PHLEGMONS AND ABSCESSES OF THE MAXILLOFACIAL AREA (MFA): CLASSIFICATION, ETIOLOGY, PATHOGENESIS, CLINICAL FEATURES, COURSE, PRINCIPLES OF TREATMENT, PREVENTION, COMPLICATIONS. THE INFLAMMATORY PROCESS OF MFA: ETIOLOGY, PATHOGENESIS, CLINICAL TYPES OF REACTIONS AND PECULIARITIES OF ODONTOGENIC INFLAMMATORY DISEASES. THE ROLE OF THE IMMUNE, HORMONAL, VASCULAR, BLOOD-COAGULABILITY SYSTEMS, ETC.

  

 

  

Phlegmon

Phlegmon is a spreading diffuse inflammatory process with formation of suppurative/purulent exudate or pus. This is the result of acute purulent inflammation which may be related to bacterial infection, however the term ‘phlegmon‘ mostly refers to a walled-off inflammatory mass without bacterial infection, one that may be palpable on physical examination.

An example would be phlegmon of diverticulitis. In this case a patient would present to the emergency department with left lower-quadrant abdominal tenderness, and the diagnosis of sigmoid diverticulitis would be high on the differential diagnosis, yet the best test to confirm it would be CT scan.

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

Etiology

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

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

Classifications

1.     By clinical course:

o    acute

o    subacute

2.     By severity of condition:

o    mild

o    average

o    severe (with spreading to 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 and non-spore forming anaerobes)

5.     By pathogenesis:

o    per continuitatem (through neighbouring tissues)

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

o    odontogenous

6.     By exudative character:

o    purulent phlegmon

o    purulent-hemorrhagic phlegmon

o    putrefactive phlegmon

7.     By presence of complications:

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

o    without complication

Clinical pictures

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

2.     Inflammatory signs – dolor (localized pain), calor (increase local tissue temperature), rubor (skin redness/hyperemia), tumor (either clear or non-clear bordered tissue swelling), functio laesa (diminish affected function).

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

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

Diagnostics

1.     Complaints and clinical appearances

2.     Anamnesis

3.     Visual and Palpations

4.     Blood test – leukocytosis (up to 10-12×10⁹/L), decrease or absence eosinophils level, shift of white count differential to the left (neutrophilia), increase ESR (up to 35–40 mm/hr).

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

6.     X-ray test

7.     Ultrasound test

Treatments

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

If the patient’s condition is mild and signs of inflammatory process are present without signs of infiltrates, then conservative treatment with antibiotics is sufficient.

If the patient’s condition is severe, however, immediate operation is usually necessary with application 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 solutions and proteolyic ferments.

In post-operative period, patients are treated with intravenous antibiotics, haemosorbtion, vitaminotherapy. Additionally, the use of i/v or i/m antistaphylococci γ-globulin or anatoxin can be taken as immunotherapy.

During operation of phlegmon dissection at any location, it is important:

1.     to avoid spreading of pus during operation;

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

3.     to avoid damaging nerves.

Information and Resources

Abscess

Abscess Overview

An abscess is a tender mass generally surrounded by a colored area from pink to deep red. Abscesses are often easy to feel by touching. The middle of an abscess is full of pus and debris.

Painful and warm to touch, abscesses can show up any place on your body. The most common sites are in your armpits (axillae), areas around 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 hair follicle can also lead to the formation of an abscess, which is called a boil (furuncle).

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

Abscess Causes

Abscesses are caused by obstruction of oil (sebaceous) glands or sweat glands, inflammation of hair follicles, or  minor breaks and punctures of the skin. Germs get under the skin or into these glands, which causes an inflammatory response as your body’s defenses try to kill these germs.

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

People with weakened immune systems get certain abscesses more often. Those with any of the following are all at risk for having more severe abscesses. This is because 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

Other risk factors for abscess include exposure to dirty environments, exposure to persons with certain types of skin infections, poor hygiene, and poor circulation.

Abscess Symptoms

Most often, an abscess becomes a painful, compressible mass that is red, warm to touch, 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.

Abscess Treatment: Self-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.

Abscess

(continued)

When to Seek Medical Care

Call your 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.

Go to a hospital’s Emergency Department if any of these conditions occur with an abscess:

• 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 swollen lymph nodes in your groin area)

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

Exams and Tests

The doctor 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.

Medical Treatment

The doctor 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.

Next Steps: Follow-up

Follow carefully 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.

Abscess

Prevention

Maintain good 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

Outlook

Once treated, 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.

Synonyms and Keywords

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

Dental Abscess Overview

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

Causes of a Dental Abscess

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

An infected tooth that has not received appropriate dental care can cause a dental abscess to form. Poor oral hygiene, (such as not brushing and flossing properly or often enough) can cause cavities to form in your teeth. The infection then may spread to the gums and adjacent areas and become a painful dental abscess.

Symptoms of a Dental Abscess

Symptoms of a dental abscess typically include:

• Pain

• Swelling

• Redness of the mouth and face

Symptoms of advanced infection may include:

• Nausea

• Vomiting

• Fever

• Chills

• Diarrhea

Other signs 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

When to Seek Medical Care for a Dental Abscess

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

• 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.

Exams and Tests for a Dental Abscess

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

Treating a Dental Abscess 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 pain and inflammation.

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

Medical Treatment for a Dental Abscess

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

Dental Abscess Follow-Up Care

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

Prevention of a Dental Abscess

Prevention plays a major role in maintaining good dental health. Daily brushing and flossing, 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 consumption can help too.

 

Outlook for Dental Abscesses

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

• 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.

The Basics of Acute Inflammation

Inflammation, described in the simplest terms is the local physiological response to tissue injury.

Many things can cause this ‘injury’, from microbial infections (bacteria, viruses, etc) through to physical agents (e.g. trauma, heat, etc).The primary goal of inflammation is to bring phagocytes and plasma proteins to the area such that they can destroy the invaders, remove debris and prepare for subsequent healing.

Inflammation is often categorised firstly by its time course; Acute & Chronic Inflammation. Acute inflammation consists of the initial response of the body to tissue injury, whilst chronic inflammation is the prolonged tissue reactions following the initial response. Today I shall focus on the former.

There are Five Cardinal Signs of Acute Inflammation which 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): Accumulation 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.

Chemical mediators of inflammation interact with other immune cells to elicit an appropriate response (in autocrine/paracrine fashion, an occasionally through the blood).
It is important to remember that there are both good and bad aspects to acute inflammation.
The 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

The Bad.

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

The interplay between Acute & Chronic Inflammation

 

The Inflammation Process

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

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

Pain

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

Swelling

The same applies to all other aspects of the acute phase response. Swelling, for example, is also a defensive process, caused by the leakage of plasma and the migration of immune cells into the area of damaged tissue. All bodily damage, whether caused by injury or infection, consists of broken cells, and when the walls of a cell rupture, an array of molecules which would not otherwise be released, spill out into the surrounding tissue. Some of these molecules trigger the sensory nerves to produce the ongoing, second type of pain just described. The sensory nerves also react by causing the blood vessels to widen, increasing local blood flow (Redness), and making the walls of the blood vessels more permeable. With greater blood flow, more white blood cells, the infantry of the immune system, can be carried to the site of the injury. The greater permeability of the blood vessel walls enables the white blood cells to flow out of the arteries and veins into the surrounding tissue to defend against possible bacterial invaders. If no bacteria have found their way into the wound, particular white blood cells known as macrophages clear up the debris of the chattered cells by engulfing and digesting it. If bacteria have gained a foothold and started to multiply, the white cells form a barrier to create a pus-filled abscess in which the blood fluid, the serum, plays a key role in healing.

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

Fever

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

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

All injuries and infections, as stated above, cause a fever. This might only manifest itself in a localised heat, and does not always produce an overall increase of the body temperature.

Lethargy, Apathy and Loss of Appetite

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

Mechanism of the Acute Phase Response

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

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

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

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

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

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

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

Problems I have with it

Let’s go through the phases again.

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

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

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

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

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

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

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

Also, prostaglandin is now encouraging the microglia to produce IL-1ß. This production of material in response to a very specific order must take time.

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

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

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

The adrenal gland now produces cortisol. That production must take time.

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

How much time do you reckon that will take?

And There is More

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

However, when we look around we find that there is more evidence we need to consider if we want to 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 human 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 then 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 given 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 in your body learns of your happiness and joins in. The fact that you can 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.

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

And secondly, it means that the immediate cell reaction we see is organised by the cell itself, producing all required attributes itself. Once these chemicals, proteins, peptides, hormones, etc. have done their job they are discarded into the surrounding tissue and dumped into the blood stream. As a reaction of the cell’s activity, not as the cause of, the levels of these substances within the surrounding tissues and the blood itself will now start to rise. Along the banks of these extensive waterways a variety of anti-pollution plants (glands, organs) are available, which identify specific materials and filter them out of the blood circulation. These materials now accumulate inside the glands where they are destroyed and the building blocks recycled. Hormones, enzymes, chemicals, etc. are not produced by glands but collected 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. In fact, the swelling of the lymph glands is most often a secondary phase in 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!

Once we know that all cells have receptors for all chemicals the body will ever use, and is capable of making these chemicals, we caow understand why everything always has an effect on every part of the body. From the fight-flight response to the influence of stress or the effect of hearing bad news, the effects of every aspect 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 inflammation 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 can 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.

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

It seems there are other problems relating 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 carbon 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 disintegration 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 main 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 proliferation 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 explain the passing on of the memory to these new leucocytes? Remember, the life span of lymphocytes is between 12 and 24 hours.

What does all this mean?

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

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

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

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

 

Neck Spaces and Infections

ANATOMY OF THE CERVICAL FASCIA

INTRODUCTION

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

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

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

ANATOMIC CONSIDERATIONS

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

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

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

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

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

The superficial cervical fascia extends from the zygoma and mimetic muscles of the face down to the chest, shoulder and axilla.  It is similar to subcutaneous 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 and submandibular), two muscles (sternocleidomastoid and trapezius) and two spaces (suprasternal space of Burns and Space of the posterior triangle) (Rule of Twos).  It is a sheet of fibrous tissue that attaches to the nuchal line, zygoma, mandible and skull base superiorly.  Inferiorly it extends to the sternum and clavicles laterally to the acromion processes.  It attaches to the body of the hyoid bone and extends to the mandible to form the floor of the submandibular space.  As the fascia encounters the mandible, it splits into two portions which cover the masseter laterally and the pterygoids medially. ¹⁷

The middle layer of the deep cervical fascia (MLDCF) is also referred to as the visceral fascia because it encloses the aerodigestive tract and thyroid gland.  Superiorly it extends from the skull base posteriorly and the hyoid bone anteriorly.  Inferiorly the fascia is continuous with the fibrous pericardium in the upper mediastinum.  The posterior portion of the fascia is also called the buccopharyngeal fascia.  The fascia 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 and the prevertebral layer.  Both layers extend from the skull base superiorly but the alar layer fuses with the MLDCF in the upper mediastinum at T1-T2.  The prevertebral layer extends down to the coccyx.  The alar layer is only present in the anterior midline between the vertebral transverse processes.  The layers fuse then into one fascial layer that surrounds the deep neck musculature, vertebral bodies, phrenic nerves, and brachial plexus.  It also extends laterally and becomes the axillary sheath. ¹⁷

ANATOMY OF THE DEEP NECK SPACES

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

SPACES SPANNING THE ENTIRE NECK

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

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

The danger space extends from the skull base to the diaphragm.  The anterior border is the alar fascia and the posterior border is the prevertebral layer of the prevertebral fascia.  It contains loose areolar tissue. ¹⁷

The prevertebral space extends from the skull base to the coccyx.  The anterior border is the prevertebral layer of the prevertebral fascia and posteriorly it is limited by the anterior longitudinal ligament of the vertebral bodies.  Laterally the space is confined by the transverse processes of the vertebral bodies. ¹⁷

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

SUPRAHYOID SPACES

The submandibular space is bounded by the mandible anteriorly and laterally, the lingual mucosa superiorly, the hyoid postero-inferiorly and the superficial layer of the deep cervical fascia inferiorly.  The mylohyoid muscle divides this space into a superior sublingual space and an inferior submylohyoid space.  The sublingual space contains loose areolar tissue, the hypoglossal and lingual nerves, the sublingual gland and Wharton’s duct.  The submylohyoid space contains the anterior bellies of the digastrics and the submandibular glands.  These two subdivisions freely communicate around the posterior border of the mylohyoid.

The pharyngomaxillary space is also known as the parapharyngeal space or lateral pharyngeal space.  It is a difficult space to visualize because of its odd shape and multiple boundaries.  It spans from the skull base to the hyoid bone.  The superior portion of the space at the skull base is larger than the space inferiorly at the hyoid.  This gives the described inverted cone shape.  The lateral border is the superficial layer of deep cervical fascia that overlies the medial portion of the medial pterygoid and deep lobe of the parotid gland.  Medially the space is limited by the buccopharyngeal fascia covering the superior pharyngeal constrictor.  The prevertebral fascia overlying the deep neck musculature is the posterior limit.  The pterygomandibular raphe (which separates the superior constrictor from the buccinator) is the anterior limit of the space.  The styloid process divides the space into two compartments.  The poststyloid portion is also referred to as the neurovascular compartment because the carotid sheath runs through it.  Cranial nerves IX, X, XI, XII and the sympathetic chain also run through this space.  The prestyloid portion is also referred to as the muscular compartment because of its proximity to the pterygoids and constrictor.  Fat, connective tissue and lymph nodes are also contained in the prestyloid compartment.  The stylopharyngeal aponeurosis of Zuckerkandel and Testus is formed by the intersection of the alar, buccopharyngeal and stylomuscular fascia and acts as a barrier to the spread of infection from the prestyloid compartment to the poststyloid compartment.

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

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

The masticator space is formed by the superficial layer of the deep cervical fascia as it surrounds the masseter laterally and the pterygoid muscles medially.  This space contains these muscles as well as the body and ramus of the mandible, the inferior alveolar nerves and vessels and the tendon of the temporalis muscle.  The masticator space is in direct communication with the temporal space superiorly deep to the zygoma.  This space is antero-lateral to the pharyngomaxillary space.

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

INFRAHYOID SPACES

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

DEEP NECK INFECTIONS (DNI)

PRESENTATION

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

Patients with deep neck infections can present in a variety of ways.  Huang et al. found that the two most common symptoms were sore throat and odynophagia.  When disregarding all patients with peritonsillar abscesses, the most common symptoms were neck swelling and neck pain.  In pediatric patients, the most common presenting symptoms are fever, decreased oral intake, odynophagia and malaise.  Depending on the location of the DNI, trismus may be present but overall it was only present in up to 20% of patients in multiple reviews.  Patients may present in respiratory distress and may have impending upper airway obstruction or concomitant pneumonia.  Dehydration from lack of oral intake and intolerance of their own secretions are also common symptoms.  Other clinical signs include torticollis from SCM inflammation, neck pain with neck movement, otalgia, headache, and vocal quality changes.  Parents and spouses may note worsening snoring and sleep apnea.

ETIOLOGY

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

MICROBIOLOGY

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

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

Table 1:  Aerobic isolates; Modified and combined data from 738 patients (1, 2, 3, 4, 5, 6, and 7)

 

Table 2:  Anaerobic Isolates: Modified and combined data from 738 patients (1, 2, 3, 4, 5, 6, and 7).

 

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

TREATMENT

Patients with suspected deep neck infections should be started on antibiotic therapy.  Most patients are given IV antibiotics targeting gram positive cocci and anaerobes.  Diabetic patients should receive antibiotics that cover gram negative aerobes as well.  Common regimens include Unasyn (Ampicillin / Sulbactam), Clindamycin or second generation cephalosporins like Cefuroxime.  In the developing world, Meher et al found that empiric therapy with penicillin, gentamycin and metronidazole was an effective therapy.  Once culture results can be obtained, antibiotic therapy can be tailored to the organism in question.  Once the patient is able to tolerate oral antibiotics then they are switched over.  There is no concensus on duration of oral antibiotic therapy.

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

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

COMPLICATIONS

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

Carotid artery rupture, although rare, carries a mortality rate between 20% and 80%.  This can occur when infection involving the carotid sheath leads to arterial wall weakening, erosion and eventual hemorrhage.  Salinger and Pearlman, in a review of 227 cases of deep neck abscess complicated by hemorrhage, found that 62% of ruptures occur from the internal carotid artery, 25% involve the external carotid and 13% involve the common carotid.  In their series, of the 73 patients who were treated with artery ligation, 64% survived.  Artery rupture may be heralded by recurrent small bleeds from the ear, nose or mouth, the onset of shock, a protracted clinical course, and hematoma in the nearby tissue, Horner’s syndrome or unexplained cranial neuropathies.  Treatment necessitates obtaining proximal and distal control, followed by ligation of the vessel.  Repair of the artery by patching or grafting is restricted by the infected environment.

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

MEDIASTINITIS

 

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

·        Clinical manifestation of severe infection.

·        Demonstration of the characteristic imaging features of mediastinitis.

·        Features of necrotizing mediastinal infection at surgery.

 

The incidence of this complication is rare.  Only 43 cases were published in the English language literature between 1960 and 1989.  The mortality rate ranges between 14 to 40% in different reviews.

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

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

BIBLIOGRAPHY

1.     Scott, BA, Stiernberg, CM, Driscoll, BP.  Deep Neck Space Infections. In: Head and Neck Surgery—Otolaryngology, 3rd ed., Bailey, BJ Ed.  Philadelphia, Lippincott-Raven Publishers, 2001; 701 – 715

2.     Kirse, DJ, Roberson, DW.  Surgical Management of Retropharyngeal Space Infections in Children.  Laryngoscope, 111: 1413-1422, 2000.

3.     Stalfors, J, Adielsson, A, Ebenfelt, A, Nethander, G, Westin, T. Deep Neck Space Infections Remain a Surgical Challenge.  A Study of 72 Patients.  Acta Otolaryngol 2004; 124: 1191-1196.

4.     Meher, R, Jain, A, Sabharwal, A, Gupta, B, Singh, I, Agarwal, AK.  Deep Neck Abscess: A Prospective Study of 54 Cases.  The Journal of Laryngology and otology.  2005 (119), 299-302.

5.     Nagy, M, Pizzuto, M, Backstrom, J, Brodsky, L. Deep Neck Infections in Children: A New Approach to Diagnosis and Treatment.  Laryngoscope. 1997; 107 (12): 1627-1634.

6.     Huang, TT, Liu, TC, Chen, PR, Tseng, FY, Yeh, TH, Chen, YS.  Deep Neck Infection: Analysis of 185 Cases.  Head and Neck.  26: 854-860. 2004.

7.     Parhiscar, A, Har-El, G.  Deep neck abscess: A retrospective review of 210 cases.  Annals of Otology, Rhinology and Laryngology, 2001; 110 (11): 1051-54.

8.     Huang, TT, Tseng, FY, Lie, TC, Hsu, CJ, Chen, YS.  Deep Neck Infection in Diabetic Patients: Comparison of Clinical Picture and Outcomes with Nondiabetic Patients.  Otolaryngol Head Neck Surg 2005; 13:943-7.

9.     Munoz, A, Castillo, M, Melchor, MA, Gutierrez, R.  Acute Neck Infections: Prospective Comparison Between CT and MRI in 47 Patients. Journal of Comp Ass Tomography.  2001. 25 (5): 733-741.

10. McClay, JE, Murray, AD, Booth, TB.  Intravenous Antibiotic Therapy for Deep Neck Abscesses Defined by Computed Tomography.  Arch Otolaryngol Head Neck Surg. 2003; 129:1207 – 1212.

11. Nagy, M, Backstrom, J.  Comparison of the sensitivity of lateral neck radiographs and computed tomography scanning in pediatric deep-neck infections.  Laryngoscope, 1999; 109 (5): 775-779.

12. Chaudhary, N, Agrawal, S, Rai, A.  Descending Necrotizing Mediastinitis: Trends in a Developing Country. Ear Nose Throat. 2005 84(4); 242-50.

13. Harar, R, Cranston, C, Warwick-Brown, N.  Descending necrotizing mediastinitis: report of a case following steroid neck injection.  Journal Laryngol Otol. 2002, vol 116; 862 – 64.

14. Kiernan, PD, Hernandez, A, Byrne, W, Bloom, R, Dicicco, B, Hetrick, V, Graling, P, Vaughan, B. Descending Cervical Mediastinitis. Ann Thorac Surg 1998; 65:1483-8.

15. Akman, C, Kantarci, F, Cetinkaya, S. Imaging in mediastinitis: a systematic review based on aetiology.  Clinical radiology 2004 (59), 573-85.

16. Baqain, Z, Neman, L, Hyde, N. How Serious are Oral Infections? Journ Laryngol Otol. 2004 (118). 561-65.

17. Paonessa, DF, Goldstein, JC. Anatomy and Physiology of Head and Neck Infections (with Emphasis on the Fascia of the Face and Neck). Otolaryngol Clin N Am.  1976; 9 (3): 561-80

18. Lee, KJ.  Essentials of Otolaryngology.

19. Rosen, EJ, Bailey, B, Quinn, FB.  Deep Neck Spaces and Infections: Grand Rounds Presentation.  Dr. Quinn’s Online Textbook of Otolaryngology Grand Rounds Archive.  2002.  http://www.utmb.edu/otoref/Grnds/Deep-Neck-Spaces-2002-04/Deep-neck-spaces-2002-04.doc