PHLEGMONS AND ABSCESSES OF THE MAXILLOFACIAL AREA n(MFA): CLASSIFICATION, ETIOLOGY, PATHOGENESIS, CLINICAL nFEATURES, COURSE, PRINCIPLES OF TREATMENT, PREVENTION, COMPLICATIONS. THE nINFLAMMATORY PROCESS OF MFA: ETIOLOGY, PATHOGENESIS, CLINICAL TYPES OF nREACTIONS AND PECULIARITIES OF ODONTOGENIC nINFLAMMATORY DISEASES. THE ROLE OF THE IMMUNE, HORMONAL, nVASCULAR, BLOOD-COAGULABILITY SYSTEMS, ETC.
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Phlegmon

Phlegmon is a spreading diffuse inflammatory process with formation of suppurative/purulent nexudate or pus. This is the result of acute purulent inflammatiowhich may be related to bacterial infection, however the term ‘phlegmon‘ mostly refers to a walled-off inflammatory mass nwithout bacterial infection, one that may be palpable on physical examination.

Aexample would be phlegmon of diverticulitis. nIn this case a patient would present to the emergency department with left nlower-quadrant abdominal tenderness, and the diagnosis of sigmoid diverticulitis would be high on the differential diagnosis, nyet the best test to confirm it would be CT scan.

Another nexample, phlegmon affecting the spine, is known as spondylodiscitis and is associated with endplate destructioand loss of disc height. In adults, the bone marrow is affected first, while in children, the ndisease starts in the disc itself and spreads rapidly to the adjacent vertebral nbodies. Phlegmon in the spine can be a diffuse nenhancement, or localized abscess, (peripheral enhancement) in the epidural, subligamentous or paraspinous nspaces. Under MRI examination, phlegmon nwill show dark with T1, and high signal (bright) with T2.

Etiology

Commonly by bacteria – streptococci, spore and non-spore forming anaerobes, etc.

Factors naffecting the development of phlegmons are virulence nof bacteria and immunity strength.

Classifications

1.     By clinical course:

o    acute

o    subacute

2.     By severity of ncondition:

o    mild

o    average

o    severe (with spreading nto other location(s))

3.     By location:

o    Superficial

§  cutaneous

§  subcutaneous

§  interstitial tissue

§  intramuscular

o    Deep

§  mediastinal

§  retroperitoneal

4.     By etiology:

o    single

o    mix (e.g.:spore nand non-spore forming anaerobes)

5.     By pathogenesis:

o    per continuitatem n(through neighbouring tissues)

o    hematogenous (through non-valvular veins nlike venous plexus of face e.g.: v. pterygoideus nplexus → inflammation of veins (phlebitis) → thrombus nformation in veins → embolization of thrombus ninto sinus venousus systems)

o    odontogenous

6.     By exudative character:

o    purulent phlegmon

o    purulent-hemorrhagic nphlegmon

o    putrefactive phlegmon

7.     By presence of ncomplications:

o    with complications n(disturbance of mastication, ingestion, speech, cardiovascular and respiratory nsystem, peritonitis, lymphadenitis, loss of conscious if very severe, etc.)

o    without complication

Clinical pictures

1.     nSystemic features of infection such as increased body ntemperature (up to 38-40 °C), general fatigue, chills, sweatings, nheadache, loss of appetite).

2.     Inflammatory signs – dolor (localized pain), calor (increase local tissue ntemperature), rubor (skiredness/hyperemia), tumor (either clear or nnon-clear bordered tissue swelling), functio laesa (diminish affected nfunction).

NB: nseverity of patient condition with phlegmons is ndirectly proportional to the degree of intoxication level i.e. the severe the ncondition, the higher degree of intoxication level.

A nnoninfectious occurrence of phlegmon be found in the acute pancreatitis nof Systemic Lupus Erythamatosis. The nimmunosuppressive aspects of this disease and the immunosuppressive medications used to treat it blunt each of the nsigns of infection.

Diagnostics

1.     Complaints and clinical nappearances

2.     Anamnesis

3.     Visual and Palpations

4.     Blood test – leukocytosis (up to 10-12×10⁹/L), decrease nor absence eosinophils level, shift of white count ndifferential to the left (neutrophilia), increase ESR (up to 35–40 mm/hr).

5.     Urine test – presence of nbacteria in urine, increase urinary leucocyte counts.

6.     X-ray test

7.     Ultrasound test

Treatments

The nmain goal of treatment is to remove the cause of the phlegmonous nprocess in order to achieve effective treatment and prevention of residives.

If the npatient’s condition is mild and signs of inflammatory process are present nwithout signs of infiltrates, then conservative treatment with antibiotics is nsufficient.

If the patient’s ncondition is severe, however, immediate operation is usually necessary with napplication of drainage system. All of these are done under general anaesthesia. During operation, the cavity or place of phlegmonous process are washed with antiseptic, antibiotic nsolutions and proteolyic ferments.

Ipost-operative period, patients are treated with intravenous antibiotics, haemosorbtion, vitaminotherapy. nAdditionally, the use of i/v or i/m nantistaphylococci γ-globulior anatoxin can be taken as immunotherapy.

During noperation of phlegmon dissection at any location, it nis important:

1.     to avoid spreading of pus nduring operation;

2.     to take into account the ncosmetic value of the operating site, especially when treating phlegmmonous process of the face; and

3.     to avoid damaging nnerves.

Information and Resources

Abscess

Abscess Overview

Aabscess is a tender mass generally surrounded by a colored area from pink to ndeep red. Abscesses are often easy to feel by touching. The middle of aabscess is full of pus and debris.

Painful nand warm to touch, abscesses can show up any place on your body. The most ncommon sites are in your armpits (axillae), areas naround your anus and vagina (Bartholin gland abscess), the base of your spine (pilonidal abscess), around a tooth (dental abscess), and in your groin. Inflammation around a nhair follicle can also lead to the formation of an abscess, which is called a boil (furuncle).

Unlike nother infections, antibiotics alone will not usually cure an abscess. Igeneral an abscess must open and drain in order for it to improve. Sometimes ndraining occurs on its own, but generally it must be opened by a doctor in a nprocedure called incision and drainage (I&D).

Abscess Causes

Abscesses nare caused by obstruction of oil (sebaceous) glands or sweat glands, ninflammation of hair follicles, or  minor breaks nand punctures of the skin. Germs get under the skin or into these glands, which ncauses an inflammatory response as your body’s defenses try to kill these ngerms.

The nmiddle of the abscess liquefies and contains dead cells, bacteria, and other ndebris. This area begins to grow, creating tension under the skin and further ninflammation of the surrounding tissues. Pressure and inflammation cause the npain.

People nwith weakened immune systems get certain abscesses more often. Those with any nof the following are all at risk for having more severe abscesses. This is nbecause the body has a decreased ability to ward off infections.

• Chronic steroid therapy

• Chemotherapy

• Diabetes

• Cancer

• AIDS

• Sickle cell disease

• Leukemia

• Peripheral vascular disorders

• Crohn’s disease

• Ulcerative colitis

• Severe burns

• Severe trauma

• Alcoholism or IV drug abuse

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Other nrisk factors for abscess include exposure to dirty environments, exposure to npersons with certain types of skin infections, poor hygiene, and poor ncirculation.

Abscess Symptoms

Most noften, an abscess becomes a painful, compressible mass that is red, warm to ntouch, and tender.

• As some abscesses progress, they may “point” and come to a head so you can see the material inside and then spontaneously open (rupture).

• Most will continue to get worse without care. The infection can spread to the tissues under the skin and even into the bloodstream.

• If the infection spreads into deeper tissue, you may develop a fever and begin to feel ill.

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Abscess Treatment: nSelf-Care at Home

• If the abscess is small (less than 1 cm or less than a half-inch across), applying warm compresses to the area for about 30 minutes 4 times daily can help.

• Do not attempt to drain the abscess by pressing on it. This can push the infected material into the deeper tissues.

• Do not stick a needle or other sharp instrument into the abscess center because you may injure an underlying blood vessel or cause the infection to spread.

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Abscess

(continued)

When to Seek Medical nCare

Call nyour doctor if any of the following occur with an abscess:

• You have a sore larger than 1 cm or a half-inch across.

• The sore continues to enlarge or becomes more painful.

• The sore is on or near your rectal or groin area.

• You have a fever of 101.5°F or higher.

• You have a red streak going away from the abscess.

• You have any of the conditions listed above.

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Go to a nhospital’s Emergency Department if any of these conditions occur with aabscess:

• Fever of 102°F or higher, especially if you have a chronic disease or are on steroids, chemotherapy, or dialysis

• A red streak leading away from the sore or with tender lymph nodes (lumps) in an area anywhere between the abscess and your chest area (for example, an abscess on your leg can cause swolle lymph nodes in your groin area)

• Any facial abscess larger than 1 cm or a half-inch across

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Exams and Tests

The ndoctor will take a medical history and ask for information about the following:

• How long the abscess has been present

• If you recall any injury to that area

• What medicines you may be taking

• If you have any allergies

• If you have had a fever at home

• The doctor will examine the abscess and surrounding areas. If it is near your anus, the doctor will perform a rectal exam. If an arm or leg is involved, the doctor will feel for a lymph gland either in your groin or under your arm.

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Medical Treatment

The ndoctor may open and drain the abscess.

• The area around the abscess will be numbed with medication.

• It is often difficult to completely numb the area, but in general local anesthesia can make the procedure almost painless.

• You may be given some type of sedative if the abscess is large.

• The area will be covered with an antiseptic solution and sterile towels placed around it.

• The doctor will cut open the abscess and totally drain it of pus and debris.

• Once the sore has drained, the doctor will insert some packing into the remaining cavity to minimize any bleeding and keep it open for a day or two.

• A bandage will then be placed over the packing, and you will be given instructions about home care.

• Most people feel better immediately after the abscess is drained.

• If you are still experiencing pain, the doctor may prescribe pain pills for home use over the next 1-2 days.

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Next Steps: Follow-up

Follow ncarefully any instructions your doctor gives you.

• The doctor may have you remove the packing yourself with instructions on the best way to do this. This may include soaking or flushing.

• Be sure to keep all follow-up appointments.

• Report any fever, redness, swelling, or increased pain to your doctor immediately.

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Abscess

Prevention

Maintaigood personal hygiene by washing your skin with soap and water regularly.

• Take care to avoid nicking yourself when shaving your underarms or pubic area.

• Seek immediate medical attention for any puncture wounds, especially if:

• You think there may be some debris in the wound

• You have one of the listed medical conditions

• You are on steroids or chemotherapy

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Outlook

Once ntreated, the abscess should heal.

• Many people do not require antibiotics.

• The pain often improves immediately and subsides more each day.

• Wound care instructions from your doctor may include wound repacking, soaking, washing, or bandaging for about 7 to 10 days. This usually depends on the size and severity of the abscess.

• After the first 2 days, drainage from the abscess should be minimal to none. All sores should heal in 10-14 days.

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Synonyms and nKeywords

abscess, abscesses, boils, carbuncles, furuncles, hidradenitis nsuppurativa, pilonidal abscess, pustules, whiteheads

Dental nAbscess Overview

A ndental abscess is an infection of the mouth, face, jaw, or throat that begins nas a tooth infection or cavity. These infections are commoin people with poor dental health and result from lack of proper and timely ndental care.

• Bacteria from a cavity can extend into the gums, the cheek, the throat, beneath the tongue, or even into the jaw or facial bones. A dental abscess can become very painful when tissues become inflamed.

• Pus collects at the site of the infection and will become progressively more painful until it either ruptures and drains on its own or is drained surgically.

• Sometimes the infection can progress to the point where swelling threatens to block the airway, causing difficulty breathing. Dental abscesses can also make you generally ill, with nausea, vomiting, fevers, chills, and sweats.

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Causes of a Dental nAbscess

The ncause of these dental abscesses is direct growth of the bacteria from aexisting cavity into the soft tissues and bones of the face and neck.

Ainfected tooth that has not received appropriate dental care can cause a dental nabscess to form. Poor oral hygiene, (such as not brushing and flossing properly nor often enough) can cause cavities to form in your teeth. The infection then may nspread to the gums and adjacent areas and become a painful dental abscess.

Symptoms of a Dental nAbscess

Symptoms nof a dental abscess typically include:

• Pain

• Swelling

• Redness of the mouth and face

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Symptoms nof advanced infection may include:

• Nausea

• Vomiting

• Fever

• Chills

• Diarrhea

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Other nsigns of an abscess might include, but are not limited to:

• Cavities

• Gum inflammation

• Oral swelling

• Tenderness with touch

• Pus drainage

• Difficulty fully opening your mouth or swallowing

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When to Seek Medical nCare for a Dental Abscess

If you nthink you have an abscess, call your dentist. If you cannot reach a dentist, go nto a hospital’s emergency department for evaluation, especially if you feel nsick.

• If an infection becomes so painful that it cannot be managed by nonprescription medicines, see your doctor or dentist for drainage.

• If you develop fever, chills, nausea, vomiting, or diarrhea as a result of a dental abscess, see your doctor.

• If you have intolerable pain, difficulty breathing or swallowing.

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Exams and Tests for a nDental Abscess

A ndoctor or dentist can determine by a physical exam if you have a drainable abscess. X-rays of the nteeth may be necessary to show small abscesses that are at the deepest part of nthe tooth.

Treating a Dental nAbscess at Home

• People who have cavities or toothaches can take NSAIDs, nonsteroidal anti-inflammatory medicines, such as ibuprofen (Advil) or naproxen (Aleve), as needed for relief of pai and inflammation.

• If an abscess ruptures by itself, warm water rinses will help cleanse the mouth and encourage drainage.

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Medical Treatment for a nDental Abscess

The ndoctor may decide to cut open the abscess and allow the pus to drain. Unless nthe abscess ruptures on its own, this is the only way that the infection can be ncured. People with dental abscesses are typically prescribed pain relievers nand, at the discretion of the doctor, antibiotics to fight the infection. Aabscess that has extended to the floor of the mouth or to the neck may need to nbe drained in the operating room under anesthesia.

Dental Abscess Follow-Up nCare

With a ndental abscess, as with each and every illness, comply with your doctor’s ninstructions for follow-up care. Proper treatment often means reassessment, nmultiple visits, or referral to a specialist. Cooperate with your doctors by nfollowing instructions carefully to ensure the best possible health for you and nyour family.

Prevention of a Dental nAbscess

Preventioplays a major role in maintaining good dental health. Daily brushing and nflossing, and regular dental checkups can prevent tooth decay and dental abscesses.

• Remember to brush and floss after every meal and at bedtime.

• If tooth decay is discovered early and treated promptly, cavities that could develop into abscesses can usually be corrected.

• Avoidance of cigarette smoking and excess alcohol consumptio can help too.

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Outlook for Dental nAbscesses

The nprognosis is good for the resolution of a small dental abscess, once it has nruptured or been drained. If the symptoms are improving, it is unlikely that nthe infection is getting worse. Proper follow-up care with your dentist is nmandatory for reassessment of your infection and for taking care of the problem ntooth.

• Care might include pulling the tooth or having a root canal performed on it.

• Dental abscesses that have extended to the floor of the mouth or to the neck can threaten a person’s airway and ability to breathe and may be life-threatening unless they are properly drained.

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The Basics of Acute Inflammation

Inflammation, described in the nsimplest terms is the local physiological response to tissue injury.
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nMany things can cause this ‘injury’, from microbial infections (bacteria, viruses, etc) through to nphysical agents (e.g. trauma, heat, etc).The primary goal of inflammation is to nbring phagocytes and plasma proteins to the area such that they can destroy the ninvaders, remove debris and prepare for subsequent healing.
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nInflammation is often categorised firstly by its time ncourse; Acute & Chronic Inflammation. Acute inflammation consists of nthe initial response of the body to tissue injury, whilst chronic inflammatiois the prolonged tissue reactions following the initial response. Today I shall nfocus on the former.
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nThere are Five Cardinal Signs of Acute Inflammation nwhich occur due to a number of reasons.

• Rubor (redness): Dilatation of small blood vessels in damaged area
• Calor (heat): Increased blood flow to area (hyperaemia)
• Tumour (swelling): Accumulatio of fluid in extracellular space (edema, British: Oedema)
• Dolor (pain): Stretching/distortion of tissue from oedema (esp. from pus), chemical mediators can induce pain
• Loss of function: Movement hindered etc.

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Chemical mediators of inflammation interact with other nimmune cells to elicit an appropriate response (in autocrine/paracrine nfashion, an occasionally through the blood).
nIt is important to remember that there are both good and bad aspects to acute ninflammation.
nThe Good.

• Dilution of toxins
• Entry of antibodies
• Transport of drugs
• Fibrin formation (traps microbes, serves as a matrix for granulation tissue)
• Delivery of nutrients & oxygen
• Stimulation of immune response

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The Bad.

• Swelling (can occlude airways, raise intra-cranial pressure and so on)
• Inappropriate inflammatory response.
• Digestion of normal tissues

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The ninterplay between Acute & Chronic Inflammation

 

The Inflammation Process

Dealing with injury nand infection is vital to survival. It is hardly surprising then, that all nanimals possess mechanisms designed specifically to deal with wound healing and nmicrobial defence. In mammals such as ourselves, nthese mechanisms are remarkably complex and, when they function correctly, nproduce an exquisitely choreographed suite of reactions which biologists are nonly now beginning to fully appreciate. The first stage in this process is nknown as the acute phase response, or, less technically, as inflammation.

Traditionally nWestern medicine has recognised the four signs of ninflammation as tumor, rubor, calor nand dolor – swelling, redness, heat and pain. Besides these physical nchanges, there are also important psychological ones, including lethargy, apathy, nloss of appetite and increasing sensitivity to pain – a suite of symptoms that nare collectively known as “sickness behaviour“. nTaken together, the four classic signs of inflammation and the psychological nsymptoms of sickness behaviour constitute the complex nset of processes referred to as the acute phase of response.

Pain

The value of nfeeling bad is nowhere better illustrated than in the case of pain. Pain, as neveryone knows, is a great protector. The acute pain, as caused by you touching na hot stove, is obviously beneficial, making you move away quickly from ndamaging objects. Even more important, however, is the second phase of paithat tends to follow the acute pain. Acute pain is sharp and stabbing, and ends nwhen you are no longer in contact with the source of damage; the second type of npain is deep and spreading, and can last for minutes, hours, days or evemonths. This kind of pain is not caused by pressure or heat from the outside nworld, but by chemicals released by the body itself. And, unlike acute pain, nwhich produces a rapid movement, the second type of pain causes you to keep the nwounded area as still as possible, and encourages you to take extra care to nshield the area from fresh injury while the process of repair is completed.

Swelling

The same applies to nall other aspects of the acute phase response. Swelling, for example, is also a ndefensive process, caused by the leakage of plasma and the migration of immune ncells into the area of damaged tissue. All bodily damage, whether caused by injury nor infection, consists of broken cells, and when the walls of a cell rupture, nan array of molecules which would not otherwise be released, spill out into the nsurrounding tissue. Some of these molecules trigger the sensory nerves to nproduce the ongoing, second type of pain just described. The sensory nerves nalso react by causing the blood vessels to widen, increasing local blood flow (Redness), nand making the walls of the blood vessels more permeable. With greater blood nflow, more white blood cells, the infantry of the immune system, can be carried nto the site of the injury. The greater permeability of the blood vessel walls nenables the white blood cells to flow out of the arteries and veins into the nsurrounding tissue to defend against possible bacterial invaders. If no nbacteria have found their way into the wound, particular white blood cells nknown as macrophages clear up the debris of the chattered cells by engulfing nand digesting it. If bacteria have gained a foothold and started to multiply, nthe white cells form a barrier to create a pus-filled abscess in which the nblood fluid, the serum, plays a key role in healing.

Besides clearing up nthe debris and attacking bacteria themselves, the macrophages also release a nnumber of chemical messengers. These signalling nmolecules, or cytokines, play a vital role in co-ordinating nthe acute phase response by facilitating both short-distance communicatioamong the immune cells themselves and long-distance communication between the nimmune cells at the injured site and the brain.

Fever

Increasing levels nof prostaglandin E2 in the brain induce an area called the hypothalamus to turup the body’s thermostat a notch. Suddenly, the same external temperature feels ncolder, and various means are employed to restore the subjective impression of nwarmth. These include involuntary processes such as shivering, which generates nheat by movement, and voluntary behaviour such as nputting on more clothes, finding a warm radiator to sit next to, and so on.

Like pain and nswelling, fever plays a vital part in defending the body against infection. nMany bacteria reproduce most effectively at normal body temperature. So by nraising body temperature the rate at which the bacteria can divide is slowed ndown. Fever has the opposite effect on most immune cells, causing them to ndivide more quickly. So fever both slows down the spread of the infection and naccelerates the counterattack by the immune system.

All injuries and ninfections, as stated above, cause a fever. This might nonly manifest itself in a localised heat, and does nnot always produce an overall increase of the body temperature.

Lethargy, Apathy nand Loss of Appetite

Fever is not cheap. nThe body has to work hard to raise its temperature. In mammals, an increase of njust one degree Celsius in core body temperature requires around 10-13 per cent nmore energy thaormal. To balance the energy budget, savings must be made nelsewhere, and the brain accordingly generates feelings of lethargy and apathy nwhich reduce the energy expended in behaviour. Sick npeople generally do not feel like doing very much, but this is not because they nhave simply “run out of energy”. They are merely saving their energy nto use in other ways.

Mechanism of the nAcute Phase Response

In response to nacute damage or entrance of foreign material monocytes nenlarge and synthesise increased amounts of enzymes nwhich help to break down the material. In doing so they are transformed to more nactive phagocytes called macrophages. Monocytes nare formed in the bone marrow, enter the blood stream and have a longer life nthan neutrophils (T and B lymphocytes, “white nblood cells”), estimated at 12 to 24 hours. Monocytes nrespond to chemotactic and immobilising nfactors (migration inhibitory factor) excreted by lymphocytes. This allows them nto “stick” at the debris site.

Macrophages have nsurface receptors for antibodies and are capable of synthesising nvarious proteins as messengers. An important function of the macrophage is the npresentation of debris material to B and T cells. Large molecules or particular nsubstances, however, require digestion by the macrophage before they can be recognised by the other cells of the immune system. Bits of nthese materials will be displayed on the surface of the macrophage and via ncontact stimulate both B and T cells into appropriate action.

Lymphocytes n(including B and T cells) mainly produce immunoglobulins n(antibodies) and are also responsible for cellular immunity. Cellular immunity nis involved in delayed hypersensitivity (allergies and various overreactions of nthe body) and homograft rejection. Lymphocytes can also damage foreign cells n(bacteria, parasites, fungi, etc.). Human lymphocytes are formed chiefly in the nbone marrow. Normal T cells develop only in the presence of a normal nfunctioning thymus. Long lived lymphocytes are primarily T cells, nthat recirculate through the spleen and the nlymph nodes, thoracic duct and bone marrow, leaving and re-entering the ncirculation repeatedly. There are subpopulations of T cells which serve to nenhance (helper T) or reduce (suppressor T) B-cell responses. It is not yet nknown precisely how the various surface receptors on T and B cells influence ncell function, but they are probably involved in antigen recognition and ncell-to-cell interactions with macrophages and other lymphocytes.

We see the various ncells involved in the process under our powerful microscopes in still pictures. nWe also can measure various substances at various points throughout the ninflammation process and we can identify certain specific sites on the cell nsurface. From this information we piece together the story of cellular nimmunity. In fact, we tell a number of “separate” stories about the nimmunological response. There is the story about how antibodies are first nformed and then used to illicit a rapid response when exposed to the same n”intruder” again. There is the story of how the immune system nresponds to a bacterial, or similar, invasion. There is the story of how the nimmune system creates tolerance for the prevention of immunologically ninduced self-injury. There is the story of autoimmunity, whereby antibodies are nformed against the body’s own tissue, which will consequently be attacked. nThere is the story of anaphylaxis, an extreme overreaction of the body defence mechanism. There is the story of the complement nsystem, which consists of at least 15 plasma proteins which interact nsequentially, producing substances that mediate several functions of ninflammation. A lot of stories in which different substances and pathways are ndescribed, but without any serious linking of the various stories or without nany knowledge as to why and how the body chooses to follow that particular npathway on that particular occasion.

Returning to the nacute phase response, the story we are particularly interested in, we know that nthere are many different cytokines (messengers) involved. One of the first ncytokines to be released by the macrophages on detecting signs of injury or ninfection is known as interleukin-1ß (IL-1ß). It diffuses into the ntissue surrounding the damaged cells, where it triggers a second wave of ncytokines which cause other types of immune cells such as neutrophils nand monocytes to migrate to the injured site. The nIL-1ß released by the macrophages also enters the blood stream, where it nis carried to the brain, but is prevented from entering the brain directly by a nlayer of cells known as the blood-brain barrier. It therefore adopts a more ncunning route into the central nervous system. First, the IL-1ß molecules nattach themselves to specially designed receptors on the surface of the cells nin the blood-brain barrier. When these receptors are activated, a chaireaction is initiated that eventually leads to the manufacturing of a molecule nknown as prostaglandin E2, which, unlike IL-1ß, is capable of passing nthrough the blood-brain barrier. When it enters the brain, prostaglandin E2 nactivates the receptors on both neurons and microglia n(immune cells in the brain), which can then initiate the other components of nthe acute phase response: fever, lethargy, apathy, loss of appetite, anxiety, nand increased sensitivity to pain in other areas of the body. But the story ndoes not end there. Once inside the brain, prostaglandin E2 encourages the microglia to manufacture IL-1ß. The net result is nthat, although IL-1ß cannot cross the blood-brain barrier directly, a nbuild-up of IL-1ß in the blood stream leads to a build-up of IL-1ß nin the brain and the cerebrospinal fluid. To complete the cycle, the nIL-1ß leads to further synthesis of prostaglandin E2 in the brain, which nin turn augments the various components of sickness behaviour.

To compensate for nthe decreased supply of new calories caused by the loss of appetite, the body nstarts to unleash old calories that have been stored up for just such times of nemergencies. These calories are stored in fat deposits around the body, but nbefore the fat can be used as a source of energy it must be broken down into nglucose. So another crucial component of the acute phase response is the nsecretion of glucocorticoids, which trigger the process nof converting fat to glucose. The key glucocorticoid nin humans is cortisol, which is released by the nadrenal glands in response to a cascade of chemical signals initiated in the nbrain by IL-1ß. First, the IL-1ß stimulates the hypothalamus to nsecrete a chemical called corticotrophin releasing hormone (CRH). nThe CRH travels to the pituitary gland, just below nthe brain, where it triggers the release of another chemical called adrenocorticotrophic hormone (ACTH). Finally, the ACTH nreaches the adrenal glands, which secrete the cortisol. nBecause of their close interconnections, the three anatomical structures ninvolved in this chemical cascade are known collectively as the hypothalamo-pituitary-adrenal axis.

You do appreciate nthat the story presented here is a simplified version – nobody knows exactly nwhat happens in all directions at any given moment in time – but it helps us to nconcentrate on that part of the story that we are particularly interested in. nAnd here is a very interesting part of the story: the fight-flight response, nwhich enables vertebrates to respond to large predators, evolved by co-opting nthe biological systems underlying the acute phase response. Both the innate nimmune response to infection and the fight-flight response to large predators activate nthe same immune-brain circuits. When a monkey or a human spots a lion moving nrapidly towards them, for example, the hypothalamo-pituitary-adrenal naxis is activated, just as it is by IL-1ß in the acute phase response. Iboth cases, the HPA axis responds with the same nchemical cascade leading to the release of cortisol nby the adrenal glands. This makes good sense, since cortisol nbreaks down the body’s fat reserves into glucose that provides vital energy. It nis of interest also to note that this whole system immediately reverses as sooas the danger has subsided. That may occur because the lion starts to run away nfrom us, or because we all of the sudden recognise nthe “lion” as our favourite dog!

Problems I have nwith it

Let’s go through nthe phases again.

The acute phase nresponse, as is the fight-flight response, has to be an instantaneous response nin order to keep you alive. The first thing that happens in damaged tissue or ninfection is a response from the macrophages, or the monocytes n- this is not quite clear from the science. How many damaged cells, or how nmany bacteria, viruses or parasites, are required to trigger off this set of nevents? Macrophages and monocytes are floating naround in the blood stream. What makes them aware of damaged tissue or foreigmaterials? Is it by sheer luck that they come across these? And if so, how do nthey get to damaged cells deep in an organ or structure, when they are mainly nfloating around in the blood? Whatever the answers to these questions, one nthing looks likely: it is going to take time.

From here on, a nnumber of different cells and a whole string of “messengers” are ninvolved in the process. Let’s follow just one line.

The macrophages, nonce they have located the problem, release IL-1ß which “diffuses ninto the tissues surrounding the damaged cells”. This interleukin leaks nfrom the macrophages into its outer-environment. In other words, for the time nbeing, it remains local. After some time, it drifts into the blood nstream. Via the blood stream it is taken up to the brain. That journey takes ntime. Of course, the blood stream will take the IL-1ß to all other nplaces in the body too but as we have no information on what it might do there, nwe are better off totally ignoring that fact! If IL-1ß triggers off a nsecond wave of cytokins which cause other immune ncells to migrate to the site, why doesn’t this happen anywhere else in the body nwhilst IL-1ß is travelling throughout the whole nbody? And furthermore, why isn’t IL-1ß picked up by any of the nelimination systems it travels past? How do the kidneys or the liver know whea molecule is needed or obsolete?

Now IL-1ß narrives at the brain, but finds that it can’t enter. It attaches itself to nspecific receptors on the membrane of the blood-brain barrier. This is said to ntrigger a chain reaction on the other side of the barrier, i.e. in the brain. How nmany IL-1ß molecules are needed in order to trigger this reaction? What nis the proportion between the number of molecules attached to the outside and nthe extent of the reaction? What is the regulatory mechanism and what will stop nit? Finding an appropriate receptor site, reading the message and nperforming the reaction on the other side surely, all of that takes time.

One of the nresponses from the brain is to produce prostaglandin E2. Producing something iresponse to a direct order surely will take time.

Prostaglandin E2 is nnow capable of pushing through the blood-brain barrier. Passing through a check npoint surely takes time.

Once inside the nbrain prostaglandin E2 has to find very specific receptors on two different ncells, the neurons and the microglia. Once this has nbeen done, the other aspects of the acute phase response are put in motion. How nmany molecules of prostaglandin E2 are required to illicit such a response? How nis the response, once it has been triggered, controlled? For the nervous ncells to carry out these instructions to put in place “loss of appetite, nfever, lethargy and increased sensitivity to pain in other parts of the nbody”, is surely going to take time.

Also, prostaglandiis now encouraging the microglia to produce nIL-1ß. This production of material in response to a very specific order nmust take time.

Oh nearly forgot, nIL-1ß also travels to the hypothalamus, a particular part of the brain. This njourney must take time. Once there, it stimulates the hypothalamus to nproduce the corticothrophin releasing hormone (CRH). This hormone travels to the pituitary gland, which is non the outskirts of the brain. This journey must take time. Do all nthese molecules know exactly where to travel to? If so, how? nOtherwise, what happens to all the stuff that goes astray? And aren’t we lucky nthat nowhere else except where it is required, tissues exist that possibly ncould respond to these drifters?

In the pituitary ngland the CRH stimulates the production of the adrenocorticothrophic hormone (ACTH). Surely, the nproduction of this must take time.

The ACTH is now nreleased into the blood stream. Don’t ask how? Are we now all of the suddeoutside the blood-brain barrier? How did that happen; we didn’t have the same nfuss coming out as we had going in, did we? Via the blood the ACTH travels nto the adrenal glands. Well, in fact, of course, it travels anywhere and neverywhere in the body. Why is it only the adrenal glands that recognise this molecule? How does a cell that is part of a ngland, and can’t move, make contact with a single molecule that happens to be nfloating by in the blood stream? How many molecules are needed to trigger the nresponse? How will the manufacturing and the amount required be regulated? The njourney must have taken time.

The adrenal gland nnow produces cortisol. That production must take ntime.

Now you are ready nfor that lion that is running towards you. And guess what, if it turns out not nto be a lion, you will turn this whole mechanism off straightaway and all the neffects will be immediately reversed.

How much time do nyou reckon that will take?

And There is More

The main questions nthese theories throw up are about the time consumed in all these chemical nreactions as well as the time spent travelling, and nthe very precision of the connections made. Don’t forget that all of this cabe switch off and on in a blink of an eye.

However, when we nlook around we find that there is more evidence we need to consider if we want nto have a better understanding of the functioning of our body.

• Blalock found that lymphocytes were secreting the mood-altering brain peptide endorphin, as well as ACTH, a stress hormone thought to be made exclusively by the pituitary gland. How can a cell of the immune system produce and secrete a hormone that relates to our moods? Candace Pert found that every neuropeptide they identified in the brain was also found on the surface of the huma lymphocyte. These emotion-affecting peptides actually appear to control the routing and migration of monocytes, which are very pivotal to the overall health of the organism. They communicate with the other lymphocytes, called B cells and T cells, by interacting through peptides and their receptors, thus enabling the immune system to launch a well-coordinated attack against disease. How can specific brain peptides not only get to the cells of the immune system, but the actually tell them what to do?
  But immune cells don’t just have receptors on their surfaces for the various neuropeptides. As demonstrated by the paradigm-shaking research of Ed Blalock at the University of Texas in the early eighties, and confirmed by research done by Michael Ruff, Sharon and Larry Wahl and Candace Pert (Department of Physiology and Biophysics at Georgetown University Medical Center in Washington, D.C.), immune cells also make, store and secrete neuropeptides themselves. In other words, the immune cells are making the same chemicals that we conceive of as controlling mood in the brain. So, immune cells not only control the tissue integrity of the body (defence system), but they also manufacture information chemicals that can regulate mood or emotion (mental state)
• Consider CCK, a neuropeptide governing hunger and satiety, which was first discovered and sequenced by chemists who were exploring its first action on the gut. If you were give doses of CCK, you would not want to eat, regardless of how long it had been since your last meal. Only recently have we been able to show that both the brain and the spleen, which can be described as the brain of the immune system, also contain receptors for CCK. So brain, gut and immune system are all being integrated by the action of the CCK.
  There are nerves that contain CCK all along the digestive tract and in and around the gallbladder. After a meal, when the fat content is moving through the digestive system to your gallbladder, you experience a feeling of satisfaction, or satiety, thanks to the signal CCK sends to your brain. CCK also signals your gallbladder to go to work on the fat in the meal, which enhances the feeling of fullness. The CCK system also signals your immune system to slow down whilst the food is still digesting. How can a brain chemical directly regulate the way the digestion works, and co-ordinate this with the function of the gallbladder and the immune system, all at the same time?
• Scientists have also established that when you intend to bite into a lemon, the digestive system is already releasing the required juices to deal with the lemon. These enzymes are specific for the type of food you are about to put in your mouth. How does the stomach know what it coming its way even before it gets there? If all the communication is of a chemical nature how can a cell produce and release specific enzymes without any part of the body being in contact with the food item? Equally, it has been demonstrated in seriously dehydrated people that the first sip of water they take, knowing that there is more available, already releases the blockade on the kidneys and that all systems instantaneously start to act as if they had enough water. If the body works as a bag of chemicals, it would be logical to assume that the dehydration emergency state would not be lifted until the sensor found that enough water was available inside the body.
• Deepak Chopra MD sums it all up. “At the very instant that you think, “I am happy”, a chemical messenger translates your emotion, which has no solid existence whatever in the material world, into a bit of matter, perfectly attuned to your desire, that literally every cell i your body learns of your happiness and joins in. The fact that you ca instantly talk to 50 trillion cells in their own language is just as inexplicable as the moment wheature created the first photon out of empty space.” Every thought is instantly translated into a balance of chemicals which direct every cell of the body to express this thought in a co-ordinated and appropriate way.
  This is only possible, on the huge scale that we are talking about, if each individual cell “knows” the thought and produces whatever is necessary to express that thought itself.

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This leads to two nserious consequences. One is the fact that somehow there must be a way that neach cell has a direct line to our mind. A thought is not a physical thing nuntil a cell produces something to make it physical. Yet, somehow the thought is n”captured” by each and every cell and it is this thought that tells nthe cell what to do. Or in other words, a non-physical thing is heard and read nby all cells and they react exactly to what is the essence of that non-physical nentity. This must mean that all cells are highly sensitive to “a nmood”, to “something in the air”, to “an atmosphere”, n”a sense of” or “an energetic alteration”. As the mind nchanges, so does the function of each and every cell in the body; and only naccording to the state the mind is in. Be happy and all your cells are nhappy. Be angry and tense and all your cells are angry and tense. From the nmoment you think something is doing you good, it is. When you think something nis damaging you, it is. It is the thought that provokes the effect, not the nsubstance or the situation.

And secondly, it nmeans that the immediate cell reaction we see is organised nby the cell itself, producing all required attributes itself. Once these nchemicals, proteins, peptides, hormones, etc. have done their job they are ndiscarded into the surrounding tissue and dumped into the blood stream. As a nreaction of the cell’s activity, not as the cause of, the levels of these nsubstances within the surrounding tissues and the blood itself will now start nto rise. Along the banks of these extensive waterways a variety of nanti-pollution plants (glands, organs) are available, which identify specific nmaterials and filter them out of the blood circulation. These materials now naccumulate inside the glands where they are destroyed and the building blocks nrecycled. Hormones, enzymes, chemicals, etc. are not produced by glands but ncollected and destroyed by them.

• Insulin, a hormone always identified with the pancreas, is now known to be produced by the brain also, just as brain chemicals like transferon and CCK are produced by the stomach.
• If the spleen and lymph nodes are the places where the cells of the immune system are woken up and directed, we would expect to see these sites swollen and most active in the early stages of an infection. I fact, the swelling of the lymph glands is most often a secondary phase i the development of the disease and appears later on. Equally, in the advanced stages of chronic destructive diseases, such as tuberculosis, you would expect to find the highest number of leucocytes and phagocytes circulating in the blood in order to put up the maximum of fight. However, the opposite is true: numbers of circulating leucocytes are well down at the advanced stage, but the lymph nodes are engorged with leucocytes!

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Once we know that nall cells have receptors for all chemicals the body will ever use, and is ncapable of making these chemicals, we caow understand why everything always nhas an effect on every part of the body. From the fight-flight response to the ninfluence of stress or the effect of hearing bad news, the effects of every naspect of our life is immediately felt in every nook and cranny of the body.

• Doctors prescribe steroids to someone who is suffering from a difficult case of arthritis. The steroids will bring down the inflammatio in the joints dramatically, but then a host of strange things might happen. The person could begin to complain of being fatigued and depressed. Abnormal fatty deposits might begin to show under the skin and the blood vessels could become so brittle that he/she would develop large bruises that are very slow to heal. What would link these entirely divergent symptoms?
  The answer lies at the level of the receptors. Corticosteroids replace some of the secretions of the adrenal cortex, a yellowish pad on the top of the adrenal glands. At the same time, they suppress the other adrenal hormones as well as the secretions from the pituitary gland, which is located in the brain. As soon as it is given, the steroids rush in and flood all the receptors throughout the body that are “listening” for a certain message. When the receptors become filled, what follows is not a simple action. The cell can interpret the adrenal message in many ways, depending on how long the site stays filled. In this case, the receptor stays filled indefinitely. Equally important is the fact that other messages are not being received due to the blockage of receptor sites, as is the loss of innumerable connections with the other endocrine glands.
  Giving steroids to an arthritis patient involves trillions of molecules and receptor sites. That is why the blood vessels, skin, brain, fat cells and so on, all exhibit their different responses. The long-term consequences of staying on steroids include diabetes, osteoporosis, suppression of the immune system (making a person more susceptible to infections and cancer), peptic ulcers, internal bleeding, elevated cholesterol, and much more. One might even include death amongst these side effects, because taking steroids for a long period causes the adrenal cortex to shrivel. If the steroid is withdrawn too quickly, the adrenal gland does not have time to regenerate. The person is left with inadequate defences against stress, which adrenal hormones help to buffer.
  Take all these details together, and what you see is that steroids ca cause literally anything to happen. They may be the immediate cause or just the first domino – the distinction makes little difference to the person involved.
  All drugs affect all systems of the body and caever be made to be specific.
• In the body’s own biochemical chain reactions cortisol (a steroid) plays a major part in the activation of the inflammation process in order to assist the body in its efforts to clean up damaged cells or invading foreign materials (bacteria, fungi, parasites). The same steroids are prescribed by doctors as a power weapon against inflammation. How can this be? – In the natural cellular process steroids are produced in minute quantities and locally by each cell wherever the steroids are needed. They also have a very short life span. The “homeopathic” quantities have an strong inflammatory effect. However, used in huge doses and indiscriminately steroids (artificially made) become anti-inflammatory by blocking a number of inappropriate receptor sites for a long period of time.

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And then there is the problem of the white blood cells nof our immune system, the gallant defenders of the tissues. We have already nasked questions about the time and very specific actions of these cells. If nthey are floating in the blood stream waiting for a call about some damage or ninvasion, how would that message “catch” these constantly moving ntargets, and how quickly would they be able to respond in adequate numbers?

It seems there are other problems nrelating to our white blood cells.

• The white blood cell is a living cell, which has a nucleus, and it has an amoeboid action, which means that it is seen to develop protrusions that are said to be the way the white blood cell moves forward. Dr Powel has found clear evidence, however, that the white blood cell is not a living cell, but a mere compact form of pathogenic material (a sophisticated rubbish bag!). When first formed the leucocytes are neither granular nor nucleated and are referred to as “young cells” or “round cells”. As the cell progresses further it looks as if a “nucleus” appears, but soon further “nuclei” are added (You would only expect one nucleus per cell). As time advances these foci increase in size as well as iumber. The constituents thereof becoming susceptible first to one dye and then to another (The nucleus, the brain of the cell, changes format?). Sometimes they undergo fatty degeneration, and are then called myelocytes.
  The distortions on which the migratory or amoeboid movement of the leucocyte depend and which seem to indicate that it is endowed with life, are chiefly attributable to the action of the carbo dioxide gas which is generated within it as it passes into decay.
  Dr Powel affirms that every nucleus or nucleolus in a leucocyte is simply a collection of residual matter (debris from damaged cells and foreign material) and is to be regarded, therefore, as a focus of decay. He further states that the segmentation of the leucocyte is not a matter of “vital duplication” as has been supposed, but of progressive disintegratio of the morbid material. The leucocyte is not a destroyer but it is the thing destroyed.
• Five types of circulating leucocytes can be identified: neutrophils, lymphocytes, monocytes, eosinophils and basophils. It is generally accepted that all these leucocyte types derive from a common pluripotent stem cell. Apart from this common origin the various types are totally independent. None of these leucocytes divide as all other living cells do.
  Precursors of the neutrophils are myeloblasts and promyelocytes. The primary granules found in these cells contain specific enzymes and proteins. With further development the cells become myelocytes and have secondary granules, containing different enzymes. From here the neutrophilic cells become condensed and the nucleus segmented.
  Lymphocytes are a reasonably homogeneous collection of singular nucleus cells; the nucleus surrounded with only a few granules. There are two mai types, T and B cells.
  Monocytes are formed in the bone marrow from promonocytes, containing granules with specific enzymes. As a result of ingesting foreign material these monocytes transform into macrophages.
  Eosinophils have a characteristic granule containing a unique peroxidase.
  Basophils have distinctive deep-blue granules, characteristically obscuring the cell nucleus, and rich in histamine.
  All together we can count twelve different cells that are said to make up our mobile defence unit. Only the very early stem cells, which live mainly in the bone marrow, divide. It is from these cells that red blood cells and platelets are made. None of the five types of circulating leucocytes know cell division. The duplication of cells through the process of cell division is the most normal way of proliferatio in any living cell. No intact cell DNA has ever been extracted from any of the five types of leucocytes.
  If these front-runners of our defence system do not produce any copies of themselves, how can we then explain the rapid proliferation of leucocytes in case of infection?
  How can we explain the increasing numbers of leucocytes at the site of a localised infection or tissue damage without a corresponding increase in blood numbers, knowing that the white blood cells caot proliferate?
  If leucocytes have a memory of all the foreign material it has ever dealt with (used in the secondary phase of the cellular immunity), but the cells never divide, never produce offspring, and just die, how can we explai the passing on of the memory to these new leucocytes? Remember, the life span of lymphocytes is between 12 and 24 hours.

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What does all this mean?

For over twenty years now scientists have proven that nevery cell in our body can produce any enzyme, hormone or protein it needs, nincluding “messengers”. At the same ntime, every cell in our body has receptors for all the messengers, so that it ncommunicates with its immediate environment.

The rapid and very precise response of the body to any nsituation leads us to believe, in view of all that scientific evidence, that nevery cell of the body is capable of “picking up” energetic signals nand respond immediately and precisely to it. Every cell of the body n”listens out” for signals in the air, not unlike the nhuman-made radio system. It registers what it “hears” by producing nthe appropriate chemicals, which in turn set off a chain reaction as a direct nresult of the energetic environment the cell, and the whole body, finds itself nin.

These chemicals, enzymes, hormones, proteins, have a nvery short shelf-life and are washed away into the lymphatic fluid that nsurrounds each and every cell, and into the blood stream. They are excreted by nthe cell and are essentially cell waste. Here it drifts around until an organ, na gland, “recognises” the material through nits own specific receptors, captures it and draws it nout of the blood stream. Within the inner workings of each gland or organ the nmechanism for dismantling the chemical and recycling the building materials nsuch as small molecules and basic elements is put to work. The higher the blood nconcentration of the specific substance the harder the gland has to work. It nmay even become swollen under a high workload pressure!

Within this system we also know that each cell nproduces its own anti-invasion chemicals, such as interferon and the lytic enzymes. In case of damage to the tissue or the ninvasion of bacteria (see “The Origin of Germs”) the nsurrounding cells start the clean up process by producing the enzymes needed nfor the destruction and disintegration of the failing tissue. The rubbish that nis consequently produced is “bagged up” in various cell-like nstructures, each equipped with the appropriate enzymes to break down the nspecific material it is carrying. It is a mobile recycling unit on its way to nthe depot, the spleen and lymph nodes. Here the “bags” are totally ndisintegrated, broken down into its basic components and recycled.

The conclusion is that:

• glands don’t produce hormones, they collect them and break them down.
• lymph glands don’t produce white blood cells; they collect the “bags” that we have come to know as “white blood cells” and recycle the basic elements.
• swollen glands are not a response from the cellular immune system to a spreading infection; they are a sign of a detoxification system under pressure.

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Neck Spaces and Infections

ANATOMY nOF THE CERVICAL FASCIA

INTRODUCTION

Deep nneck space infections most commonly arise from a septic focus of the mandibular teeth, tonsils, parotid gland, deep cervical nlymph nodes, middle ear, or sinuses. These deep cervical space infections have nbecome relatively uncommon in the postantibiotic era. nConsequently, many clinicians are unfamiliar with these conditions. Iaddition, with widespread use of antibiotics and/or profound immunosuppression, the classic manifestations of these ninfections, such as high fever, systemic toxicity, and local signs of erythema, edema, and fluctuance, nmay be absent.

Deep nneck space infections often have a rapid onset and can progress to nlife-threatening complications. Thus, clinicians must be aware of such ninfections and should not underestimate their potential extent or severity.

The nrelevant anatomy, microbial etiology, clinical manifestations, diagnosis, and ntreatment of deep neck space infections will be reviewed here. Peritonsillar abscesses and submandibular nspace infections (Ludwig’s angina), suppurative parotitis, and odontogenic, nmiddle ear, and sinus infections are discussed in detail separately.

ANATOMIC CONSIDERATIONS

Knowledge nof the cervical compartments and interfascial spaces nis essential for understanding the pathogenesis, clinical manifestations, and npotential routes of spread of infections involving these spaces.

The neck can be divided into several layers and npotential spaces.  Some anatomists have divided the neck into visceral and nsomatic portions.  Others have divided the neck into triangles in order to nhelp organize the crowded and complicated anatomy.  Knowledge of the fascial layers and the potential spaces of the neck are nimportant to clinical practice because of the potential complications that narise from spread of infection.

Despite the constant nature of human anatomy there nhave been many permutations of the cervical fascial nlayers.  Each anatomist that has charged themselves with describing the nlayers has used different terminology which has ultimately muddled an already ncomplicated subject.  It seems that each time you learn the nomenclature; nyou encounter yet another set of synonyms.  Levitt nsummarizes it best when he said “It is essentially the terminology which is nconfusing, not the basic anatomy.”

The majority of otolaryngology papers addressing the nsubject have accepted the nomenclature reviewed by Paonessa net al.  Papers from other surgical and radiology journals continue to use ndifferent terms, so there is no universally accepted standard across different nfields.

There are two main divisions of the cervical fascia: nthe superficial layer and the deep layer.  The superficial cervical fascia ndoes not have any subdivisions.  The deep layer has multiple nsubdivisions.  All three divisions of the deep layer contribute to nformation of the carotid sheath.

The superficial cervical fascia extends from the zygoma and mimetic muscles of the face down to the chest, nshoulder and axilla.  It is similar to nsubcutaneous tissue and is divided into two potential compartments by the platysma muscle. ¹⁷

The superficial layer of the deep cervical fascia (SLDCF) surrounds the neck and encloses two glands (parotid nand submandibular), two muscles (sternocleidomastoid nand trapezius) and two spaces (suprasternal nspace of Burns and Space of the posterior triangle) (Rule of Twos).  It is na sheet of fibrous tissue that attaches to the nuchal nline, zygoma, mandible and skull base nsuperiorly.  Inferiorly it extends to the sternum and clavicles laterally nto the acromion processes.  It attaches to the nbody of the hyoid bone and extends to the mandible to form the floor of the submandibular space.  As the fascia encounters the nmandible, it splits into two portions which cover the masseter nlaterally and the pterygoids medially. ¹⁷

The middle layer of the deep cervical fascia (MLDCF) is also referred to as the visceral fascia because nit encloses the aerodigestive tract and thyroid ngland.  Superiorly it extends from the skull base posteriorly nand the hyoid bone anteriorly.  Inferiorly the nfascia is continuous with the fibrous pericardium in the upper mediastinum.  The posterior portion of the fascia is nalso called the buccopharyngeal fascia.  The nfascia has two divisions: the muscular division which encloses the infrahyoid strap muscles and the visceral division. ¹⁷

The deep layer of the deep cervical fascia (DLDCF) has two divisions: the alar nand the prevertebral layer.  Both layers extend nfrom the skull base superiorly but the alar layer nfuses with the MLDCF in the upper mediastinum nat T1-T2.  The prevertebral layer extends dowto the coccyx.  The alar layer is only present nin the anterior midline between the vertebral transverse processes.  The nlayers fuse then into one fascial layer that nsurrounds the deep neck musculature, vertebral bodies, phrenic nnerves, and brachial plexus.  It also extends laterally and becomes the axillary sheath. ¹⁷

ANATOMY nOF THE DEEP NECK SPACES

The potential spaces of the neck can be divided into ngroups in relation to the hyoid bone.  There are six suprahyoid nspaces, one infrahyoid space and five spaces that nspan the length of the neck.

SPACES nSPANNING THE ENTIRE NECK

The superficial space can be divided into two parts by nthe platysma muscle.  This space is similar to nsubcutaneous tissue and contains lymphatic channels.  The deep portiocontains the external jugular vain and lymph nodes.  Abscesses that npresent in this space can be drained by incising along Langer’s lines.  nSuperficial space infections can potentially extend to the axilla nand chest along the subcutaneous fat planes but they rarely extend deeper past nthe superficial layer of the deep fascia. ¹⁷

The retropharyngeal space extends from the skull base nto the upper mediastinum at the level of T1-T2.  nIts anterior border is the buccopharyngeal fascia and nits posterior border is the alar fascia.  It ncommunicates with the anterior visceral space inferiorly.  The space is ndivided in the midline by a raphe that attaches the nsuperior constrictor muscle to the alar fascia.  nIt contains retropharyngeal lymph nodes (Glands of Henle) nthat typically atrophy after the age of five. ^{17, 18}

The danger space extends from the skull base to the ndiaphragm.  The anterior border is the alar nfascia and the posterior border is the prevertebral nlayer of the prevertebral fascia.  It contains nloose areolar tissue. ¹⁷

The prevertebral space nextends from the skull base to the coccyx.  The anterior border is the prevertebral layer of the prevertebral nfascia and posteriorly it is limited by the anterior nlongitudinal ligament of the vertebral bodies.  Laterally the space is nconfined by the transverse processes of the vertebral bodies. ¹⁷

The visceral vascular space is the potential space nwithin the carotid sheath.  It extends from the skull base to the mediastinum.  It contains the carotid artery, internal njugular vein and vagus nerve.  It also receives nlymphatic drainage from all the lymphatic vessels in the head and neck. ¹⁷

SUPRAHYOID SPACES

The submandibular space is nbounded by the mandible anteriorly and laterally, the nlingual mucosa superiorly, the hyoid postero-inferiorly nand the superficial layer of the deep cervical fascia inferiorly.  The mylohyoid muscle divides this space into a superior nsublingual space and an inferior submylohyoid nspace.  The sublingual space contains loose areolar ntissue, the hypoglossal and lingual nerves, the sublingual gland and Wharton’s nduct.  The submylohyoid space contains the nanterior bellies of the digastrics and the submandibular nglands.  These two subdivisions freely communicate around the posterior nborder of the mylohyoid.

The pharyngomaxillary space nis also known as the parapharyngeal space or lateral npharyngeal space.  It is a difficult space to visualize because of its odd nshape and multiple boundaries.  It spans from the skull base to the hyoid nbone.  The superior portion of the space at the skull base is larger thathe space inferiorly at the hyoid.  This gives the described inverted cone nshape.  The lateral border is the superficial layer of deep cervical nfascia that overlies the medial portion of the medial pterygoid nand deep lobe of the parotid gland.  Medially the space is limited by the buccopharyngeal fascia covering the superior pharyngeal nconstrictor.  The prevertebral fascia overlying nthe deep neck musculature is the posterior limit.  The pterygomandibular nraphe (which separates the superior constrictor from nthe buccinator) is the anterior limit of the nspace.  The styloid process divides the space ninto two compartments.  The poststyloid portiois also referred to as the neurovascular compartment because the carotid sheath nruns through it.  Cranial nerves IX, X, XI, XII and the sympathetic chaialso run through this space.  The prestyloid nportion is also referred to as the muscular compartment because of its nproximity to the pterygoids and constrictor.  nFat, connective tissue and lymph nodes are also contained in the prestyloid compartment.  The stylopharyngeal naponeurosis of Zuckerkandel nand Testus is formed by the intersection of the alar, buccopharyngeal and stylomuscular fascia and acts as a barrier to the spread of ninfection from the prestyloid compartment to the poststyloid compartment.

The parotid space is created by the superficial layer nof deep cervical fascia as it splits to surround the mandible and parotid ngland.  The fascia sends dense connective tissue septa from the capsule ninto the gland.  In addition to the parotid gland, this space contains the nparotid lymph nodes, the facial nerve and posterior facial vein.  The fascial envelope is deficient on the supero-medial nsurface of the gland, facilitating direct communication between this space and nthe parapharyngeal space.

The peritonsillar space is nbound by the capsule of the palatine tonsil medially, the superior pharyngeal nconstrictor medially.  The superior border is the anterior tonsillar pillar and the posterior tonsillar npillar is the inferior border.  The space contains loose areolar tissue and minor salivary glands.

The masticator space is formed by the superficial nlayer of the deep cervical fascia as it surrounds the masseter nlaterally and the pterygoid muscles medially.  nThis space contains these muscles as well as the body and ramus nof the mandible, the inferior alveolar nerves and vessels and the tendon of the ntemporalis muscle.  The masticator space is idirect communication with the temporal space superiorly deep to the zygoma.  This space is antero-lateral nto the pharyngomaxillary space.

The temporal space has as its lateral boundary the nsuperficial layer of deep fascia as it attaches to the zygoma nand temporal ridge and its medial boundary the periosteum nof the temporal bone.  It is subdivided into superficial and deep spaces nby the body of the temporalis muscle.  This nspace contains the internal maxillary artery and the mandibular nnerve.

INFRAHYOID SPACES

The anterior visceral space is a potential space nwithin the middle layer of deep cervical fascia.  It also referred to as nthe pretracheal space.  It is continuous with nthe retropharyngeal space laterally.  It is bounded by the thyroid ncartilage superiorly and the anterior superior mediastinum ndown to the aortic arch inferiorly.  Posteriorly nit is limited by the anterior esophageal wall.  It contains the thyroid nand parathyroid glands and surrounds the trachea.

DEEP nNECK INFECTIONS (DNI)

PRESENTATION

When considering both adult and pediatric patients, nthe average age of patients presenting with DNI is nbetween 40 to 50 years.  Some papers site a higher incidence in patients nin their twenties as well.  Overall there is a npredominance in patients over 50.  Reviews from India point to na higher prevalence in the lower socioeconomic groups mainly due to poor oral nhygiene and lack of dental care.  In pediatric patients, these infections ncan occur at any age.  The most common age group is between three to five nyears of age with a slight male predominance.  Retropharyngeal abscesses nare more common in the pediatric population because of the presence of lymph nnodes that atrophy with age.

Patients with deep neck infections can present in a nvariety of ways.  Huang et al. found that the two most common symptoms nwere sore throat and odynophagia.  Whedisregarding all patients with peritonsillar nabscesses, the most common symptoms were neck swelling and neck pain.  Ipediatric patients, the most common presenting symptoms are fever, decreased noral intake, odynophagia and malaise.  Depending non the location of the DNI, trismus nmay be present but overall it was only present in up to 20% of patients imultiple reviews.  Patients may present in respiratory distress and may nhave impending upper airway obstruction or concomitant pneumonia.  nDehydration from lack of oral intake and intolerance of their own secretions nare also common symptoms.  Other clinical signs include torticollis from SCM ninflammation, neck pain with neck movement, otalgia, nheadache, and vocal quality changes.  Parents and spouses may note nworsening snoring and sleep apnea.

ETIOLOGY

When considering all deep neck infections, the most ncommon etiology is probably pharyngitis or ntonsillitis.  When excluding peritonsillar nabscesses, the most common etiology is odontogenic ninfection.  These infections occur in patients who have had recent dental nextractions and in patients in lower socioeconomic groups who have no access to ndental health care.  In pediatric patients, these infections are usually a nresult of suppurative lymph node following upper nrespiratory infections, pharyngitis, otitis media, and tonsillitis.  In areas where nintravenous drug abuse is prevalent, these infections can result from ncontaminated injections into the jugular veins.  Traumatic injury to the npharynx and neck, including iatrogenic trauma, is also a potential source of ninfection.  Other less common causes include foreign bodies, sialoadenitis, parotitis, osteomyelitis, and epiglottitis.  nIn patients with recurrent deep neck infections, you should have a high nsuspicion for underlying congenital anomalies (second branchial ncleft cyst, first, third and fourth branchial cleft ncysts, lymphangiomas, thyroglossal nduct cysts and cervical thymic cysts).

MICROBIOLOGY

The available culture data for 738 patients from nseveral reviews were combined to make the following tables.  The most ncommonly isolated organisms in these infections are gram positive aerobes nfollowed by anaerobes, gram negative aerobes and fungi.  Polymicrobial infections are common (25%) with some series nindicating an incidence of up to 65%.  The estimation of anaerobic ninfections may be low because of the difficulty in growing these norganisms.  Gram negative aerobes were found in 19% of patients.  nHuang et al found that 56% of diabetic patients in their series grew Klebsiella pneumonia.  Sterile pus was nnoted in 9.6% of patients.  Fungal species were isolated in less than 1% nof patients.

The most common gram positive aerobes were nStreptococcal species followed by Staphylococcal species.  Beta hemolytic nstreptococci were the predominant subgroup followed by Streptococcus viridans and Staphylococcus aureus.  nThe predominant gram negative aerobes were Klebsiella nspecies and Neisseria species.  Peptostreptococcus and Bacteroides nspecies were the most common anaerobic isolates.

Table n1:  Aerobic isolates; Modified and combined data from 738 patients (1, 2, n3, 4, 5, 6, and 7)

 

Table n2:  Anaerobic Isolates: Modified and combined data from 738 patients (1, n2, 3, 4, 5, 6, and 7).

 

Table n3: Polymicrobial and Sterile Cultures: Modified and ncombined data from 738 patients (1, 2, 3, 4, 5, 6, and 7).

TREATMENT

Patients with suspected deep neck infections should be nstarted on antibiotic therapy.  Most patients are given IV antibiotics ntargeting gram positive cocci and anaerobes.  nDiabetic patients should receive antibiotics that cover gram negative aerobes nas well.  Common regimens include Unasyn (Ampicillin / Sulbactam), Clindamycin or second generation cephalosporins nlike Cefuroxime.  In the developing world, Meher et al found that empiric therapy with penicillin, gentamycin and metronidazole was nan effective therapy.  Once culture results can be obtained, antibiotic ntherapy can be tailored to the organism in question.  Once the patient is nable to tolerate oral antibiotics then they are switched over.  There is nno concensus on duration of oral antibiotic therapy.

Patients should undergo imaging studies to determine nif there is an abscess of phlegmon present.  nNagy et al found that lateral neck films were not useful in patients in which nthere was a high suspicion of deep neck infection.  CT of the neck with ncontrast is the most used imaging modality because of its ability to delineate ncellulites versus abscesses and also because it can be used for surgical nplanning.  When compared to MRI, CT if faster, ncheaper and more widely available but MRI decreases ntoxic exposure to radiation and iodine based contrast.  MRI is superior in assessing the origin of infection and nalso has decreased interference from dental artifacts.  Roberson et al nfound that lesions with regular cavity walls and ring enhancement on CT with ncontrast were 89% sensitive but 0% specific in identifying abscess ncavities.  Irregular (scalloped), ring enhancing lesions on CT were 64% nsensitive, 82% specific and had a positive predictive value of 94% iidentifying abscess cavities.

Surgical therapy and approaches can be determined by nevaluating the CT neck of the patient.  In patients with definitive nabscesses by CT drainage was the usual treatment choice.  Patients with nevidence of cellulites or phlegmon by CT but no ndefinitive abscess, IV antibiotics alone have been shown to be effective.  nMcClay et al showed that use of IV antibiotics alone nin pediatric patients with a definitive abscess by CT scan was reported to be neffective in clinically stable patients.  In patients receiving IV nantibiotics that show no clinical improvement (febrile, not tolerating po intake) then repeat imaging and surgical drainage should nbe pursued.  External approaches are widely used and transoral napproaches have been controversial depending on the site of the ninfection.  Transoral approaches have been showto be safe in patients with retropharyngeal, pharyngomaxillary nand prevertebral abscesses that are medial to the ngreat vessels.  Some patients may need a tonsillectomy to facilitate nexposure to the abscess.  Lesions that extend lateral to the great vessels nshould be approached externally.  For external drainage, incisions can be nmade anterior or posterior to the SCM and may be ncarried transversely as a submaxillary or submental incision.  Since the infection may distort nnormal anatomy, useful landmarks include the: tip of greater horn of hyoid, cricoid cartilage, styloid nprocess, and SCM.  Repeated needle aspiration is nalso used to drain these abscesses.

COMPLICATIONS

The incidence of complications from deep neck space ninfections has remarkably decreased since the advent of antibiotic ntherapy.  Despite this, the potentially devastating outcomes associated nwith these complications remind the physician to remain vigilant for their nsigns.  Airway obstruction and asphyxia is a potential complication of any ndeep neck infection, but has been most commonly associated with Ludwig’s nangina.  Early evaluation and management of these patients is nparamount.  About 10-20% of patients reviewed required a tracheostomy and up to 75% of patients with Ludwig’s angina nrequired a tracheostomy.  Rupture of the nabscess, either spontaneously or with manipulation such as intubation, nwith associated aspiration can result in severe pneumonia, lung abscess or empyema. Other complications include sepsis, internal njugular vein thrombosis, upper GI bleeding, mediastinitis, nand vocal cord palsy.

Carotid artery rupture, although rare, carries a nmortality rate between 20% and 80%.  This can occur when infectioinvolving the carotid sheath leads to arterial wall weakening, erosion and neventual hemorrhage.  Salinger and Pearlman, in a review of 227 cases of ndeep neck abscess complicated by hemorrhage, found that 62% of ruptures occur nfrom the internal carotid artery, 25% involve the external carotid and 13% ninvolve the common carotid.  In their series, of the 73 patients who were ntreated with artery ligation, 64% survived.  nArtery rupture may be heralded by recurrent small bleeds from the ear, nose or nmouth, the onset of shock, a protracted clinical course, and hematoma in the nearby tissue, Horner’s syndrome or unexplained ncranial neuropathies.  Treatment necessitates obtaining proximal and ndistal control, followed by ligation of the nvessel.  Repair of the artery by patching or grafting is restricted by the ninfected environment.

Patients at risk for complications are older patients nand patients with systemic disease including HIV/AIDS, myelodysplasia, ncirrhosis and diabetes.  Huang et al found that 33% of diabetic patients nhad complications and two of three mortalities in their series were patients nwith diabetes.

MEDIASTINITIS

 

By definition descending necrotizing mediastinitis is a mediastinal ninfection in which the pathology originates in fascial nspaces of head and neck and extends down.  The most common cervical spaces nthat spread to the mediastinum are the retropharyngeal nand danger space (71%), visceral vascular space (20%) and the anterior visceral nspace (7-8%).  Estrera et al’s criteria for ndiagnosis are:

·        nClinical nmanifestation of severe infection.

·        Demonstration of the ncharacteristic imaging features of mediastinitis.

·        Features of necrotizing mediastinal infection at surgery.

 

The incidence of this complication is rare.  Only n43 cases were published in the English language literature between 1960 and 1989.  nThe mortality rate ranges between 14 to 40% in different reviews.

Clinically, these patients are usually diagnosed with na deep neck infection and are already undergoing antibiotic therapy.  Some nreports of patients presenting to the emergency room with this condition have nbeen reported as well.  Symptoms include increased respiratory difficulty, ntachycardia, chest pain, back pain, erythema/edema of nthe neck and chest, crepitus and shock.  It is nimportant to have a low threshold for further workup in patients with these nsymptoms.  Unstable patients should be moved to an ICU setting and imaging nstudies and an ECG should be obtained.  Plaichest films do not show changes until late in the course of the disease.  nPatients with mediastinitis will have a widened mediastinum superiorly, mediastinal nemphysema, and pleural effusions.  CT of the neck and thorax are the best nmodalities to determine if there is a descending infection.  Findings oCT thorax include esophageal thickening, air fluid levels, pleural neffusions and obliterated normal fat planes.  The CT thorax establishes nthe diagnosis and aids in the surgical planning.

Treatment for descending necrotizing mediastinitis should include some sort of drainage nprocedure along with IV antibiotics.  Consultation with thoracic surgeons nshould be obtained.  Access to the superior mediastinum nfrom a cervical incision is adequate for fluid collections above the tracheal nbifurcation (T4).  Transthoracic drainage should nbe performed for abscesses that extend below T4.  Abscesses in the nanterior mediastinum may be approached by a subxyphoid incision.  Thoracostomy ntubes should be placed for pleural effusions.  n

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