ASSIMILATION OF LAW ON REGISTRATION OF OUTPATIENT MEDICAL CARD PATIENT WITH PERIODONTITIS, ABSCESS, PERICORONITIS, OSTEOMYELITIS. CONSOLIDATION OF SKILLS FILLING OUTPATIENT MEDICAL CARD (FOLLOWING WRITING SAMPLE). ERYSIPELAS FACE, NOME
Dental records: An overview
Abstract
Dental records consist of documents related to the history of present illness, clinical examination, diagnosis, treatment done, and the prognosis. A thorough knowledge of dental records is essential for the practicing dentist, as it not only has a forensic application, but also a legal implication with respect to insurance and consumerism. This article reviews the importance of dental records in forensics.
Introduction
Forensic odontology is the application of the art and science of dentistry to resolve matters pertaining to the law. Some of the diverse facets of this unique discipline can range from the identification of human remains to mass disaster management, from the assessment of bite marks and patterned skin injuries to the use of dental materials in the examination of evidence.
A dental record is the detailed document of the history of the illness, physical examination, diagnosis, treatment, and management of a patient. Dental professionals are compelled by law to produce and maintain adequate patient records. With the increasing awareness among the general public of legal issues surrounding healthcare, and with the worrying rise in malpractice cases, a thorough knowledge of dental record issues is essential for any practitioner. The ability of clinical practitioners to produce and maintain accurate dental records is essential for good quality patient care as well as it being a legal obligation. The dental record provides for the continuity of care for the patient and is critical in the event of a malpractice insurance claim.
Comprehensive and accurate records are a vital part of dental practice. Good record keeping is fundamental for good clinical practice and is an essential skill for practitioners. The primary purpose of maintaining dental records is to deliver quality patient care and follow-up. Dental records can also be used for forensic purposes and have an important role in teaching and research, as well as in legal matters. The code of practice on dental records documents the minimum requirements for recording and maintaining dental records and describes some of the underlying principles to be applied by the practitioners in their record keeping.
Patient Record
The record may consist of several different elements, which include writteotes, radiographs, study models [Figures [Figures11–2], referral letters, consultants’ reports, clinical photographs, results of special investigations, drug prescriptions, laboratory prescriptions, patient identification information, and a comprehensive medical history. Obviously this is a large amount of information and it is essential that a practitioner maintains this in an easily accessible manner.
Dental records
Cartoon on significance of dental records
The information in the dental record should primarily be clinical iature. The record includes a patient’s registration form with all the basic personal information. The dental team should be very meticulous and thorough in the dental office record keeping tasks. All information in the dental record should be clearly written, and the person responsible for entering new information should sign and date the entry. The information should not be ambiguous or contain many abbreviations. In practices with more than one dental practitioner, the identity of the practitioner rendering the treatment should be clearly noted in the record. All entries in the patient record should be dated, initialed, and handwritten in ink and / or computer printed. Although no specific color of ink is required, any copy of the record should be easy to read. Handwritten entries should be legible.
Within the writteotes the following are examples of what is typically included in the dental record:
1. Identification data — name, date of birth, phone numbers, and emergency contact information.
2. Dental history
3. Clinical examination to include an accurate charting
4. Diagnosis
5. Treatment plan
6. Documentation of informed consent
7. Medical history — a thorough investigation, to include a minimum of:-
· Name and phone number of physician
· Dentists’ own evaluation of patient’s general health and appearance
· List of systemic disease — diabetes, rheumatic fever, hepatitis, and the like
· Any ongoing medical treatment
· Any bleeding disorders, drug allergies, smoking and alcohol history
· Any cardiac disorders
· Relevant family medical history
· Pregnancy
· Physical and emotional tolerance for procedures
No financial information should be kept in the dental record. Ledger cards, insurance benefit breakdowns, insurance claims, and payment vouchers are not part of the patient’s clinical record. Financial records should be kept separately from the dental record. Other information best left out of the record would be personal opinions or criticisms. Do document a patient’s refusal to accept the recommended treatment plan and cancelled appointments.
The outside cover of the chart should only display the patient’s name and / or account number. Use of abstract is advantageous in the in-office system (color or symbol coding), so that only your office staff will be able to decipher it. For all offices, a single sticker on the outside cover can alert the team to look on the inside for important information regarding allergies, medications, antibiotic pre-medications, and clinical conditions that can affect dental treatment. All medical notations inside the chart, to be seen only by the authorized personnel.
Maintenance of dental records
Most dentists make notes on paper dental records. However, many more dentists are making use of computerized filing systems to maintain patient dental records. Electronic records have great quality and patient-safety benefits, and will likely increase as more dental clinics and hospitals become computerized. Many dental clinics use the traditional paper charts; the traditional filing systems are labeled with the following information,
- Patient’s surname
- Patient’s first name
- Patient’s middle name
- Patient’s degree or seniority (i.e., Senior, II)
The files are then arranged in a way for easy retrieval — usually in a lateral, open-shelf filing system.
Color Coding
Many dental offices use a color-coded filing system for patient record files. Color-coded labels — usually the first two letters of the patient’s last name and active date of treatment — are placed on the patient’s file. This can help make record retrieval fast and easy.
Active and Inactive
Most offices have two categories of patient records files: (1) Active and (2) Inactive.
Active files hold the records of patients currently having their dental care provided by the practice. Inactive patients are considered to be those who have not returned for 24 months. Keep files of active patients on-site. These records should be conveniently located in the office.
Inactive files hold the records of patients who have been treated in the office in the past, but are not currently under care in the office. These files are generally located in the office, but in a remote area.
A system should be established in the office to identify a change from active to inactive status on a timely basis. All records, active and inactive, should be maintained carefully to be certain that they are not destroyed or lost.
Lawney describes a simple ten-step procedure to ensure that your records are adequate. A modified and expanded version, appropriate to the National Health Service and
1. Use a consistent style for entries — the appearance of the record is enhanced by using the same colour and type of pen, use the same abbreviations and notations, and so on
2. Date and explain any corrections — it may be a fatal error in a malpractice case if records appear doctored in any way. These unexplained corrections can undermine the credibility of the entire record and of the treating dentist
3. Use single-line crossout — this preserves the integrity of the record and shows that you have nothing to hide
4. Do not use correction fluids — not only is this messy, but it is conspicuous and may indicate that there has been an attempt to hide information.
5. Use ink — pencil can fade and opens up the question of whether or not the records have been altered.
6. Write legibly — an illegible record may be as bad as no record at all. Difficult to read entries can lead to guesswork by others and this may not be favorable to you.
7. Express concerns about patient needs — by doing this you are documenting that you have listened, empathized, understood, and acted upon the wishes of your patient. It also enables an explanation to be given should a patient’s wishes be unobtainable or unrealistic, and can help instantly diffuse a malpractice case. Use quotations to indicate patient comments as distinct from your own.
8. Never write derogatory remarks in the record — Superfluous entries only serve to convey a feeling of unprofessionalism and may create doubts regarding the overall credibility of the remainder of the record. Negative views about patients, such as their failure to follow your advice or attend appointments, should be recorded in a dispassionate and objective manner.
9. Document fully — there is no need to be sparse with notes, a detailed explanation is always better than one lacking information.
10. Only use accepted abbreviations for treatments — this is helpful both in a malpractice situation and also when transferring records to a different dentist for referral, prior approval or a change in dentist.
11. Collate documents — insurance details and other materials from third parties should be separate from those items that pertain directly to patient care.
12. Maintain a chronological order — the use of a hole punch and metal retainer clips on the top of the record may be helpful to keep loose sheets organized.
By following these steps the production of accurate and defensible records is possible.
Record Management
The recording of accurate patient information is essential to dentistry. The dental record, also referred to as the patient chart, is the official office document that records all diagnostic information, clinical notes, treatment given, and patient-related communications that occur in the dental office, including instructions for home care and consent to treatment. Protecting health information — and diligent and complete record keeping — is extremely important for many reasons,
Care for the patient: Patient records document the course of treatment and may provide data that can be used in evaluating the quality of care that has been provided to the patient.
Means of communication: Records also provide a communication between the treating dentist and any other doctor who will care for that patient. Complete and accurate records provide enough information to allow another provider who has no prior knowledge of the patient to know the patient’s dental experience.
Defense of allegations of malpractice: Besides, the dental record may be used in a court of law to establish the diagnostic information that was obtained and the treatment that was rendered to the patient. This information helps in determining whether the diagnosis and treatment conformed to the standards of care in the community.
Aid in the identification of a dead or missing person: Another way the dental record may be used is to help provide information to appropriate legal authorities that will aid in the identification of a dead or missing person. The most common element of forensic dentistry that a general practitioner is likely to encounter is to supply antemortem (before death) records to a forensic odontologist.
Retention and storage
There is usually a different requirement for the retention of records of children. These records must be kept for a certain period after the child becomes a major. The dental office should have a records retention policy and all the staff should understand it. The office’s professional liability insurance company will likely have recommendations about retention.
Dental records may be preserved on microfilm or microfiche, stored with a records storage service (fairly common in many jurisdictions) or scanned for electronic storage. The great benefit of storing records electronically or on microfilm or microfiche is that they take up less space than paper records. Diagnostic and / or treatment casts may be photographed and stored in some cases. However, prior to completely converting the records to one of these methods, a dentist should consult with his / her own attorney and a professional liability insurance company.
The accurate health / dental history may provide important and valuable information for the dentist, prior to beginning treatment. All dentists should take health histories initially and update the same periodically as necessary. Dentists have a responsibility to obtain and maintain the current health histories of patients. Team members are most often responsible for having patients complete their health / dental history forms, but that is only part of the process. It is also important that a patient understands the questions, provides appropriate answers, and signs the completed form. A health history form provides a starting point for the dental team to fulfill its professional obligations.
The NHS Terms of Service, state that dental records should be kept for a period of two years. The Regulations state that treatment records, radiographs, photographs, and study models should be retained after the completion of any course of treatment and care, under a continuing care or capitation arrangement for this period. There are strict time limits applied to such actions,
1. Within three years of the date when the cause of action occurred
2. Within three years of the patient’s date of knowledge that the treatment may have been negligent
3. If a claim is based upon a Breach of Contract, the action must be raised within five years in
It is therefore possible that a claim for negligence could happen many years after the event, and that retention of records for the minimum of two years is inadequate. The defense organizations suggest that records be kept permanently. This is often impossible due to space constraints and so the advice given by defense organization is as follows,
1. Treatment Records, X-rays, Study Models, and Correspondence is to be retained for 11 years after the completion of treatment
2. For children, retention of records until the patient is 25 years old
3. Orthodontic Models — retain the original pre- and post-operative models permanently, discard any intermediates after a period of five years.
The storage area of these records should be secure and access strictly controlled. By following these guidelines the dental records of a patient will be available whenever they are needed. Following these guidelines will be very supportive for forensics at our place.
Confidentiality
Dentists are in a privileged position to learn a lot about their patients and this knowledge is acquired under the assumption that it is confidential. Confidentiality encourages open and honest communication, enhancing the dentist–patient relationship, and encourages respect for patient autonomy and privacy.
There are certain circumstances when information can be disclosed and they include,
1. Sharing of relevant information with other healthcare professionals involved in a patient’s treatment
2. Information may be passed to a third part if the patient or legal adviser gives written consent, for example, an insurance company
3. Where information is requested about a deceased patient and consent of the estate or relative is sought and there is an investigation of sudden, suspicious or unexplained death
4. Information is required in the preparation of legal reports containing only relevant dental treatments
5. Access to dental records by the police. Search and seizure warrants may not include dental records, and therefore should be carefully checked
6. Clinical research protocols and peer review procedures. The name of the patient must be kept confidential. If information is to be used for teaching purposes then the patient’s consent must be obtained
The area of confidentiality of childrens’ dental information can be confusing. Those individuals of 16 years and older should be considered adults, however, for those who are 16 years and under, the dentist still has a duty of care and therefore confidentiality to the child. This duty is combined with a duty to the parents, especially in the area of consent to treatment. Children who are victims of abuse require special management and the dentist may have an overriding responsibility to break confidentiality and report their findings to the appropriate authorities.
Special guidelines exist for patients with AIDS / HIV and sexually transmitted diseases. Strict confidentiality must be maintained when dealing with these individuals. Disclosure of such information could lead to a complaint of serious professional misconduct.
Forensic Uses of Patient Records
Forensic dentistry is the overlap of the dental and legal professions. The most common element of forensic dentistry that a general practitioner is likely to encounter is to supply antemortem (before death) records to aid in personal identification. Forensic dentists are frequently called upon to identify the remains of individuals who cannot be identified visually. This encompasses a large number of situations such as burnt, grossly decomposed or mutilated remains. The identification is normally carried out by the comparison of antemortem (before death) and postmortem (after death) records.
The identification of the deceased individuals is an essential element in the process of death certification and is a crucial component in the investigation of homicides or other suspicious deaths. It is vital to have expeditious and accurate identification both for law enforcing authorities and relatives. Until identification can be confirmed, estates cannot be settled, death benefits cannot be paid, and surviving spouses are unable to remarry. Perhaps of most importance is that the identification of the dead is an essential component of the grieving process and is a necessary part of human dignity in a civilized society.
The police officers in charge of the case will normally call upon the dentist to provide details of dental records. It must be remembered that police officers have no statutory rights to inspect or remove a patient’s records without their consent. However, the law allows for special circumstances and it is reasonable to hand over an individual’s record if it enables them to be identified or excluded. The consent of the nearest relative or estate executor may also be sought if required.
The availability of contemporaneous and clear notes is essential in forensic dental identification. If notes are incorrectly dated, it can complicate and even negate a positive identification. It is in such situations where the errors highlighted by Borrman and others can cause crucial mistakes to be made. When a request for records is received the entire record is useful, including such items as laboratory prescriptions and study models. Many documented cases have used the unique pattern of the palatal rugae recorded on an orthodontic study model to identify young individuals with no dental restorations.
The police may require access to an individual’s record for another criminal matter. They may, for example, want to see an appointment book to establish an alibi or time line. In these circumstances a warrant is required if the patient has not agreed to the release, as it can be argued that the release of notes in this instance is not in the patient’s best interest. If in doubt always contact your legal adviser.
Summary and Conclusion
Doubt about what should be documented or how records need to be kept, practitioners should ask themselves: “Will this action serve the best interests of my patient? Does this action helps in my patient’s safety and the continuity of his or her dental care?” The principles applying to handwritten records also apply to computer records, for example, entries must be date, time, and operator-stamped, all changes made must be traceable, and any codes used must be readily convertible to conventional language. Records must be readily accessible and understandable data needs to be controlled, for example, via use of passwords.
The production, retention, and release of clear and accurate patient records are an essential part of the dentist’s professional responsibility. Success in this task will assist the dentist should a medicolegal claim be made and can assist the police and coroners in the correct identification of individuals.
ERYSIPELAS – PICTURES, SYMPTOMS, CAUSES, TREATMENT
Background
Erysipelas is a bacterial skin infection involving the upper dermis that characteristically extends into the superficial cutaneous lymphatics. Erysipelas has been traced back to the Middle Ages, where it was referred to as St. Anthony’s fire, named after the Christian saint to whom those afflicted would appeal for healing. Around 1095, the Order of St. Anthony, a Roman Catholic congregation, was formed in
Pathophysiology
Bacterial inoculation into an area of skin trauma is the initial event in developing erysipelas. Thus, local factors, such as venous insufficiency, stasis ulcerations, inflammatory dermatoses, dermatophyte infections, insect bites, and surgical incisions, have been implicated as portals of entry. The source of the bacteria in facial erysipelas is often the host’s nasopharynx, and a history of recent streptococcal pharyngitis has been reported in up to one third of cases. Other predisposing factors include diabetes, alcohol abuse,[1] HIV infection, nephrotic syndrome, other immunocompromising conditions, and vagrant lifestyle.
Preexisting lymphedema is a clear-cut risk factor for erysipelas. Recurrent erysipelas complicating the lymphedema from breast cancer treatment is well documented.[2, 3] Lymphoscintigraphy in patients with a first-time episode of lower extremity erysipelas has documented lymphatic impairment in both affected and nonaffected legs. Thus, subclinical lymphatic dysfunction is a risk factor for erysipelas.[4]
In erysipelas, the infection rapidly invades and spreads through the lymphatic vessels. This can produce overlying skin “streaking” and regional lymph node swelling and tenderness. Immunity does not develop to the inciting organism.
Epidemiology
Frequency
United States
Isolated cases are the rule with erysipelas, although epidemics have been reported. The incidence of erysipelas declined throughout the mid-20th century, possibly due to antibiotic development, improved sanitation, and decreased virulence.[5] The change in distribution from the face to the lower extremities is most likely related to an aging population with risk factors such as lymphedema. Approximately 85% of cases of erysipelas occur on the legs rather than the face.
International
Erysipelas is somewhat more common in European countries. Isolated cases are still the rule, and distribution and etiology remain similar to that in the
Mortality/Morbidity
The most common complaints during the acute infection include tenderness of the involved area, fever, chills, and swelling. Predisposed patients often develop local recurrence, and this can lead to disfiguring and disabling healing reactions, such as elephantiasis nostras verrucosa. This chronic warty, edematous condition is caused by lymphatic destruction from repeated infection. Death as a direct result of erysipelas is exceedingly rare.
Race
Erysipelas infections affect persons of all races.
Sex
Erysipelas has been reported to be more common in females, but occurring at an earlier age in males, likely because of their more aggressive activities and resultant skin injuries. Other studies indicate that predisposing factors, rather than gender, account for any male/female differences in incidence.
Age
Cases of erysipelas have been reported in all age groups, but it does appear that infants, young children, and elderly patients are the most commonly affected groups. The peak incidence has been reported to be in patients aged 60-80 years, especially in patients who are considered high-risk and immunocompromised or those with lymphatic drainage problems (eg, after mastectomy, pelvic surgery, bypass grafting).
History
Patients often cannot recall an inciting event, but a history of recent trauma or pharyngitis may be elicited. Prodromal symptoms, such as malaise, chills, and high fever, often begin before the onset of the skin lesions and usually are present within 48 hours of cutaneous involvement. Pruritus, burning, and tenderness are typical complaints.
Physical
Erysipelas begins as a small erythematous patch that progresses to a fiery-red, indurated, tense, and shiny plaque, as shown in the image below.
Facial erysipelas exhibiting classic fiery-red plaque with raised, well-demarcated borders.
The lesion classically exhibits raised, sharply demarcated, advancing margins. This is in opposition to the slightly deeper involvement seen in cellulitis, with which lesions present with limited edema and less well-defined borders. Local signs of inflammation, such as warmth, edema, and tenderness, are universal. Lymphatic involvement often is manifested by overlying skin streaking and regional lymphadenopathy. More severe infections may exhibit numerous vesicles and bullae along with petechiae and even frank necrosis. With treatment, the lesion often desquamates and can resolve with pigmentary changes that may or may not resolve over time.
Causes
Streptococci are the primary cause of erysipelas. Most facial infections are attributed to group A streptococci, with an increasing percentage of lower extremity infections being caused by non–group A streptococci. Streptococcal toxins are thought to contribute to the brisk inflammation that is pathognomonic of this infection. No clear proof has emerged that other bacteria cause typical erysipelas, although they clearly coexist with streptococci at sites of inoculation. Recently, atypical forms reportedly have been caused by Streptococcus pneumoniae, Klebsiella pneumoniae, Haemophilus influenzae, Yersinia enterocolitica, and Moraxella species, and they should be considered in cases refractory to standard antibiotic therapy.
The role of Staphylococcus aureus, and specifically methicillin-resistant S aureus, remains controversial. No conclusive evidence demonstrates a pathogenic role for staphylococci in typical erysipelas. The infection’s predictable response to penicillin, even when S aureus is present, argues against S aureus as an etiologic agent. However, analogous to what occurs in bullous impetigo or staphylococcal scalded skin syndrome, exotoxins from coexisting S aureus may account for the clinical presentation of bullous erysipelas.
Differential Diagnoses
- Cellulitis
- Dermatitis, Contact
- Erysipelas Carcinomatosum
- Erythema Induratum
- Erythema Nodosum
- Granuloma Faciale
- Necrotizing Fasciitis
- Stasis Dermatitis
- Systemic Lupus Erythematosus
Laboratory Studies
In classic erysipelas, no laboratory workup is required for diagnosis or treatment. However, leukocytosis and elevations in erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are common.[7, 8]
Routine blood and tissue cultures are not cost-effective because they have an extremely low yield and results have a minimal impact on management. Cultures are perhaps best reserved for very immunosuppressed hosts in whom an atypical etiologic agent might be more likely.[9]
Bacterial cultures from the portal of entry may be most helpful in persons with atypical clinical presentations.
Imaging Studies
Imaging studies are not usually indicated and are of low yield. MRI and bone scintigraphy are helpful when early osteoarticular involvement is suspected. In this setting, standard radiographic findings typically are normal.
Histologic Findings
The histologic hallmarks of erysipelas are marked dermal edema, vascular dilatation, and streptococcal invasion of lymphatics and tissues. This bacterial invasion results in a dermal inflammatory infiltrate consisting of neutrophils and mononuclear cells. The epidermis is often secondarily involved. Rarely, bacterial invasion of local blood vessels may be seen.
Medical Care
Elevation and rest of the affected limb are recommended in erysipelas treatment to reduce local swelling, inflammation, and pain.
Saline wet dressings should be applied to ulcerated and necrotic lesions and changed every 2-12 hours, depending on the severity of the infection.
Streptococci cause most cases of erysipelas; thus, penicillin has remained first-line therapy.[10, 11] Penicillin administered orally or intramuscularly is sufficient for most cases of classic erysipelas and should be given for 10-20 days.
A first-generation cephalosporin or macrolide, such as erythromycin or azithromycin, may be used if the patient has an allergy to penicillin. Cephalosporins may cross-react with penicillin and should be used with caution in patients with a history of severe penicillin allergy such as anaphylaxis.
Hospitalization for close monitoring and intravenous antibiotics is recommended in severe cases and in infants, elderly patients, and patients who are immunocompromised.
Coverage for Staphylococcus aureus is not usually necessary for typical infections, but it should be considered in patients who do not improve with penicillin or who present with atypical forms of erysipelas, including bullous erysipelas. Some authors believe that facial erysipelas should be treated empirically with a penicillinase-resistant antibiotic, such as dicloxacillin or nafcillin, to cover possible S aureus infection, but supporting evidence for this recommendation is lacking.[6]
Patients with recurrent erysipelas should be educated regarding local antisepsis and general wound care. Predisposing lower extremity skin lesions (eg, tinea pedis, toe web intertrigo, stasis ulcers, asteatotic dermatitis) should be treated aggressively to prevent superinfection. Use of compression stockings should be encouraged for as long as 1 month in previously healthy patients and long term in patients with lower extremity edema. Long-term management of lymphedema is essential. Long-term prophylactic antibiotic therapy generally is accepted, but no true guidelines are available. Treatment regimens should be tailored to the patient. One reported regimen is benzathine penicillin G at 2.4 MU intramuscularly every 3 weeks for up to 2 years.[12] Two-week intervals have also been used.[2]
Two drugs, roxithromycin and pristinamycin, have been reported to be extremely effective in the treatment of erysipelas. Several studies have demonstrated greater efficacy and fewer adverse effects with these drugs compared with penicillin.[13] Currently, the Food and Drug Administration has not approved these drugs in the
Also see a clinical guideline summary from the Infectious Diseases Society of America, Practice guidelines for the diagnosis and management of skin and soft-tissue infections.
Surgical Care
Debridement is necessary only in severe infections with necrosis or gangrene.
Consultations
Most patients with erysipelas respond very well to conventional antibiotic therapy. However, in atypical infections that are unresponsive to first- and second-line agents, an infectious disease consult may be useful.
Activity
Patients with acute infections involving the extremities should be encouraged to limit their activity and keep the limb elevated to decrease swelling.
Medication Summary
The objective of pharmacotherapy is to reduce morbidity and to prevent complications.
Antibiotics
Class Summary
Penicillin is the standard therapy for typical erysipelas, although coverage for S aureus should be considered in the appropriate setting.
Penicillin VK (Wycillin, PenVeeK)
Penicillin G procaine (Wycillin) and penicillin VK (PenVeeK) are currently recommended as first-line agents for the treatment of moderately severe infections of skin and skin structure. In adults, administer penicillin G procaine by deep IM injection only into upper, outer quadrant of buttock. In infants and small children, the midlateral aspect of the thigh may be a better site for administration.
Dicloxacillin (Dycill, Dynapen)
Treatment of infections caused by penicillinase-producing staphylococci. Penicillinase-resistant penicillin that will cover for S aureus.
Nafcillin (Unipen)
Initial therapy for suspected penicillin G-resistant streptococcal or staphylococcal infections.
Use parenteral therapy initially in severe infections. Change to oral therapy as condition warrants.
Because of thrombophlebitis, particularly in elderly patients, administer parenterally only for short term (1-2 d); change to
Erythromycin (E-mycin, E.E.S., Eryc)
Macrolide used for penicillin-allergic individuals. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes causing RNA-dependent protein synthesis to arrest. For treatment of staphylococcal and streptococcal infections.
In children, age, weight, and severity of infection determine proper dosage. When bid dosing is desired, half total daily dose may be taken q12h. For more severe infections, double the dose.
Complications
The most common complications of erysipelas include abscess, gangrene, and thrombophlebitis. Less common complications (< 1%) are acute glomerulonephritis, endocarditis, septicemia, and streptococcal toxic shock syndrome. Rare osteoarticular complications involve joints contiguous with the erysipelas plaques and include bursitis, osteitis, arthritis, and tendinitis.
Prognosis
The prognosis for patients with erysipelas is excellent. Complications of the infection usually are not life threatening, and most cases resolve after antibiotic therapy without sequelae. However, local recurrence has been reported in up to 20% of patients with predisposing conditions.
What is Erysipelas?
This is a kind of bacterial caused infection which is very rare. It normally only affects the legs or the face. It’s a variant of cellulitis which is another skin disease. But, cellulitis may develop on any location on the body and may be infected by many different bacteria, where erysipelas is normally just caused by streptococcus pyogenes as well as merely developing in the locations that have already been mentioned.
One type of erysipelas, known as “swine erysipelas”, before the discovery of antibiotics was a relentless problem for farmers with pigs. Pigs normally died as well as whole farms suffered from this infection. Beginning only as lesions, in this situation, over the entire body, it would rapidly develop to do damage to organs and finally caused the pigs to die. Currently pigs are normally immunized for this erysipelas with defensive doses of antibiotics so as to avoid getting this disease.
In humans erysipelas is very rare. And, immediate treatment is needed. If left not treated, it often can damage the heart as well as the joints. When anyone looks at the biography of interesting people from the past or in past family histories, you can find the deaths of many people by erysipelas. Anybody living before the time in which antibiotics were developed would have seen this disease progressively and particularly settled in the joints and it is there where it caused an awful lot of pain. Numerous people especially in the Victorian Era became addicts to opium in an effort to deal with the pain caused by this condition.
This disease is characterized by very well demarcated areas of heat, redness, pain and swelling and also can be associated with symptoms including:
- Pus-filled blisters
- Face rash
- Arm rash
- Leg rash
- Shiny red rash
- Painful, extremely red, warm skin and swollen under the lesion or sore
- Skin lesion have raised border
- Sores – erysipelas lesions – on the bridge of the nose as well as the cheeks
- Fever, chills and shaking
- Enlarged and tender local lymphatic nodes
- Headaches
- Vomiting
- Fatigue
Currently, erysipelas is always recognizable. The face rash follows a butterfly outline, extending over the cheeks as well as the nose. The symptoms start quickly and develop a raised rash. This rash is purple or orange because of the bleeding from the smallest blood vessels into the skin. The marked swelling as well as the color of this rash is quite hard to confuse this disease with several types of cellulitis.
This rash is very painful and will come with a fever as well as chills. If there is a rash such as this, the individual should be seen by a physician as soon as possible in order to start treatment.
Erysipelas Causes
Risk factors include:
- Cut in the skin
- Problems with drainage thru veins or lymphatic system
- Skin sores or ulcers
Anybody can develop erysipelas although it develops mostly among the elderly as well as the exceptionally young. There are many factors for developing this disease. Often this bacterium will enter a new wound from surgery and any swelling surrounding the wound normally indicates in most case some kind of cellulitis. Pimples, insect bites as well as cuts can all put a person at risk to the underlying bacteria. Bacteria are normally found in the nasal area and are accountable for the majority of cases of erysipelas established on the area of the face.
Several groups are much more prone to developing erysipelas. A person with a disease which is autoimmune such as HIV or lupus is most prone. Those with poor blood flow thru veins which are blocked, heart function which is reduced or heart defect are also most apt to get this infection. Individuals who exist in any constant unsanitary conditions, for instance the homeless appear to be more disposed to develop erysipelas. Also, alcoholism is another risk issue for developing erysipelas as well as a multitude of additional infections.
Erysipelas Treatment
In the early stages treatment consist of a 2-weeks of doses of oral penicillin or a penicillin-derivative antibiotic. If the individual is allergic to penicillin, some of the newest antibiotics may be used instead. In cases of erysipelas which are severe, antibiotics may need to be given thru an intravenous line or IV.
Erysipelas spreads quickly, eventually settling in the joints. When the rash on the legs or face is left untreated, those with this infection will need to be treated with lifelong daily doses of antibiotics to keep this infection in the joints to a minimum. But most of the times the symptoms and signs of this infection are so marked as well as painful, people will seek treatment rapidly.
In some individuals, the bacteria may migrate to the blood. This causes a condition known as bacteremia. The infection can spread to the heart valves as well as the joints and bones.
Other complications include:
- Septic shock
- Return of infection
Red wind – erysipelas
Red wind or erysipelas is an acute infectious skin disease which is caused by bacteria in the streptococcus family (streptococcus beta hemolytic group A), which enters the skin through small epithelium injuries. It usually occurs at the feet or on the head. The disease is manifested by sharply bordered red swelling of the skin and general infection signs. Factors that can contribute to the development of the disease are excessive alcohol consumption, malnutrition and systemic diseases of the organism.
How is the disease transmitted?
Erysipelas is transmitted only by direct contact with the infected person. The incubation last from three to four days.
What is the course of the disease?
In most patients, there is a rapid increase in body temperature, which can go up to 40°C, with intense fewer. Also, at the same time general malaise, headache, sickness and an urge to vomit are present. After 12 to 24 hours there is an itch and straining of the skin in the affected area, and after 24 hours there is an intense redness, which spreads and rises from the skin. The area of the skin that is caught in the red wind is warm, tense, tight, shiny, with clearly strained edges, extremely red and painful.
If you talk to the doctor in time, you will be given adequate treatment, the temperature goes away after seven days and the stain on the skin becomes less red and pronounced. With the use of therapy other symptoms of the disease disappear.
Are there other types of disease?
Besides the typical red wind – erysipelas, there are also the attenuated, migrating and relapsing types of the disease.
Attenuated erysipelas
Attenuated erysipelas has a limited expansion of lesions and less general nuisances such as headache or sickness.
Migrating erysipelas
Migrating erysipelas, as its name suggests, is characterized by expanding skin lesions, followed by temperature.
Relapsing erysipelas
Relapsing erysipelas is characterized by creation of new red spots in certain time spans, after curing the ones before.
How is the diagnosis established?
The diagnosis is established by the dermatologist by examining the characteristics of the skin lesion, frequency of the phenomenon and the symptoms that follow it. Also, the diagnosis is confirmed by laboratory blood analysis. If the blood analysis results in a severe leukocytosis, speeded up sedimentation and fibrinogen, it is a sign that a disease is present in the patient.
How is the disease cured?
Treating erysipelas is done by antibiotics, and penicillin is the most effective antibiotic in the therapy which needs to be administered as soon as possible, in order to avoid heavier infection and spreading to other organs. If the patient is allergic to penicillin, therapy can be administered by using other antibiotics or sulfonamides.
NOMA
Noma disease is a potentially fatal medical condition that normally begins as a gum infection and can cause extreme tissue destruction involving the face. This condition is most prevalent in developing countries, and children are the most likely to be affected. Early symptoms of noma disease usually involve gum discoloration and the formation of one or more ulcers inside the mouth. The ulcer then grows larger or deeper and may reach the bone as tissue death begins to spread. Treatment for noma disease involves surgery as well as any life-support measures deemed necessary, including breathing assistance and tube feeding.
Classification of nomas
Poverty, malnutrition, and poor dental hygiene are the most common contributing factors to the development of noma disease. Children who live in areas where poor sanitation practices exist are at a higher risk of developing this condition. Certain illnesses, such as typhoid or whooping cough, may also increase susceptibility to noma disease.
Symptoms of the disease often begin with bad breath and the production of an excessive amount of salivation. The gums and surrounding tissues may then start to take on a gray-colored appearance. A type of sore known as an ulcer tends to develop as the condition progresses.
After the ulcer develops, noma disease can rapidly become medically devastating. Tissue death begins to occur and can spread from the mouth to the nose, cheeks, and bones. While this process is usually painless, it can prove fatal if not treated adequately and quickly. Hospitalization is almost always required in order to treat this disease.
A combination of antibiotics is typically given in an effort to slow tissue death. A small tube known as an IV catheter may be inserted into a vein so that the antibiotics and any additional medications can be delivered directly into the bloodstream. Fluids may be given through the IV as well to guard against dehydration.
Depending on the severity of the damage to the face, the patient may need help breathing. This may include the delivery of extra oxygen into the lungs or, in the more severe cases, a machine may be used to do most or all of the breathing until normal respiratory capacity is restored. The patient may need to be fed through a tube if the ability to chew or swallow has been diminished. Corrective or cosmetic surgery is ofteeeded due to the disfigurement left behind by the effects of noma disease.
Noma is a type of gangrene that destroys mucous membranes of the mouth and other tissues. It occurs in malnourished children in areas of poor cleanliness.
Causes
The exact cause is unknown, but may be due to bacteria called fusospirochetal organisms.
This disorder most often occurs in young, severely malnourished children between the ages of 2 and 5. Often they have had an illness such as measles, scarlet fever, tuberculosis, cancer, or immunodeficiency.
Risk factors include Kwashiorkor and other forms of severe protein malnutrition, poor sanitation and poor cleanliness, disorders such as measles or leukemia, and living in an underdeveloped country.
Symptoms
Noma causes sudden, rapidly worsening tissue destruction. The gums and lining of the cheeks become inflamed and develop ulcers. The ulcers develop a foul-smelling drainage, causing breath odor and an odor to the skin.
The infection spreads to the skin, and the tissues in the lips and cheeks die. The process can eventually destroy the soft tissue and bone. Eventual destruction of the bones around the mouth cause deformity and loss of teeth
Noma can also affect the genitals, spreading to the genital skin (this is sometimes called noma pudendi).
Exams and Tests
Physical examination shows inflamed areas of the mucous membranes, mouth ulcers, and skin ulcers. These ulcers have a foul-smelling drainage. There may be other signs of malnutrition.
Treatment
Antibiotics and proper nutrition helps stop the disease from getting worse. Plastic surgery may be necessary to remove destroyed tissues and reconstruct facial bones. This will improve facial appearance and the function of the mouth and jaw.
Outlook (Prognosis)
In some cases, this condition can be deadly if left untreated. Other times, the condition may heal over time even without treatment. However, it can cause severe scarring and deformity.
Possible Complications
- Disfigurement
- Discomfort
When to Contact a Medical Professional
Medical care is needed if mouth sores and inflammation occur and persist or worsen.
Prevention
Measures to improve nutrition, cleanliness, and sanitation may be helpful.
Face-Eating NOMA Disease Spreads In Nigeria
NOMA, a severe disease that affects the face is silently spreading in
Studies carried out in the last two years have revealed that about 126,000 Nigerians die from NOMA disease every year.
Although it is relatively unknown, the disease has been plaguing lives especially of people in the North. Victoria Nkong, the coordinator of the campaign against NOMA disease, explains the symptoms as initial sore or rash inside the mouth of a victim, which if left untreated gradually grows and in the process, part of the face is eaten up with gangrene. She says that in extreme cases, the disease eats its way into the heart and vital organs of the victim’s body leading to death.”
Although most of the cases of NOMA disease can be found in the Northern part of the country, we have recorded a few cases in
NOMA disease is prevalent among the poor and it is caused by acute malnutrition. Children and young people from the ages of two to seven years are mostly affected but in rare cases, adults can fall victims. If detected early, it can be treated with common antibiotics but when it is left untreated, the disease eats out the whole face, at which point the victim will have to undergo a very expensive corrective surgery,” says Nkong.
Nkong emphasises the existence and spread of the disease in the country, urging sufferers to get treatment and possibly surgery.
“Most medical practitioners in
Noma – the Devastating Disease
During a mission in
Noma (cancrum oris), which borrows its name from the Greek term “to devour”, is an infectious yet non-contagious disease that destroys the soft and hard tissue of the face. The lesion is thought to begin as a localized ulceration in the gingiva or the mucosa of the cheek or lip and to spread rapidly through the surrounding tissues. At the same time, there is swelling of the corresponding part of the face. Untreated, the swollen skin will become gangrenous and will perforate, within a week, leaving a hole in the face. Noma is thought to lead to death in 70–90 per cent of cases. Most deaths are attributed to complications such as pneumonia, diarrhoea and septicaemia associated with severe malnutrition.
– Study of the Human Rights Council Advisory Committee on severe malnutrition and childhood diseases with children affected by noma as an example, para 31, citations omitted.
Malnutrition as one of the main causes of Noma
The main victims of Noma are children aged 1 to 6 years. Medical studies are unanimous in their findings: malnutrition is one of the main risks factors of Noma.
The disease was common in Europe and
Today Noma remains a problem there where high malnutrition rates are rampant. Doctors, NGOs and reports by the WHO confirm that Africa, in particular, but not exclusively, the sub-Saharan states
it is likely that it is much more frequent in remote Asian rural communities than is currently appreciated.
– M.L. Srour et al, “Noma in
According to estimates released by WHO in 1998, 140,000 individuals contract noma on a yearly basis; 100,000 of these are children. The survival rate is between 10 and 20 per cent, which means that at least 110,000 people, the vast majority of which are children, die every year because of noma. According to the WHO World Health Report 1998, 770,000 persons survived the disease with heavy sequelae. (para 31).
The Human Rights Council Advisory Committee has termed Noma in its Study as “the most brutal face of poverty and malnutrition in children” which “thus gives rise to some of the worst violations of the rights of the child.” Perhaps the most tragic aspect of Noma is that it is easily preventable if cost-effective treatment consisting in mouth rinses, antibiotics and nutritious food is administrated early on. Reconstructive surgery performed on survivors can repair the disfigurement and functional impairment which is the certain consequence of Noma. Without reconstructive surgery a “child who survives is unlikely ever to be able to speak or eat normally again.” (D.E. Barmes et al., “The need for action against oro-facial gangrene (noma)”, Tropical Medicine and International Health, vol. 2, No. 12, 1997, p. 1113.) Reconstructive surgery is performed by volunteer medical teams funded by some NGOs and charities.
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Certainly the main challenges concerning Noma concern raising awareness about the existence of this disease, removing the attached social stigma which stifles action of families and states, and convincing states, UN institutions, and in particular the WHO, to show political will in addressing Noma in a global, coordinated effort.
Noma on the agenda of the Human Rights Council
In August 2009 during the third session of the Human Rights Council Advisory Committee, Jean Ziegler presented the study “The Tragedy of Noma“. Jean Ziegler flagged the preventable plight of children affected by Noma and pointed to malnutrition as the main factor of this disease therefore analyzing Noma from a right to food perspective. “The Tragedy of Noma“ was prepared to serve as a background paper for the Study on discrimination in the context of the right to food. This latter Study was entrusted to the Advisory Committee by the Human Rights Council through resolution 10/12 of 26 March 2009.
The preliminary and the final Study on discrimination in the context of the right to food both listed children affected by and at risk of Noma as a vulnerable group and as victims of de facto discrimination in relation to the right to food. The Human Rights Council agreed with the findings of the Advisory Committee as it mandated it in resolution 16/27 of 25 March 2011, to undertake a comprehensive study on the relationship between severe malnutrition and childhood diseases, taking children affected by Noma as an example, and on ways to improve the protection of malnourished children.
Jean Ziegler and his collaborators embarked on a thorough process of research and consultations with NGOs working in the field of Noma, human rights and humanitarian organizations – among which CARE International, Dutch Noma Foundation, Ecumenical Advocacy Alliance, Facing Africa, GESNOMA, Hilfsaktion Noma, Label Vert, Medico International, Noma-Hilfe-Schweiz, Médecins sans Frontières, Sentinelles, Winds of Hope Foundation, No-Noma International Federation – UN institutions including the WHO and the UN Secretary General’s High Level Task Force on Food Security, medical doctors and other individuals. Jean Ziegler and Ioana Cismas attended numerous meetings, participated and organized in conferences in order to both learn and raise awareness about Noma and the importance of a human rights perspective in relation to this disease. Members of the Advisory Committee, some States, and several NGOs have shown great support in this process.
The research and consultation process overwhelmingly pointed to the following conclusions that:
- Noma can be prevented by tackling malnutrition and through detection during oral checks performed by health workers;
- Noma is certainly a neglected disease while not being formally recognized as such by the WHO, which in turn represents a disservice to raising awareness and funding opportunities;
- A global approach to monitoring the incidence, prevention, treatment and etiological study of Noma is needed beyond the current efforts of the few dedicated NGOs and the WHO Regional Office in Africa, which is tasked with the activities concerning Noma, and develops program only in few countries of the African continent, yet not in other parts of the world.
In February 2012, during the eighth session of the Advisory Committee, Jean Ziegler presented the Study of the Human Rights Council Advisory Committee on severe malnutrition and childhood diseases with children affected by noma as an example, which concluded
The persistence of Noma – the disease of Nazi concentration camps – in today’s world raises doubts not only about our morality, but it comes to prove that the human rights of children, the most vulnerable members of the international community are being severely ignored and violated. Sates and international organizations should assume responsibility for the neglected victims of Noma. (para 67)
The three key messages of the Study are:
- The exclusive focus on Noma in Africa through the WHO Regional Office in
Africa is insufficient; therefore Noma should be addressed at the global level. This includes worldwide surveillance, prevention, primary health care, surgical and rehabilitation treatment and etiological study. - Noma should be formally acknowledged as a WHO neglected disease. States should promote a resolution at the World Health Assembly to list Noma as a neglected disease.
- States should implement the Human Rights Principles and Guidelines to improve the protection of children at risk or affected by malnutrition, specifically at risk of or affected by Noma, which are contained in the Annex of the Study.
The Human Rights Council in its resolution on the right to food of March 2012 put out an important call to states encouraging them to implement the Human Rights Principles and Guidelines to improve the protection of children at risk or affected by malnutrition, specifically at risk of or affected by Noma.
What lies ahead for advancing the fight against Noma is for states and the WHO to address the conclusions of the Advisory Committee and follow the call for action of the Human Rights Council. If you or your organization want to contribute to the future of children at risk or affected by this disease by ensuring that their human rights, including their right to food, are respected write to your Government, your Congressmen or Parliamentarians, to your embassies and missions worldwide raising awareness about Noma and urging them to take action!
The Study of the Human Rights Council Advisory Committee on severe malnutrition and childhood diseases with children affected by noma and the annexed Human Rights Principles and Guidelines to improve the protection of children at risk or affected by malnutrition, specifically at risk of or affected by Noma can be consulted here. The Study is available also in Arabic, Chinese, French, Russian and Spanish on this website.
NECROSIS
Structural changes of cells undergoing necrosis or apoptosis
Necrosis (from the Greek νεκρός, “dead”, νέκρωσις, “death, the stage of dying, the act of killing”) is a form of cell injury that results in the premature death of cells in living tissue.[1] Necrosis is caused by factors external to the cell or tissue, such as infection, toxins, or trauma that result in the unregulated digestion of cell components. In contrast, apoptosis is a naturally occurring programmed and targeted cause of cellular death. While apoptosis often provides beneficial effects to the organism, necrosis is almost always detrimental and can be fatal.[2]
Cells that die due to necrosis do not follow the apoptotic signal transduction pathway but rather various receptors are activated that result in the loss of cell membrane integrity and an uncontrolled release of products of cell death into the intracellular space.[1] This initiates an inflammatory response in the surrounding tissue: Nearby phagocytes are prevented from locating and engulfing the dead cells.[2] The result is a build-up of dead tissue and cell debris at, or near, the site of the cell death. A classic example is gangrene. For this reason, it is ofteecessary to remove necrotic tissue surgically, a process known as debridement.
Classification
Necrosis is the sum of cell changes after localized cellular death through a process known as autolysis. Structural signs that indicate irreversible cell injury and the progression of necrosis include: dense clumping and progressive disruption of genetic material: and disruption to membranes of cells and organelles.[3]
Morphological patterns
There are five distinctive morphological patterns of necrosis:
1. Coagulative necrosis is characterized by the formation of a gelatinous (gel-like) substance in dead tissues in which the architecture of the tissue is maintained,[4] and can be observed by light microscopy. Coagulation occurs as a result of protein denaturation, causing the albumin in protein to form a firm and opaque state.[3] This pattern of necrosis is typically seen in hypoxic (low-oxygen) environments, such as infarction. Coagulative necrosis occurs primarily in tissues such the kidney, heart and adrenal glands.[3] Severe ischemia most commonly causes necrosis of this form.[5]
2. Liquefactive necrosis (or colliquative necrosis), in contrast to coagulative necrosis, is characterized by the digestion of dead cells to form a viscous liquid mass.[4] This is typical of bacterial, or sometimes fungal, infections because of their ability to stimulate an inflammatory response. The necrotic liquid mass is frequently creamy yellow due to the presence of dead leukocytes and is commonly known as pus.[4] Hypoxic infarcts in the brain presents as this type of necrosis, because the brain contains little connective tissue but high amounts of digestive enzymes and lipids, and cells therefore can be readily digested by their own enzymes.[3]
3. Caseous necrosis can be considered a combination of coagulative and liquefactive necroses,[3] typically caused by mycobacteria (e.g. tuberculosis), fungi and some foreign substances. The necrotic tissue appears as white and friable, like clumped cheese. Dead cells disintegrate but are not completely digested, leaving granular particles.[3] Microscopic examination shows amorphous granular debris enclosed within a distinctive inflammatory border.[4] Granuloma has this characteristic.[6]
4. Fat necrosis is specialized necrosis of fat tissue,[6] resulting from the action of activated lipases on fatty tissues such as the pancreas. In the pancreas it leads to acute pancreatitis, a condition where the pancreatic enzymes leak out into the peritoneal cavity, and liquefy the membrane by splitting the triglyceride esters into fatty acids through fat saponification.[4] Calcium, magnesium or sodium may bind to these lesions to produce a chalky-white substance.[3] The calcium deposits are microscopically distinctive and may be large enough to be visible on radiographic examinations.[5] To the naked eye, calcium deposits appear as gritty white flecks.[5]
5. Fibrinoid necrosis is a special form of necrosis usually caused by immune-mediated vascular damage. It is marked by complexes of antigen and antibodies, sometimes referred to as “immune complexes” deposited within arterial walls[4] together with fibrin.[4]
Other clinical classifications of necrosis
1. There are also very specific forms of necrosis such as gangrene (term used in clinical practices for limbs which have suffered severe hypoxia), gummatous necrosis (due to spirochaetal infections) and hemorrhagic necrosis (due to the blockage of venous drainage of an organ or tissue).
2. Some spider bites may lead to necrosis. In the
3. In blind mole rats (genus Spalax), the process of necrosis replaces the role of the systematic apoptosis normally used in many organisms. Low oxygen conditions, such as those common in blind mole rats’ burrows, usually cause cells undergo apoptosis. In adaptation to higher tendency of cell death, blind mole rats evolved a mutation in the tumor suppressor protein p53 (which is also used in humans) to prevent cells from undergoing apoptosis. Human cancer patients have similar mutations, and blind mole rats were thought to be more susceptible to cancer because their cells cannot undergo apoptosis. However, after a specific amount of time (within 3 days according to a study conducted at the
Causes
Necrotic leg wound caused by a brown recluse spider bite
Necrosis may occur due to external or internal factors. External factors may involve mechanical trauma, physical damage to the body (that causes cellular breakdown), any damage to blood vessels (which may disrupt the blood supply to that area); and ischemia.[9] Thermal effects (extremely high or low temperature) can result iecrosis due to the disruption of cells. In frostbite, crystals form, increasing the pressure of remaining tissue and fluid causing the cells to burst.[9] Under extreme conditions tissues and cells die through an unregulated process of destruction of membranes and cytosol.
Internal factors causing necrosis include trophoneurotic disorders; injury and paralysis of nerve cells. Pancreatic enzymes (lipases) are the major cause of fat necrosis.[9] Necrosis can be activated by bacterial toxins and components of the immune system, such as the complement system, activated natural killer cells, and peritoneal macrophages. Pathogen-induced necrosis programs in cells with immunological barriers (intestinal mucosa) may alleviate invasion of pathogens through surfaces affected by inflammation.[1] Toxins and pathogens may cause necrosis; toxins such as snake venoms may inhibit enzymes and cause cell death.[9]
Pathological conditions are characterized by inadequate secretion of cytokines. Nitric oxide (NO) and reactive oxygen species (ROS) are also accompanied by intense necrotic death of cells.[9] A classic example of a necrotic condition is ischemia that leads to a drastic depletion of oxygen, glucose and other trophic factors and evokes massive necrotic death of endothelial cells and non-proliferating cells of surrounding tissues (neurons, cardiomyocytes, renal cells, etc.).[1] Recent cytological data indicates that necrotic death occurs not only during pathological events but it is also a component of some physiological process.[9]
Activation-induced death of primary T-lymphocytes, and important constituents of the immune response, are caspase-independent and necrotic by morphology; hence current researchers have demonstrated that the occurrence of necrotic cell death caot only occur during pathological processes but also during normal processes such as tissue renewal, embryogenesis and immune response.[9]
Pathogenesis
Until recently, necrosis was thought to be an unregulated process.[11] There are two broad pathways in which necrosis may occur in an organism.[11]
The first of these two pathways initially involves oncosis, where swelling of the cells occur.[11] The cell then proceeds to blebbing, and this is followed by pyknosis, in which nuclear shrinkage transpires.[11] In the final step of this pathway the nucleus is dissolved into the cytoplasm, which is referred to as karyorrhexis.[11]
The second pathway is a secondary form of necrosis that is shown to occur after apoptosis and budding.[11] Cellular changes of necrosis occur in this secondary form of apoptosis, where the nucleus breaks into fragments, which is known as karyolysis.[11]
Cellular changes
The nucleus changes iecrosis and characteristics of this change are determined by the way in which the DNA is broken down, as shown in figure 3. There are three different ways in which the DNA can be broken down, which are; karyolysis, pyknosis and karyorrhexis.[4]
Karyolysis is a process where the chromatin of the nucleus fades due to the loss of the DNA by degradation.[4] Pyknosis is where the nucleus shrinks and the chromatin in the nucleus condenses.[4] Karyorrhexis follows on from the process of pyknosis, and involves the shrunkeucleus proceeding to fragmentation until the nucleus completely disappears.[4]
Plasma alterations are also seen iecrosis. Plasma membranes appear discontinuous when viewed with an electron microscope. This discontinuous membrane is caused by cell blebbing and the loss of microvilli.[4]
Treatment
There are many causes of necrosis, and as such treatment is based upon how the necrosis came about. Treatment of necrosis typically involves two distinct processes. Usually, the underlying cause of the necrosis must be treated before the dead tissue itself can be dealt with.
• In the case of ischemia, which includes myocardial infarction, the restriction of blood supply to tissues causes hypoxia and the creation of reactive oxygen species (ROS) that react with, and damage proteins and membranes. Antioxidant treatments can be applied to scavenge the ROS.[12]
• Wounds caused by physical agents, including direct physical trauma and injury, can be treated with antibiotics and anti-inflammatory drugs to prevent bacterial infection and inflammation. Keeping the wound clean from infection also prevents necrosis.
• Chemical and toxic agents (e.g. pharmaceutical drugs, acids, bases) react with the skin leading to skin loss and eventually necrosis. Treatment involves identification and discontinuation of the harmful agent, followed by treatment of the wound, including prevention of infection and possibly the use of immunosuppressive therapies such as anti-inflammatory drugs or immunosuppressants.[13] In the example of a snake bite, the use of anti-venom halts the spread of toxins whilst receiving antibiotics to impede infection.[14]
Even after the initial cause of the necrosis has been halted, the necrotic tissue will remain in the body. The body’s immune response to apoptosis, which involves the automatic breaking down and recycling of cellular material, is not triggered by necrotic cell death due to the apoptotic pathway being disabled.[15] The standard therapy for necrosis is removal of the dead tissue (debridement) either by surgical or non-surgical means. Depending on the severity of the necrosis, this may range from removal of small patches of skin, to complete amputation of affected limbs or organs. Chemical removal of necrotic tissue is another option in which enzymatic debriding agents, categorised as proteolytic, fibrinolytic or collangenases, are used to target the various components of dead tissue.[16] In select cases, special maggot therapy using Lucilia sericata larvae has been employed to remove necrotic tissue and infection.[17]
In plants
If calcium is deficient, pectin cannot be synthesized, and therefore the cell walls cannot be bonded and thus an impediment of the meristems. This will lead to necrosis of stem and root tips and leaf edges.
