Introduction

The middle ear is an air space behind the ear drum that houses the three ear bones-the “hammer” or malleus, the “anvil” or incus, and the “stirrup” or stapes (see figure 1). When sound travels down the ear canal it vibrates the eardrum and sets in motion the connected middle ear bones. Finally, the bones transmit the sounds into the nerve endings of the inner ear or cochlea, where the signals of sound are sent to the brain. The brain then interprets between sounds as diverse as the chirping of birds, the blast of a firecracker, or the communication of human speech.

Infections of the middle ear are quite common in children and account for more visits to pediatricians than any other cause. Today middle ear infections are diagnosed two to three times more commonly than 25 years ago. Subsequently, the use of antibiotics and other treatments has increased substantially. This may be in part due to an increased awareness of the condition by practitioners. However, changing lifestyle changes, such as the increased reliance on day care, may actually be increasing the frequency of the problem. Middle ear infections happen most often between six and eighteen months of age. Children who have had few problems with such infections by age three are unlikely to encounter future episodes.

Children with frequent infections early in life pose two problems. First, there are the repeated illnesses and possible complications from the infections themselves. Back and forth visits to the pediatrician, fevers, awakenings in the middle of the night, and a constantly irritable child can put physical and emotional strain on the entire family. Unusual but potential complications include infection of the mastoid space behind the ear, infections around the brain, and infections causing permanent inner ear hearing loss and dizziness. Second, some relatively mild but prolonged ear infections can produce enough temporary hearing loss to affect development of speech and language. In many ways this second condition can lead to even more profound, long-term educational problems for the affected children. Detection, treatment and prevention of middle ear infections are the cornerstones of proper care and avoidance of such consequences.

Causes and Risks

Bacteria and viruses can lead to infection in the middle ear space. The organisms get into the space through a tube that links the middle ear to the back of the nose (see figure 2). Problems with the angle, shape, and size of this so-called “Eustachian tube” are thought to lead to repeated infections. We know that heredity plays a role in determining how the Eustachian tube works early in life. Many children with frequent infections have siblings with similar problems. As the Eustachian tube grows and matures, it develops a sharper downward angle and a larger opening. This helps mucus that builds up during colds to drain into the nose. Changes in air pressure are also more easily adjusted and oxygen can enter the middle ear. These changes affect how well bacteria can grow since the organisms thrive on the “sugar” of middle ear mucus and the lower oxygen levels.

Certain races have increased tendencies toward ear infections, which goes along with the hereditary or genetic nature of the problem. Native American Indians and Eskimos are particularly prone and often suffer the complications of longstanding middle ear inflammation.

Other factors include breastfeeding, which seems to offer some protection against infection, possibly by transferring immune proteins that help the infant fight bacteria. Bottle-feeding while lying down in a crib may increase infections by encouraging bacteria to back up into the Eustachian tube. Children living in households where there are smokers or woodstoves have higher rates of infection. Cleft palate children, who have a gap in the roof of the mouth, have more middle ear infections because of missing muscles that open the Eustachian tube. The tube can also malfunction because of allergies and colds that cause swelling of the nasal mucous membranes and because of overgrowth of the adenoids, nearby tissues that help fight infection.

Daycare is possibly the factor most responsible for the increase in ear infections in the last 25 years. A child’s exposure to a large number of other children early in life typically leads to more frequent colds and flu’s that often lead to middle ear inflammation.

How Infections Occur

Ear infections often begin during colds or flu’s, when viruses cause inflammation and swelling of the nasal and Eustachian tube passages. The tube has trouble opening, which leads to a lack of oxygen flowing into the middle ear. This also prevents mucus from leaving the middle ear. Bacteria from the nose virtually feast on the “sugar-laden” mucus and they thrive at low oxygen levels. This results in inflammatory cells entering the middle ear to defend against the organisms. The resulting inflammation causes fever, pain, and build up of pus (bacteria and inflammatory cells). Additionally, there is temporary hearing loss from the pus restricting movement of the eardrum. Since the pus cannot escape through the Eustachian tube, it puts intense pressure on the eardrum, occasionally leading to rupture of the drum with drainage of pus out through the ear canal. This is often alarming, but is actually an excellent way for the body to release the pus and help heal the infection. Occasionally doctors will help this process along by recommending a “myringotomy,” during which a small nick is made in the eardrum to allow the pus to escape. Physicians refer to this type of infection as “acute otitis media.”

Although half of all ear infections get better on their own, antibiotics should be used for 7 to 10 days to insure recovery, speed improvement and prevent complications. The antibiotics have no effect on viruses, but are aimed at destroying the most common bacteria that cause infections (Pneumococcus, Hemophilus Influenzae, and Mycoplasma pneumoniae). Some common antibiotics used are Amoxicillin and Bactrim. For difficult or resistant infections, “broad spectrum” antibiotics such as Augmentin, Ceftin and Suprax are used to cover heartier bacteria.

As the infection improves, the fever, pain and ill feeling resolve. The pus becomes transformed into a liquid or fluid that may be thick or watery. This continues to cause hearing loss and can remain for up to several weeks. Occasionally the fluid will remain indefinitely and needs to be treated more aggressively. Physicians refer to the fluid as “effusion.”

Another type of middle ear infection is subtler and occurs without pain or fever. Commonly a cold leads to Eustachian tube blockage and build up of fluid in the middle ear, but there are few bacteria and only limited inflammation. Often hearing loss from the fluid is the only symptom. However, in very young children the hearing loss may not be apparent since they are not yet speaking. Occasionally parents notice their children’s lack of response to softer sounds and turn to their doctors for help. This type of chronic ear problem is referred to by physicians as “otitis media with effusion.”

Antibiotic Resistance

Over the last 25 years the vast use of antibiotics has lead to a problem referred to as “resistance.” Bacteria have learned how to alter their attacks in ways that they overcome the actions of antibiotics. As they have “evolved” over the years, some of the common antibiotics like Amoxicillin have failed to be effective in up to 30% of infections. Parents mistakenly think this is due to their child’s “immunity” towards the antibiotic. In fact this is not an effect on the child’s immune system, but a tendency for the bacteria themselves to “resist” the effects of the antibiotics. Resistance is more common in parts of the country where antibiotics are used most frequently. Therefore, it is critical that these medicines only be used for short courses (7 to 10 days) and only when bacterial infections are suspected. Giving antibiotics to prevent infections in the winter or during colds (so called “prophylaxis”) is probably no longer warranted in the face of this problem of resistance.
Overcoming resistant bacteria involves using “broad spectrum” antibiotics that outsmart these organisms. In some cases increasing the dosage or strength of common antibiotics such as Amoxicillin is necessary to break the resistance. More importantly, avoiding the use of antibiotics for colds or for prolonged periods of time will go far to reduce this problem.

Tympanostomy Tubes

Children who have three to four ear infections over a six-month period or who have fluid in the middle ear that does not go away after three months despite antibiotics need further treatment. There is no proof that decongestants or antihistamines have any impact in treating or preventing ear infections. As mentioned, occasionally draining the middle ear by nicking the eardrum, so-called “myringotomy,”can relieve persistent pain and fever and prevent complications. Tympanostomy tubes are a common way to prevent infections and keep middle ear fluid away. After the eardrum is nicked and any fluid is vacuumed from the middle ear, a small plastic tube is placed into the opening. The flange on the tube keeps it in place for about a year. The tube maintains an opening in the eardrum, so that air and oxygen pressures are maintained and any fluid is allowed to drain. The tympanostomy tube behaves as a substitute for the poorly functioning Eustachian tube until it develops and works normally.

Tympanostomy tube placement or “myringotomy and tubes” is the most common procedure performed in this country. The child is briefly given “laughing gas” while the tubes are placed. The child is usually back to normal within an hour or two and the procedure has very few risks. Tubes not only prevent the illnesses associated with ear infections and their possible complications in the vast majority of patients, but can also prevent prolonged periods of middle ear fluid build-up that causes hearing loss and possible speech and language problems.

Other Treatments

Occasionally older children continue to have recurrent ear infections, despite the chances that the Eustachian tube has matured. This can be due to an enlarged adenoid. The adenoid is a mound of inflammatory tissue that helps fight infection at the back of the nose. It can become quite enlarged in some children, causing blockage of the Eustachian tube openings and harboring bacteria that can easily climb up the Eustachian tube. Removal of the adenoid is recommended in these cases as an adjunct to placement of tympanostomy tubes.

More recently, an office procedure employing a laser to create a small opening in the eardrum (laser-assisted tympanostomy) has been suggested as an alternative to tympanostomy tubes for some patients. The procedure does not require anesthesia at the hospital or surgicenter, which is an advantage. The laser opening is made in such a way that the hole remains for at least several weeks. For children who only require a temporary opening in the eardrum, this may be an alternative to tympanostomy tubes.

Speech Development

A child’s speech and language development goes through two phases early in life. In the first two to three years of life there is a predominantly “receptive” period. During this time speech centers are developing in the brain as nerve connections and networks are forming. Adequate hearing, especially hearing for speech sounds, is critical for these pathways to develop properly. The first two to three years of life represent a “window” of time during which these speech centers form. If hearing is diminished for long periods the speech areas form abnormally. Even if hearing is adequate beyond this two to three year “window”, the child’s speech may “catch up” slowly or incompletely. This can lead to substantial delay and limitation of educational development even with speech and language therapy.

The second phase of speech and language is “expressive,” during which the child begins to make speech sounds and use words. This may begin as early as one year of age. However, use of words in phrases and sentences usually becomes more obvious after age two years. Therefore, problems with hearing that interfere with speech development may not be detected until after the critical window of the receptive language phase. Children with chronic middle ear fluid additionally may not suffer pain, fever or obvious illness, giving little warning that this type of ear problem is even occurring. This more “silent” form of chronic middle ear infection can therefore have far-reaching consequences, affecting the intellectual, academic, social, and even financial potential of the child.

Solutions

Prevention of hearing loss and language delay is clearly critical. Many states now test hearing at birth as a screen. However, ear infections causing middle ear fluid tend to occur after birth. Therefore, both parents and physicians need to maintain vigilance over possible hearing loss from ear infections. Subtle changes in the way a child reacts to softer sounds should alert the parent to a possible problem of persistent middle ear fluid that requires medical intervention. The child who is prone to episodes of ear infections with fever, pain and illness usually presents less of a dilemma because of all the warning signs and subsequent frequent visits to the doctor. Physicians need to follow children with detected middle ear fluid to ascertain that the problem resolves within a few weeks and does not keep returning. When the fluid is persistent or recurrent in the absence of signs of infection (fever, pain, and illness), referral to an ear, nose and throat specialist (otolaryngologist) should be made. The specialist can determine the degree of hearing loss by performing a hearing test. Pressure tests of the eardrum or “tympanograms” can be easily administered to confirm the presence of fluid, which is typically apparent during the routine ear examination as well. Children can then be treated with tympanostomy tube placement to prevent long-term problems with speech and language development.

Conclusion

Middle ear infections are common and usually temporary in childhood. Because they often interfere with hearing for prolonged periods of time, they can impact the development of speech and language. The potential impact of this on the individual and society is enormous. Therefore, treatment and prevention of childhood ear infections is important not only to deal with the illness, but also to avoid intellectual developmental delay and deterioration.

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METHICILLIN RESISTANT STAPHYLOCOCCUS AUREUS
VANCOMYCIN RESISTANT ENTEROCOCCUS

SUMMARY: Staphylococci and Streptococci are normal flora of the skin, intestinal and female genital tract. Ordinarily, they do not cause infections. They may be carried for months in the nose and on the skin. However, under certain circumstances, where the skin is broken or there is medical instrumentation, such as a prosthesis, of major surgery, they may become invasive and pathogenic. This may result in abscesses, deep wounds, and even septicemia and death. They may directly infect the tissues or emit toxins which are deleterious to the body.

Since the introduction of antibiotics, there prevalence had been controlled to some extent, only for them to develop resistance to these medications. This has caused serious illness and presented difficult treatment decisions and approaches, since our armamentarium has been seriously curtailed. Combinations of antibiotics, universal hygiene hospital precautions, preoperative culturing of the skin and nares, and isolation have all been employed with some salutary results. More will be need to be done in the future, since these organisms can transmit resistance to each other.

Staphylococci are one of the most common inhabitants of the skin and mucous membranes of humans. Generally, they are non-pathogenic, causing no significant problems. However, they will become pathogenic when they are able to invade into the body and contribute to superficial deep infections, as well systemic toxicity. They are particularly troublesome as a source of surgical wounds, peri-prosthetic and systemic infections. In the hospital setting, they are the most common source of nosocomial infections. They may be incriminated in many cases of food poisoning.

Staphylococcus Aureus is the most significant organism in this genus that afflicts humans. This group is divided into those that can cause plasma to clot (coagulase positive) and those, less virulent, which are unable to cause clotting (coagulase negative). These organisms enjoy a non-pathogenic colonization, living and being carried in the nasopharynx, maxillae, vagina, skin and perineum. During menstruation, their numbers double in the vagina.

This bacterium is found in 20-30% of the anterior nares of normal healthy people. Conversely, in the hospital setting, where the personnel are exposed frequently and repeatedly to staphylococcal, a colonization approaching 60% is demonstrated. Frequent health care visitors, such as dialysis patients, are ready recipients of staphylococcal colonization. Individuals with compromised immune systems, and chronic skin conditions, as well as type I Diabetics are especially susceptible to colonization. It is estimated that 5-6% of all new hospital admissions will develop Hospital acquired infections, of which Staphylococci are the most common.

Once an individual is colonized, the organism can persist for long periods and has a half-life of 40 months. Those organism acquired in the health setting are very likely to be resistant to the more commonly used antibiotics, especially Oxacillin and Methicillin and are referred to as MRSA (Methicillin Resistant Staphylococcal Aureus). Up to 50% of Staphylococcal strains seen in the hospital are resistant to Methicillin. Outside of the health arena, MRSA is rarely a danger to the general public. But in the health setting, this organism is responsible for 25% of hospital bloodstream infections. Debilitated, burned, post-operative surgical and orthopedic wound patients are especially vulnerable to this bacterium. “It is estimated that the odds of dying from an MRSA infection in the hospital are almost twofold higher than if the infection were not caused by a resistant infection“.

Since the introduction of antibiotics, bacteria and virus have begun to develop mechanism whereby resistance to these antibiotics are achieved, resulting in the emergence of very virulent organisms such as MRSA and VRE. Particularly in the hospital setting, where antibiotics are used so often, this transformation from common antibiotic sensitive organisms to resistant organism has been observed with alarming frequency. This has begun to manifest itself even in the long term setting such as nursing homes and rehabitative centers. Even in the community setting with the frequent and increasing use of antibiotics to treat Sinusitis and childhood ear infections, antibiotic resistant organisms have begun to flourish. Patients failing to take the full course of treatment, stopping the medication before they are all taken, because they feel better, has allowed the surviving bacteria, even though reduced in number, to develop antibiotic resistance.

In recent years, studies have demonstrated that MRSA is often picked up in the hospital and carried home by both the patient and the visitors. Screening patients, who are transferred from other hospitals has begun to gain a foothold in an effort to stem this spread.

Pathogenesis

Colonization, either from the individual or other human contacts and surfaces, affords the staphylococcus access to disrupted epithelial or mucosal barriers, where it may become pathogenic. Once it gains access to the inner tissues, it is able to set up infection, inflammation and fever. This invasion may manifest clinically as skin infections (ulcers and boils), pneumonia, sepsis, deep abscesses and even death. Spread of the organism is by direct physical contact, as well as contact with objects, such as sheets, towels, dressings, clothes, etc. that have been contaminated by either infected skin or
Respiratory droplets. Airborne spread is felt to be possible in some situations.

Some of these organisms, especially Staphylococci, can manifest there pathological influence by the emission of toxins, which can be deadly to humans. The Toxic Shock Syndrome, from vaginal tampons, left in for extended periods, has been associated with Staphylococcal toxins, and is associated with many deaths.

Epidemics of MRSA have occurred in Intensive care units, Orthopedic units, premature nurseries, where neonates, with immature immune systems, reside. The economic and health impact of MRSA has become enormous. Now, certain groups are suggesting that women have their babies at home where resistant organisms are less likely to be found.

It has been postulated, from studies, that the longer one is required to stay in the hospital, or in the Intensive care unit, had numerous antibiotics, or antibiotics for a long period of time, or is exposed to medical devices, the more likely they will contact MRSA. Chronic Staphylococcal infections with recurrent infections has been proposed by some researchers, and is currently under investigation. Even Chronic Fatigue Syndrome has been linked as one possible result of chronic infection as a reaction to toxins emitted by the staphylococcal. Septic Arthritis has been associated with MRSA, among other organisms.

TREATMENT

Colonized patients, who are not scheduled for surgery, are not candidates for treatment. The pre-antibiotic era management of wounds is still an acceptable approach to superficial wounds and abscesses. Incision and drainage of the wound or sore can often heal the lesion without the use of antibiotics. Intravenous antibiotics are necessary for deep seated infections, and consist of potentially toxic drugs, which require hospitalization, intravenous administration and close vigilance.

Removal of prosthetic apparatuses may be necessary if the deep peri- prosthesis infection is discovered some time after the initial implantation. This may require re-implantation of a new prosthesis after the wound has healed.

PREVENTION

The use of antibiotics, either systemically or topically or both has been tried in order to decrease the colonization of MRSA in the hospital setting. Initially there were many failures in eradicating colonization in the nares and preventing recolonization. The relatively successful combinations have been rifampin with trimthoprim sulfamethoxazole, rifampin and minocycline, and mupirocin ointment alone.

Mupirocin ointment has received particular attention of late, since it is easy to apply and has few side effects. Typically, this agent is applied twice a day for 5 days. This has been fairly successful in patients who were to undergo surgery, where the risk of developing MRSA surgical site infection varies from 2 to 14 times higher than those with negative nares cultures. In studies, there was an approximate 50% decrease in the rate of infections in those who received the ointment. It decolorized the nares in 83% of those who received it for 5 days, and 90% in those, who received it for 6 days.

Recently, there have emerged rapid tests able to identify Staphylococcus Aureus within 15 min. to 2 hrs., which may allow to institution of this therapy to be implemented expeditiously, in those scheduled to undergo surgery or who are susceptible to infection, because of reduced resistance.

Even a recent DNA vaccine has been tried, and may offer a different and effective approach to MRSA.

Antibiotics, such as Vancomycin have been used to treat MRSA successfully, but resistance is rapidly developing and these are very virulent drugs, with serious potential side effects, and must be given intravenously in the hospital. New drugs are being sought for in an ever increasing frenzy.

Finally, simple universal rules of health, such as washing of hands by the health personnel between patients, for 20 seconds with an antibacterial soap, and using paper hand towels to flush toilets and open bathroom doors, after washing, will help in diminishing the prevelance of this organism in the hospital surroundings, where it is most dangerous. Insisting that your
Nurse and Physician wash his hands, as described, before touching you or room furniture or articles may deter transfer of resistant organisms. Wearing and changing gloves would be a better approach, but has yet to be accepted.

A Japanese study suggested the following steps to control MRSA: 1.) Constant and careful surveillance, 2.) regular risk factor analyses, 3.) the optimal administration of antibiotics, 4.) the education of all hospital staff. They strategically placed hand washing equipment, used disposable gloves and contaminated waste bags, and noted the hospital incidence if MRSA to be reduced considerably.

“Patients with MRSA should be physically isolated in a single room with the door remaining closed and the room regularly damp dusted, or they should be nursed in a special ward away from other non-infected patients. If a patient is readmitted to the original hospital or to another hospital, within some specified period of time and was know to have a previous MRSA infection, this patient should be physically separated or placed in isolation immediately to reduce the possibility of spread to others. After an MRSA patient is discharged from the hospital, their room should be comprehensively cleaned and all linen and other clinical waste disposed of in special bags.” (4)

VANCOMYCIN RESISTANT ENTEROCOCCUS

Enterococcus, like Staphyloccus, is a normal inhabitant of the body. It resides, generally, in a non-pathogenic manner in the intestinal and female genital tracts of humans. But, it too, can become a pathogen, once it gains access within the body, especially in an enviroment conducive to inflammation or where the immune system is impaired.

And like Staph, it too has, over the years, from exposure to antibiotics, developed resistance, which now expresses itself as a resistance to Vancomycin, leaving us almost defenseless before it’s onslaught. It too, was originally thought to be attributed to endogenous sources within the individual patient, as the origin of the bacteria’s presence. But, like MRSA, recent outbreaks have indicated that patient-to-patient transmission of the microorganism can occur, either through direct contact or even through indirect contact. This can occur via a) the hands of the personnel or b) contaminated environment or equipment.

Also, like Staph, certain patient groups are susceptible to it’s invasion. These include the immunologically compromised, critically ill or debilitated patients, persons who have had an intraabdominal or cardio-thoracic surgical procedure, as well as those with indwelling urinary or central venous catheters or those with implantations of prosthetic materials or devices. It too, is often found to be plentiful in Special care units such as ICU. Streptococci have also been associated with Toxic Shock Syndrome, because of their penchant to produce toxins.

And it has recently been discovered, that one genus of bacteria can share it’s antibiotic resistance to that of another. So an MRSA, which is not resistant to Vancomycin, can, in the presence of VRE, rapidly develop an equal resistance to Vancomycin.

PREVENTION AND TREATMENT

Prevention involves all the aforementioned Universal health precautions referable to MRSA. They include, judicious hand washing, use of gloves, isolation precautions, care and cleaning of equipment and the patient environment. In this particular case, intensified fecal screening for VRE might facilitate earlier identification of colonized patients, leading to more efficient containment of the microorganism. And equally, since colonization can remain for prolonged periods of time after discharge from the hospital, there should be a method of highlighting those patients with previous VRE infections, so that they can be immediately identified, when they return to the hospital environment.

Although, in contrast to MRSA, hospital personnel have rarely been associated with the transmission of this microorganism, the possibility still remains. So, hospital personnel should still be examined for chronic skin and nail problems and perform hand and rectal swab cultures for completeness sake.

As to prophylaxis for major surgical procedures, which involve implantation of prosthetic materials or devices, a single dose of vancomycin administered immediately before surgery is sufficient unless the procedure lasts greater than 6 hours, in which case the dose should be repeated. No more than 2 doses should be administered.

Since Vancomycin is the most common medication used for MRSA, the HICPAC ( Hospital Infection Control Practices Advisory Committee, has published guidelines concerning situations in which the use of Vancomycin should be discouraged. Their advice also includes recommendation for Screening procedures for detecting VRE in Hospitals where VER have not been detected and Detecting and Reporting MRSA and VRSE.

Treatment of VRE, presently consists of a combination of a penicillin and an aminoglycoside.

References:

1.) The significance of MRSA infection in genl sugery: a multivariate analysis of risk factors and preventive approaches: Surg Today. 1993;23(10):880-4/

2.) Risk factors for persistent carriage of MRSA: Clin Infec Dis. 2000 Dec;31(16): 1380-5. Epub 2000 Nov.

3.) Nasal carriage of Staph aureus is a major risk factor for surgical-site infections in orthopedic surgery: Infect Control Hosp Epidemiol. 2000 May;21(5):319-23.
4.)MRSAAssociationofMedicalMicrobiologists.(http://www.amm.co.uk/pubs/fa_mrsa.htm)

5.) Recommendations for Preventing the Spread of Vancomycin Resistance Recommendations of the Hospital Infection Control Practices Advisory Committee (HICPAC): http://aepo-xdv-www.epo.cdc.gov/wonder/prevgiud/m0039349/m0039349.asp

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Image yourself as a physician, having a patient who is quite ill from an overwhelming infection or major trauma or cancer, or even a premature separation of the placenta in pregnancy, and the patient suddenly shows signs of multiple Blood Clots developing in many different areas of the body. They may manifest as reddened indurated areas in the surface of the skin, or even small areas of cyanosis, as in the fingers. Sometimes, small areas of necrosis (gangrene) are evident. These are areas, which do not receive enough blood, because the clots block off the circulation. This is often referred to as “Ischemia”. Numerous bruises may become evident. And just as you are deciding to place your patient on blood thinners (Anticoagulants), designed to combat this excessive clotting tendency, the patient starts to bleed everywhere. This bleeding may occur from as many as three different areas of the body, such as by having nosebleeds, urinary bleeding and hemorrhages in the gums or into the skin. So now you’re really up against it. What causes this phenomenon be where the patient clots excessively and then bleeds excessively, and often, both at once?

Many Physicians now encounter a condition where most of the clotting factors in the blood stream are being used up because numerous clots are occurring within the blood vessels in many of the organs. The organs involved, unfortunately, are often vital, for life, such as the lungs, kidneys, liver and brain. And then, to complicate matters, when most of the clotting factors necessary to cause clotting are used up, bleeding develops. This phenomenon is called Disseminated Intravascular Coagulation (DIC). The balance between the clotting (thrombosis) and the bleeding tendency determines the constellation of symptoms.

As you can see, it occurs in very sick patients and often results in death. It is incumbent for the physician to anticipate, recognize and promptly treat this condition when it occurs, or death will, surely ensue. As DIC progresses, the patient may experience a fall in blood pressure, onset of elevated temperature, and shortness of breath. Since less blood is reaching the brain, the patient’s sensorium may deteriorate, manifested by somnolence, confusion and even coma. Or the patient may become restless and agitated from diminished oxygen to the brain. Jaundice, secondary to breakdown of clots may manifest itself. Shock is often the final episode, resulting in death.

Fortunately, there are clues which the physician must recognize. As expected, since the clotting system is involved, these clues present as abnormal values revealed by the blood tests. The signs and symptoms may be varied and complex and the diagnosis is not often detected until hemorrhage ensues. So the laboratory values are paramount in pointing to the proper diagnosis.

A fall in the platelet count, suggesting that the platelets are being used up to form the multiple clots is one of the first and most striking, obvious findings. The fibrinogen level is diminished, since that also, is used up in the clotting frenzy. The CBC will show a rapidly developing anemia, as the clotting and bleeding process is progressing. Once DIC is suspected, other blood tests are helpful in confirming it’s presence. A D-dimer and Fibrin Degenerative Product confirm the fact that clots are being formed and destroyed, as bleeding occurs. Fragmented red blood cells, called Schistocytes may be observed on the blood slide.

Pathophysiology
Some initiation of coagulation is necessary to trigger off this chain reaction. In these sick patients, injury of the lining of the blood vessels or injury of the tissue initiates this reaction. The vessel lining, in an effort to repair this injury, by its usual mechanism, releases substances which promoters clotting. The clotting is the body’s first approach to healing of that disrupted lining. Then, the other processes of healing go into action. This material, which previously was not in contact with the blood, before the vessel lining was disrupted, now interacts with the blood clotting mechanisms and the cascade of clotting goes forward. Unfortunately, in DIC, so much of these clot-promoting substances are released that a clotting frenzy ensues. Although bleeding may be the most prominent recognizable symptom, it’s the small clots in the microcirculation that jeopardizes the vital organs and results in organ failure, which is irreversible.

TREATMENT
The treatment of DIC must be begun early and aggressively.

1.) The most important thing to treat is the underlying stimulus. Sepsis must be treated with aggressive antibiotic therapy. The retained placenta must be evacuated. The trauma must be addressed and treated;

2.) To prevent shock, bleeding must be addressed by replacement of fluid. This helps by elevating the blood pressure and clearing the blood of Fibrin Degenerative Products, which continue the cascade of clotting and bleeding;

3.) Oxygen to keep the blood oxygenated and to try and deliver more oxygen to the tissues deprived of blood flow by the clots;

4.) Treat the clotting with Anticoagulants;

5.) Replace the lost clotting components, so the bleeding will stop;

6.) If all else fails, Antifibrinolytic agents may be of help, especially if a hyperfibrinolysis state exists, as in some forms of Leukemia and Cancer. Such a drug is Amicar or Cykokapron, as an alternative.

SUMMARY
Disseminated Intravascular Coagulation is a continuum of events that occurs in the coagulation pathway, associated with severe illnesses or trauma. It is accompanied by physical findings suggesting small vessel clotting and laboratory findings of a decreased or falling platelet counts. Other findings of enhanced clotting activity is evidenced by utilization of numerous blood clotting factors such as Fibrinogen. Bleeding occurs when these clotting factors are used up and occurs in multiple areas of the body. Both the clotting and the bleeding may occur simultaneously. The patient may go into shock from blood loss or become confused by poor oxygen transportation. The prognosis is guarded and often related to the underlying stimulus and its severity, such as Sepsis or Trauma.

The physician must anticipate and think of this condition and move swiftly to verify its presence with laboratory confirmation, and treat the underlying etiology, as well as monitor the thromboembolic and bleeding complications which occur.

Although there is no specific laboratory test for DIC, looking for a fall in the platelet count, the presence of FDP/D-dimer, and a prolonged PT and a PTT are considered indicative of its presence. Treatment is directed towards the underlying etiology, replacement of blood products, and the utilization of anticoagulants and, if necessary, the addition of fibrinolytics.

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