make
breathing easier and their feet hang immobile on the floor. Immobility is perhaps
the commonest of all causes of edema, because clearance of fluid via the
lymphatics needs muscle action. Thirdly, in severe heart failure endocrine and
neural changes alter the way tissues are perfused in ways that are not fully
understood.
• In lymphedema abnormal removal of interstitial fluid is caused by failure of the
lymphatic system. This may be due to obstruction from, for example, pressure from
a cancer or enlarged lymph nodes, destruction of lymph vessels by radiotherapy, or
infiltration of the lymphatics by infection (such as elephantiasis). It is most
commonly due to a failure of the pumping action of muscles due to immobility, most
strikingly in conditions such as multiple sclerosis, or paraplegia. Lymphatic return of
 fluid is also dependent on a pumping action of structures known as lymph hearts. It
has been suggested that the edema that occurs in some people following use of
aspirin-like cyclo-oxygenase inhibitors such as ibuprofen or indomethacin may be
due to inhibition of lymph heart action.
Fluid deficit

Compartments of
Body and Distribution of Water by Weight
Plasma 5%
Interstitial 15%
Intracellular 40%

Total 60 % Water
Solids - 40%
fat, protein, carbohydrates,
minerals

Fluid and Electrolyte Balance

The main fluid in the body is water. Total body water is 60% of body weight. The water is distributed in three main
compartments separated from each other by cell membranes. The intracellular compartment is the area within the cell.
The extracellular compartment consists of the interstitial area (between and around cells) and the inside of the blood
vessels (plasma).

ELECTROLYTE DISTRIBUTION

Extracellular Intracellular
Electrolyte Function
meq/liter meq/liter
fluid balance, osmotic
Sodium 142 10
pressure
Neuromuscular excitability
Potassium 5 100
acid-base balance
Calcium 5 - bones, blood clotting
Magnesium 2 123 enzymes
Total Positive ions 154 205

Electrolyte Distribution

Extracellular Intracellular
Electrolyte Function
meq/liter meq/liter
fluid balance, osmotic
Chloride 105 2
pressure
Bicarbonate 24 8 acid-base balance
Proteins 16 55 osmotic pressure
Phosphate 2 149 energy storage
Sulfate 1 - protein metabolism
Total Negative ions 154 205

Electrolytes are the chemicals dissolved in the body fluid. The distribution has important consequences for
the ultimate balance of fluids.
Sodium chloride is found mostly in extracellular fluid, while potassium and phosphate are the main ions in
the intracellular fluid.

table 2: Some high-sodium condiments.

Onion salt Baking soda Mustard
Celery salt Monosodium glutamate (msg) Worcestershire
Garlic salt Soy sauce sauce
Seasoned Steak sauce Salad dressings
salt Barbeque sauce Pickles
Meat Catsup Chili sauce
tenderizer Relish
Bouillon
Baking
powder

Low Sodium sources

Sodium occurs naturally in most foods. The most common form of sodium is sodium chloride, which is table salt. Milk,
beets, and celery also naturally contain sodium, as does drinking water, although the amount varies depending on the
source. Sodium is also added to various food products. Some of these added forms are monosodium glutamate, sodium
nitrite, sodium saccharin, baking soda (sodium bicarbonate), and sodium benzoate. These are ingredients in condiments
and seasonings such as Worcestershire sauce, soy sauce, onion salt, garlic salt, and bouillon cubes. Processed meats, such
as bacon, sausage, and ham, and canned soups and vegetables are all examples of foods that contain added sodium. Fast
foods are generally very high in sodium.[3]

Foods that are naturally low in sodium

Seasonings: Black, cayenne, or lemon pepper, mustard, chili or hot sauce
Herbs: Dried or fresh garlic, garlic/onion powder (no salt), dill, parsley, rosemary, basil, cinnamon, cloves, paprika,
oregano, ginger, vinegar, cumin, nutmeg
Fresh fruits and vegetables (celery, carrots, beets, spinach)
Dried beans, peas, rice, lentils
Macaroni, pasta, noodles, rice, barley (cooked in unsalted water)
Honey, sugar
Unsalted butter
Unsalted dry curd cottage cheese
Fresh beef, pork, lamb, fish, shrimp, egg
Skim milk, yogurt
Hot cereals
Club soda, coffee, seltzer water, soy milk, tea[7]