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This finding suggests that the effect of smoking decrease through the end of life. The prevalence of chronic periodontitis increases with When compared with females, males expressed more dis- age, and the disease usually becomes clinically significant ease as measured by greater loss of attachment and deeper only in adults.

Increasing age is correlated with an pocket depths. This association spanned all ages, except increased prevalence of periodontal disease, as well as an in ages 85 to 90 years, when males had better periodontal increase in both the extent and severity of the disease. Men also expressed a more severe peri- both humoral and cellular. Soon after the United States.

African-Americans experience the high- subgingival colonization occurs, an influx of PMNs est prevalence of chronic periodontal disease and the great- occurs which is accompanied by an increase in crevicular est severity of disease. Compared with white Americans, fluid. Gingival crevicular fluid is a serous exudate or tran- Mexican-Americans have both a higher prevalence and sudate that collects in the gingival sulcus. The inter- more severe disease presentation.

This mechanism of action pro- mation increased with age and this increase in prevalence by duces a localized response to the bacterial insult. As noted in periodontal disease patterns, males including production of cytotoxic proteins, results in the expressed a higher prevalence of bleeding than females. When the dental plaque either African-Americans or whites, respectively.

An increase in cellular immunity occurs odontal disease are not as clear as for other oral diseases. An increase in collagenase activity behaviors, including oral hygiene behaviors and access to results from the induction of cellular immunity and the care, gingival inflammation is related to lower socioeco- proliferation of PMNs, macrophages, and fibroblasts see nomic status, including income and education.

Studies Figure In the oral cavity, the of an immune response to that insult are primary to the production of secretory immunoglobulin A sIgA in clinical manifestation of the disease process. As a chronic saliva provides the initial defense. Either opsinization of disease, the disease process is a bit more complex than the the bacteria occurs or the bacteria survive and are able to traditional infectious disease model with many factors adhere to the mucosa and colonize in the resident contributing to the induction and progression of peri- biofilm.

Initially, the response is predominantly a secre- odontal disease. Because periodontal disease is multifac- tory response, with IgA as the primary antibody. After torial, we must also consider the impact of lifestyle the organism invades the tissue, the humoral antibody behaviors, systemic and genetic determinants, and social response shifts to a serous response with IgG as the pri- and cultural factors in this causal framework.

These factors mary responder antibody. On invasion of the tissue, IgE are discussed in Chapter 5. This event activates both the date, none of the organisms have been identified as cellular and humoral response at the site of invasion. Only Aggregatibacter actinomycetemcomitans has In response to the insult, plasma cells and lymphocytes been causally linked to aggressive periodontitis previously produce IgG specific to the invading organism.

C-reactive protein CRP , complement and fibrinogen The host response to the bacterial colonization of the by local cells, which further exacerbate the inflammatory subgingival niche is a complex reaction of local and sys- response.

In response to the colonization of the systemic linkages that were reported in the literature. A detailed description of will greatly enhance our ability to assess risk and to apply these relationships is presented in Chapters 5 and The prevention. Population-based measures for gingivitis and strongest evidence for an association with periodontal periodontitis are not uniform or standardized, which hin- disease is between diabetes both type 1 and type 2.

To adopt a Diabetes and the relationship to periodontal disease are standard of measure of periodontal health at the popula- well documented in the literature. The association tion level is critical to have a greater understanding of appears to be bidirectional, that is, the severity of the dia- changes in this disease nationally.

The prevalence of betes is related to the severity of periodontal disease and destructive periodontal disease has remained fairly stable the severity of the periodontal condition affects the abil- over time, but as the population in the United States shifts ity to maintain adequate glycemic control. Ramifications of this related to both the bacterial infection and the host increase will challenge oral health care providers, and with response to the insult. In cross-sectional and retrospective case-control Continued research into periodontal disease pathogenesis studies, linkages have been suggested among periodontal is instrumental in solidifying the oral-systemic connec- disease and cardiovascular disease, osteoporosis, and neg- tion.

Armitage GC: Development of a classification system for peri- largely unknown, theories have emerged to describe the odontal diseases and conditions, Ann Periodontol , Although peri- 2. Ciancio SG: Current status of indices of gingivitis, J Clin odontal disease was long thought to be a localized or Periodontol , Silness J, Loe H: Periodontal diseases in pregnancy.

Because of the vascular nature of the gingival Correlation between oral hygiene and periodontal condition, Acta tissue and the chronic nature of periodontitis, the poten- Odontol Scand , It has been suggested that the ulcerated 7. Albander JM: Periodontal diseases in North America, Periodontol from 50 to cm,2 although more conservative figures , Although the larger 9.

Loesche WJ, Syed SA: Bacteriology of human experimental estimate is equivalent to ulcerated skin covering a fore- gingivitis: effect of plaque gingivitis score, Infect Immun arm, even the smaller estimate is a considerable chronic , Listgarten MA: Pathogenesis of periodontitis, J Clin Periodontol results from the periodontal infection and contributes to , Suzuki JB: Diagnosis and classification of periodontal diseases, condition. Although the exact mechanism of these Dent Clin North Am , National Center for Health Statistics: Third national health and logical aspects of periodontal disease, Acta Odontol Scand nutrition examination survey, , Department of Health , Accessed May 18, National Center for Health Statistics: National health and nutrition , Page RC, Schroeder HE: Current status of the host response in tooth loss in the permanent dentition of adults: United States, chronic marginal periodontitis, J Periodontol , The rate of periodontal destruction before age 40, periodontitis, JADA , J Periodontol , Study design and baseline data, J Periodontal Oral Investig , Res , Zambon JJ: Actinobacillus actinomycetemcomitans in human Page RC: The role of inflammatory mediators in the pathogene- Soskolne WA, Klinger A: The relationship between periodontal gingival indices: a methodology study, J Periodontol , diseases and diabetes: an overview, Ann Periodontol , Loe H: The gingival index, the plaque index, and the retention Russell AI: A system of classification and scoring for prevalence betes mellitus, J Clin Periodontol , Ramjford SP: Indices for prevalence and incidence of periodontal odontal therapy in diabetics and smokers, J Periodontol disease, J Periodontol , Ainamo J, Ainamo A: Validity and relevance of the criteria of the Survey Datafile Public Use Data file Documentation.

Periodontol , Healthy people statisti- lial surface area revisited, J Periodontal Res , Department of Health and Human Services: Healthy People Porphyromonas gingivalis infection on inflammatory mediator , ed 2, with understanding and improving health and objectives response and pregnancy outcome in hamsters, Infect Immunity for improving health, 2 vols, Washington, DC, U.

Government , Printing Office, November, Chapter 3. Oropharyngeal cancer adds the base of the tongue, the tonsil, and the posterior pha- Clinical Examination ryngeal wall. For simplicity, this chapter will refer to cancers at. Al Or Floor of mouth. Tonsils Population-based research in the area of oral cancer ca phar. In general, they Or. Larynx ICD codes C Head and nc h. Cancers of the oral cavity and pharynx comprise Head and neck cancers.

Although most oropharyngeal sites can be neck cancer includes nonoral or oropharyngeal sites in the viewed or palpated during a standard oral examination, head and neck, oropharyngeal cancer sites, and oral cancer others, such as the nasopharynx, pyriform sinus, and sites.

Oropharyngeal cancers, which include both oral cancer sites and oropharyngeal cancer sites, account for hypopharynx cannot be easily visualized or palpated. Oral cancer sites Consequently, although cancers of the oral cavity and phar- account for Figure Age-adjusted, site-specific year cancer incidence rates and percent change from Released April , based on the November submission. Incidence per , Estimated new head and neck cancer cases Projections for oral cavity and pharynx components made using SEER incidence rates.

To date, no medical advances have been effec- factors associated with oral cancer. Because of the associ- tive in eradicating disseminated disease. Ulcerated lesion mutation. When exposed to carcinogens, cells in the oral cavity undergo genetic changes that lead to malignant transformation. Malignant transformation is a multistep process.

With time and repeated exposures, cells accumulate numerous genetic mutations that lead to increased cell proliferation and cellular immortalization the ability to replicate indefinitely , which develop into invasive carcinomas that are capable of metastatic spread. Some of these genetic changes may be present in premalignant lesions that often appear as a small white patch lesion called oral leukoplakia. These lesions are described later in the chapter. When the cells accumulate multiple mutations and move from a premalignant state to a malignant state, changes can be observed, which are detected on biopsy and are diagnostic for cancer.

Early lesions will display differ- Figure Squamous cell carcinoma. Exophytic, ent grades of epithelial dysplasia, ranging from mild dys- papillary mass of the buccal mucosa. A subpopulation of these ed 2, Philadelphia, , Saunders. A lesion that has broken through the basement membrane is classified as carcinoma. Identifying premalig- nant lesions with the potential of malignant transforma- tion is important to improve OSCC survival rates.

Figure Squamous cell carcinoma. Deeply invasive The three most common sites for OSCC, in order of and crater-like ulcer of the anterior floor of mouth and alveolar ridge. The lesion had eroded into the underlying prevalence, are the vermillion border of the lower lip, the mandible.

Metastatic spread to regional nodes Saunders. Epithelial dysplasia is graded as mild, moderate, severe, and carcinoma in situ. Distinctions between mild, moder- ate, and severe are made on the basis of a histological examination. Knowledge of the degree of dysplasia assists with diagnostic decision-making and helps to predict whether the lesion will progress to cancer or will resolve on its own after removal of the irritant.

Carcinoma in situ is the highest grade of dysplasia and consists of abnormal cells that have not invaded adjacent tissue. The risk of progressing to cancer is high but treatment at, or before, this stage is considerably more successful. A diagnosis of malignancy occurs when abnormal cells have invaded the Figure Squamous cell carcinoma.

Red, granular underlying tissues and are identified on histological exam- lesion of the left lateral soft palate and tonsillar region. Oral epithelial dysplasia does not follow a predictable sequential progression from mild to moderate to severe.

It is not uncommon for a mild dysplasia to rapidly progress to an invasive carcinoma; however, not all Upper lip epithelial dysplasias will develop into carcinoma. Carcinomas may arise from lesions in which epithelial dysplasia has not been diagnosed. Because of this unpre- Dorsal surface dictable progression, biopsy of suspect lesions is essential Lateral surface to managing precancerous and cancerous lesions.

Staging provides a clinical estimate of how Figure Examination of the oral cavity. The tip of the advanced the disease is and whether or not it has spread tongue should be grasped with a piece of gauze and pulled from the original site to regional lymph nodes, other parts out to each side.

TNM clinical Philadelphia, , Saunders. Stages III and IV eral border of the tongue will metastasize to regional are advanced stages in which the tumor is either larger in lymph nodes. Therefore, examination of these sites should size or has spread to distant sites of the body or lymph be performed routinely to identify and treat these lesions nodes.

Both the Oral Epithelial Dysplasia presence and the number of lymph nodes with metastases predict the risk of distant metastases and the increased Oral epithelial dysplasia is the earliest form of precan- risk of local recurrences. Oral cancer patients with no cerous lesion. The diagnosis of oral leukoplakia is made when all other potential causes for a white patch lesion have been eliminated.

A large number of patients diag- nosed with leukoplakia also have a history of using smok- Figure Leukoplakia. Area of leukoplakia on floor ing or smokeless tobacco. Cessation of tobacco use results of the mouth and ventral aspect of the tongue. Interestingly, tobacco-associated leukoplakias seem to have less malignant potential than leukoplakias found in patients that do not use tobacco.

Silverman et al. Homogenous lesions Figure are uniformly white. Nonhomogenous lesions have areas of redness interspersed within the white lesion, producing a lesion with a less uni- form appearance Figure The presence of oral leuko- plakia in a non-smoker should trigger clinicians to suspect that the lesion has a high malignant potential and to per- Figure Nonhomogenous leukoplakia.

This mixed form a biopsy for a definitive diagnosis. If the patient uses white and red lesion of the buccal mucosa showed tobacco, these lesions can be followed over time. In the moderate epithelial dysplasia. It is impossible to visually determine which oral leuko- plakia will transform into carcinoma. The only definitive way to differentiate a benign white patch lesion from a pre- malignant or malignant lesion is through biopsy.

Erythroplakia Erythroplakia is a clinical term that describes a red lesion that cannot be defined clinically or pathologically as any other condition. Erythroplakias occur more frequently in older men and are found on the lateral border of the tongue, the floor of the mouth, the retromolar pad, and on the soft palate Figure Clinically, they appear as red macules or plaques with a soft, velvety texture that tend to bleed easily when rubbed.

This small, subtle, red lesion on the right lateral border of the tongue shows carcinoma ness or burning sensations. Oral and maxillofacial pathology, ed 2, Philadelphia, , Histological examination of erythroplakia invariably Saunders. In nonhomogenous leukoplakias, the red com- ulation-based cancer registries. Therefore, the red area of mixed lesions should present , cover 9. Among the data collected are lichen planus OLP , measured over a period of 6 months patient demographics place of birth, age at diagnosis, to more than 20 years, ranged from 0.

Thus, an increased risk of associ- ated malignancy appears to exist in patients with OLP. Incidence and Mortality This risk appears to be greatest in the erosive form of OLP and in erythematous areas. Oral cancer comprises 2. Worldwide, cancers of the includes identifying and monitoring short and long-term oral cavity and pharynx were responsible for an estimated disease trends, and determining disease-related morbidity 2. Population-based cancer registries are the males, and 1.

Deaths attributed to cancer of. All White Black. All sites Oropharyngeal cancers, which include both oral cancer sites and oropharyngeal cancer sites, account for Oral cancer sites account for Underlying mortality data provided by National Center for Health Statistics www. Five-year relative survival varies cavity and pharynx. A comparison of site-specific inci- among sites ranging from On the females45 and this disparity is observed worldwide other hand, after cancer of the larynx, which accounted Figure Male-female site-specific incidence ratios for The hard palate is the In the United States, more than half the cancers of the only site where gender parity exists.

The disparity between oral cavity and pharynx occur at three sites: the tongue, males and females has become less pronounced during tonsil, and salivary glands see Table Although the the past 50 years because of the increase in the proportion incidence of these cancers increased substantially of women who use tobacco products, drink alcohol, between and , the incidence of cancers of the or both.

Age-adjusted incidence per , person-years. Male Age-adjusted incidence per , person-years Female. Figure Age-adjusted oral cancer incidence by region and country, to Figure Age-adjusted, incidence site-specific, oral cancer incidence, to , by gender. Five-year relative survival for oral cancer is low floor of the mouth, and gingiva decreased substantially, Although apparent increases or decreases in cancer inci- The proportion of individuals diagnosed at a late dis- dence with time may reflect changes in diagnostic meth- tant stage has declined from Only The 5-year the mids and declined from the mids to the survival rate for individuals diagnosed with oral cancers present.

In , Blacks have primarily in white men who work in outdoor occupa- a higher incidence of cancers of the hard palate, soft tions, such as farmers. Although the incidence rate for black Americans is geneity of the site-specific incidence trends. Although the higher, the reduction in incidence from to incidence of cancers of the vermilion border of the lip, was one fifth that of white Americans see Table Pancreas Cancer Oral and pharynx 7.

Figure Age-adjusted, site-specific, 5-year survival for cancer diagnosed in and percent change from Underlying mortality data provided by NCHS www. Both oral cancer diagnosis and death from oral cancer occur pyriform sinus see Table During this time, whites at younger ages for blacks than for whites. Furthermore, showed modest decreases in incidence of cancers of the black males have the highest probability of developing oral lip, floor of the mouth, and pyriform sinus, and blacks cancer until the eighth decade Figure Blacks have a substantially higher incidence rates for can- In addition to having a higher incidence rate for many cers of the oropharynx, tonsil and floor of the mouth see oral cancers, black Americans had significantly poorer Table From to , whites showed a substan- 5-year survival rates than white Americans Figure Blacks are glands and blacks showed a marked increase in cancers diagnosed with oral cancer at later stages than whites see of the anterior tongue, oropharynx, nasopharynx, and Table In , , and , the proportion of.

Localized Regional Distant. Cumulative probability of developing oral 0. Figure Cumulative probability of developing oral cancer by a given age based on to incidence data. Figure Cancers diagnosed in Five-year oral cancer relative survival rate, by race. Survival rates for black Americans decreased 0. Black 5-year survival rates are consistently lower for cancers of the hypopharynx, tongue, and tonsil see than those of whites for all sites except for cancer of the Table The reasons for these improvements in survival lip Figure Most troubling, incidence rates for can- are complex; however, it is likely that increased awareness cers of the nasopharynx, hypopharynx, and oropharynx of oral cancer by dental professionals—especially for can- have more than doubled for black Americans from cers of the tongue and tonsil—is a factor.

Improvement in to see Table These cancers have the low sur- these site-specific survival rates is consistent with the vival rates see Table , and because they are difficult to increasing proportion of blacks diagnosed at earlier stages visualize, these lesions tend to be diagnosed at later stages. Most recently Although these findings are promising, the survival rate remains lower for Too often, oral cancer is not diagnosed until the patient blacks than for whites.

During the past 20 years, survival is symptomatic. This delay may explain the fact that the rates for blacks have only improved by 7. Blacks are younger at diagnosis In fact, only Because survival rates for Table shows trends in 5-year survival rates many oral cancers that are diagnosed in the later stages between and Although overall survival rates are low, early diagnosis is important to improving survival increased For example, the 5-year survival rate for oral cancer.

Other oral cavity and pharynx. Figure Age-adjusted, site-specific, to oral cancer incidence by race. Accessed May 9, These two objectives are as compared with Reduce deaths resulting from cancer of the oral cavity and nosed at the earliest stage, however see Table The mortality rate for black males, however, Reduce the annual age-adjusted oropharyngeal cancer higher risk should be given even closer, more frequent death rate from 3.

Risk assessment 2. Increase the proportion of oral and pharyngeal cancers for oral cancer is described in Chapter 6. Lesions in this population of patients must be treated very 3. Increase the proportion of adults aged 40 years and older quickly and aggressively. This examination should be done both visu- has not been repeated. All suspect lesions should be biopsied and sent for histological analysis. The role of the Dental Care for OSCC Patients dentist in many cases is to diagnose oral cancer and coor- dinate care for surgical resection and adjunctive radiation, Many patients will be immunocompromised when they chemotherapy, or both.

National Oral Health Objectives Dental providers are responsible for removing all sources of oral infection before the start of these treatments. Healthy People is a set of national health objectives Xerostomia dry mouth , mucositis, and Candida infec- designed to identify the most significant preventable tions are common sequelae of chemotherapy and radia- threats to health and to establish national goals to reduce tion treatment.

Dental professionals must work closely these threats. These measurable objectives can be used to with these patients, and their physicians, in managing provide a framework for establishing prevention pro- these common problems associated with OSCC treat- grams for the United States. Current Healthy People ini- ment.

Some patients will lose a portion of their mandible tiatives reflect efforts during the past two decades. It is the dental practitioner that will assist with In , the Department of Health and Human fabrication of prosthesis to assist in postsurgical eating Services published Healthy People ,41 which describe and speaking. Last, the dental professional plays a crucial national health promotion and disease prevention objec- role in monitoring patients regularly for local recurrences tives for the year Two of the oral health objectives and additional primary tumors.

Silverman S: Demographics and occurrences of oral and pharyn- Sudbo J: Novel management of oral cancer: a paradigm of predic- geal cancers. Assoc suppl7SS , Clinical and histologic signs of malignancy, Cancer J Clin , Acta Odontol Scand , Institute of Medicine: The future of public health, Washington, association between human papillomavirus and a subset of head DC, , National Academy Press.

A rare neoplasm with an aggressive course, Oral Surg , Oral Med Oral Pathol , Oral Pathol , Reibel J: Prognosis of oral pre-malignant lesions: significance of rates in the United States, , Oral Oncol , Lagiou P, Adami H: Burden of cancer. Trichopoulos D, editors: Textbook of cancer epidemiology, New York, Organization: histological typing of cancer and precancer of the oral Anticancer Res , Mashberg A, Samit A: Early diagnosis of asymptomatic oral and Anneroth G, Hansen LS: A methodologic study of histologic 3-oropharyngeal squamous cancers, CA Cancer J Clin , classification and grading of malignancy in oral squamous cell A new care utilization estimates in the United States across three nation- system for the clinico-pathological classification and identifica- ally representative surveys, Health Serv Res , Reibel J: Prognosis of oral pre-malignant lesions: Significance of Understanding and Improving Health, ed 2, Washington, clinical, histopathological, and molecular biological characteris- DC, , U.

Underlying mortality Underlying mortality data provided by Chapter 4. Salivary Assessment Hyposalivation Arguments have been raised against the risk-based Tooth Morphology approach to prevention. He based this argu- Caries Risk Assessment Method ment on the ethical constructs of social justice and equity.

The discriminative ability of combinations of risk factors for heart disease, though modest, is better than that achieved using specific risk KEY TERMS factors. The Host Agent shaded area is designed to suggest the dynamic interac- tooth resistance- dento- tion of host, environment, and agent, and represents by its bacterial variable area the intensity of caries activity that can fluorides, plaque e m saliva Ti change with time when any or all of the factors change in response to altered environmental or genetic influences.

Until the s, scientific interest focused on subgroups Environment of the population who did not develop dental caries. However, a coherent or systematic clinically Figure Traditional Venn diagram of caries causation. In , a highly systematized approach to clinical risk assessment was published. This assessment included Clinicians are drawn to risk-based prevention because gathering data from multiple sources to identify a detailed they usually care for individual patients, rather than preventive history, elements of clinical observation, and populations.

Because of the multifactorial nature of caries longitudinal records so that one might implement a longi- and other oral diseases, a comprehensive preventive pro- tudinal evaluation. As with other chronic disease prevention, the com- infants and children, a short, practical, risk-based guide bination of population-based public health promotion and for caries prediction and prevention emerged. This chapter time, a risk-based approach to caries prevention for indi- will identify risk factors and indicators that are associated viduals has been advocated.

The rationale for using a risk with the induction, progression, and severity of dental caries assessment approach is to tailor appropriate preventive in individuals. This chapter explains the mechanisms for strategies to the individual patient. Those patients who these processes on the basis of the current science. The are at greater risk for disease require more aggressive background, rationale, and description of the state of the intervention at more frequent intervals.

In patients with science in oral health risk assessment are a major focus of on-going caries activity and progression, the desired this chapter. Several approaches to the assessment of caries intensity of prevention and frequency of reevaluation are risk are discussed. Risk assessment has its foundation in a scientific under- standing of caries etiology.

Their work Absolutely essential to any risk-based system are valid and demonstrated that a number of organisms were impli- reliable methods of disease detection and recording. Dean and others helped to develop the notion caries incorporate both traditional caries detection of tooth susceptibility, especially as influenced by fluor- approaches, such as visual and radiographic methods, and ides.

Although at present the new substrate in the mouth was necessary for caries to technologies may be used infrequently in clinical practice, develop. The light source should be of the small- nal clinical observation and documentation of an early car- est possible diameter.

Posterior approximal caries can be ious lesion is necessary. A system of recording both the observed when the light probe is positioned above the absence of caries lesions and caries at the early and later gingival margin of the tooth. The light source should be stages, and the ability to review and evaluate these records directed perpendicular to the approximal area to prevent over time, is required.

Electronic recordkeeping can facili- direct observation of the beam and allow diffraction tate this evaluation and can provide a visual representation between demineralized and sound tooth structure. Longitudinal assess- structure. Approximal decay will produce a dark shadow ment, which includes multiple measures over time of an on the occlusal marginal ridge. When dental caries is existing caries lesion, is mandatory to determine caries present, this tool is a highly accurate indicator of approx- activity, whether the lesion is demineralizing, static, or imal caries.

The observed image can be easily modified by remineralizing, and to tailor prevention or treatment reangulating the tip of the light probe to address any pro- strategies. As the new caries detection systems become jection effects on perceived lesion depth. An attribute or exposure that increases the proba- examine the patient for further evidence of demineraliza- bility of occurrence of a disease is a determinant.

If the tion. Evidence of remineralization may not be evident determinant factor or marker can be changed by an inter- either on visual or radiographic examination, but stasis or vention it is said to be modifiable. If the determinant lack of lesion progression is a positive sign. Rationale for longitudinal assessment is zation of conventional film radiographs or by direct digi- supported by the reality that modifiable factors change tal radiography.

Digital The basic test for determining the presence or absence intraoral radiographic systems appear to be as accurate as of dental caries is a careful visual examination. A dental traditional radiographic methods for caries detection, even explorer probe should not be used routinely. Dental though the image quality may appear degraded upon explorers can be used to remove dental plaque to enhance visual examination.

Investigators have reported that the use of an the conductivity of an electrical current that results from explorer does not enhance the added validity or reliability in a decrease in the mineral content of carious enamel and fissure caries detection when compared with visual exami- dentin. Enamel demineralization results in increased nation alone. This increase in poros- dental explorer when compared with visual examination has ity is filled with fluid, which facilitates the conduction of been established for 40 years.

The probe tip is placed in the fissure false positive diagnoses of caries in which the fissure is and the level of conductivity is recorded on a scale reflect- deep and narrow. Vigorous use of an explorer to detect ing increased levels of demineralization. The use of an available. Current research on the validity and reliability explorer can produce cavitation, which may contribute to of these tests identifies important issues that should demineralization and inhibit remineralization.

QLF relies on the natural fluorescence of the Because decayed tooth structure has a lower index of light tooth to distinguish between carious and sound enamel. This examination is performed using the ture. This inherent fluorescence of the enamel is reduced by light from the hand piece coupler in the dental operatory demineralization of the enamel structure.

The demineralized tissue will appear darker SES. There are some limitations to QLF technology. QLF is not able to distinguish between active and arrested caries and Risk factors Knowledge between caries and stains on the tooth surface, increasing Preventive factors Modulating factors the rate of false positive diagnoses.

QLF technology is presently limited to detection of caries on smooth sur- Figure Factors involved in caries development. Lancet , DIFOTI, digital imaging fiber optic transillumina- tion, produces a high-contrast image of early caries, but is very susceptible to invalidation by both extrinsic and factors, exposure to fluoride, sealants, and antibacterial intrinsic staining.

These are discussed in detail in Chapters 9 and The validity and reliability of early caries detection Modulators of dental caries identified in the model in methods be understood. The mere detection of dental Figure include demographic factors that are specifi- caries using these methods does not justify active treatment. Knowledge, individual risk factors that contribute to the disease and attitudes and beliefs related to understanding of oral suggest a change to current preventive strategies.

The approach depicted in dental professional. A review of these behavioral inter- Figure emphasizes interactions, rather than a narrow vention strategies with scientific justification of efficacy is focus on any one single factor. It likewise provides a in Chapters 16 and A discussion of the individual components of Bacteria caries etiology is merited to explain the independent and collective causal theories discussed in Chapter 1.

The plaque biofilm is essential to caries; however, not all Dental caries is a multifactorial disease initiated by of the more than species of bacteria found thus far in microbiological virulence and proliferation within the the plaque biofilm are cariogenic.

With gene technology, biofilm that is modified by salivary flow and composition, additional oral bacterial species are being identified diet, and preventive strategies, including fluoride expo- in plaque. Only a few species of microorganisms have sure. Although their virulence varies, theoretically lead to a reduction or increase in disease.

This these organisms are indicator organisms. Bacteria live on concept provides the basis for caries risk assessment. The cariogenic bacteria present in the biofilm mass ferment Preventive variables that have a direct impact on caries risk dietary sugars into weak acids that lower the plaque pH include saliva flow, composition and buffer capacity, dietary and cause demineralization.

Therefore, the activity, not just the presence of the lesions, may be impor- trend has been to define caries not simply as a plaque- tant to predict caries32; however, the only way at present to mediated disease, but rather as a disease associated with a determine lesion activity is by longitudinal assessment. Rather than an Dental caries predominates in specific teeth in both pri- exogenous infection, dental caries results from an ecolog- mary and permanent dentition.

This observation would suggest surfaces. These grooves are more retentive and difficult to Acquisition of these microorganisms occurs at a young clean using routine oral hygiene. Adults continue to be at age. Transmission of the bacteria is through a vertical risk for initial caries, in addition to secondary or recurrent pathway, typically from mother to child, and not horizon- caries that form around existing restorations.

Because more tal, or person to person. Once introduced into the oral lowing gingival recession. These observations underscore cavity, the bacteria colonize the erupting teeth that offer a the role of the tooth morphology in caries development. Kohler et al. Fluoride provides resistance to demineraliza- the longer the delay in transmission to the child, the less tion, favoring remineralization of smaller, less acid solu- caries prone the child is later in childhood.

Saliva is an essential source of calcium and a direct association exists between the oral health of the phosphate ions for remineralization. This important finding the oral cavity. Diet Because of the nature of the bacteria in the oral cavity, the disease of dental caries occurs throughout the life Caries is a diet- and biofilm-dependent oral disease.

Caries risk can be lowered through a systematic pre- Sugar and other fermentable carbohydrate exposures are ventive approach that includes, when indicated, decreas- an essential etiological factor in caries development. This can be accomplished by diet Dietary fermentable carbohydrates act to change the bio- modification, oral hygiene, and increasing the tooth resist- chemical and physiological composition in dental biofilm ance with fluorides and salivary stimulation. Caries lesions are prone to develop where oral reproduction.

The energy sources may be exogenous biofilms are allowed to mature and remain on the teeth from immediate food sources or endogenous from for long periods of time. Teeth provide nonshedding sur- stored polysaccharides within biofilm. Cariogenic bacte- faces for microbial colonization, and large numbers of ria can metabolize any monosaccharides glucose, fruc- bacteria accumulate in the biofilm of the tooth surface in tose, and galactose or disaccharides sucrose and maltose both health and disease.

Cooked starches are an available source of glu- the tooth in caries risk, consideration must be given to cose. The result of this sugar catabolism is the production tooth morphology and caries history. Studies have shown of organic acids in the dental plaque fluid, which lower that previous caries experience is an important consider- the plaque pH. When the pH decreases to approximately ation for caries risk and that the presence of caries, 5.

Once the decalcification reaches the dentin- dietary factors that address the quantity and frequency of enamel junction, acid decalcification of the dentin can fermentable carbohydrate in the diet, the pattern of food progress, and the bacteria themselves later invade the and beverage consumption, and an identification of protein of the dentin and destroy it through proteolysis.

If screening and risk assess- Sucrose further reduces concentrations of calcium, ment indicate a need for more detailed dietary informa- inorganic phosphorus and fluoride ions that are impor- tion, there are numerous approaches to dietary assessment tant in maintaining mineral equilibrium between the listed in Table , which provides additional dietary tooth and the oral environment.

Possible mechanisms for information and complete dietary assessment. Prevention requires longitudinal assessment and tions have shown a clear relationship between sucrose monitoring. The onset of this disease can progress from a consumption and caries prevalence and incidence. These preclinical phase of exposure to etiological bacteria and include the Vipeholm study from the s,38 the substrate with undetectable demineralization to gross Hopewood House study from the s,39 and the Turku cavitation of tooth structure and tooth loss.

For caries to Sugar studies from the early s. With the decline in caries to date. This study showed that the quantity of sugar con- prevalence, this time has increased. Therefore, time is on sumed and whether it was consumed with or between meals the side of the patient and dental professional, allowing were important factors in caries development.

Raw starches for nonsurgical, preventive intervention. Development, are considered less cariogenic than simple sugars such as equilibrium, progression, and remineralization may reoc- sucrose, glucose, and fructose. Sucrose, in particular, pro- cur over a lifelong period; however, this can be controlled motes higher enamel mineral loss, and when combined with in several ways.

Lifestyles and behaviors, including oral cooked starch enhances the cariogenic potential of starch. Thus, caries risk assessment and reassessment terizes caries. Retentive foods such as dried fruit, highly must be an on-going and integral component of long- processed grains, and some cooked starches, like potato term dental patient care.

Food form may also be to categorize persons into risk groups with respect to the important. Sugar in drinks appears to be somewhat less potential to develop new carious lesions over time. The cariogenic than those in solid form such as candies. The use of risk assessment in the clinical management of increased frequency and duration of exposure to sugary caries is outlined in Box The dated method to assess caries risk has been developed and sugar in beverages merits full consideration in assessing adopted universally by dental professionals.

The first caries risk. This textbook sets out to address this deficiency. Conversely, the discomfort was developed at the University of Texas Health Science and possible tooth loss caused by caries can affect Center at San Antonio, Dental School. BOX among the models because of differences in emphasis and.

P C R A interpretation of the science among the various designers. Questions on dietry screen- specific type of appropriate interventions. This sions, or both. The inabil- planned interventions. One possible solution to the inability to communicate and facilitate needed change in validate the model is the implementation of electronic health behaviors to prevent caries.

On the basis of the initial screening questions, additional testing may be indicated. Testing approaches specific to various outcomes are described in Chapter 9. This program was an online instrument used prevention. See Chapter 15 for a discussion of preventive to determine the future probability estimates of develop- strategies that may be included in a treatment plan.

Today, each of the U. The U. Navy adopted past and present caries Identification of present and past individual preventive and status in preventively oriented treatment planning,49 and health practices is essential to motivate patients to adopt the U. Army50 and Air Force51 adopted a risk-based healthy behaviors, reduce caries risk, and to improve their caries assessment protocol.

The American Academy of oral health. Quality of life measures are important to the broader a broad approach to risk assessment, considering the effect impact of oral function on daily living. Knowledge of indi- of both systemic disease and reported behavioral factors in vidual patient health and disease history, attitudes toward the interpretation of caries risk.

In , the California health attainment and disease occurrence, and preventive Dental Association published a comprehensive caries risk and risky health behaviors need to be identified and evalu- assessment guide that targeted the adult patient. Caries and cultural context, so that cultural filters do not obscure Management by Risk Assessment CAMBRA attempts knowledge, attitudes, or behaviors of the patient, or cause to address the management of caries in a systemic way.

This topic is addressed in The risk assessment models that are currently used rely Chapter Caries indicators—consider clinical findings, radiographic interpretation, and other findings incorporated into caries charting approved by faculty. Use caries assessment and management decision trees. Fluoride exposure 11 No fluoride from water, tablets, or drops? Strep count for lab OR are not indicated for caries.

Figure Oral health evaluation. Motivational interviewing techniques are dis- delivering the preventive message so that patient adher- cussed in Chapter As a component of communication, ence will be enhanced. The dental professional should acknowledge the health risk communication. Many common diseases and drugs impact the health plan of prevention.

It is important to differntiate between status of the oral cavity and caries risk. Endocrine and the early lesion in enamel and the lesion clearly extending other disorders impact oral health status and are impor- into dentin is important. Research shows that early caries tant in the determination of caries risk. Radiation therapy lesions are more predictive than either filled surfaces or associated with management of head and neck cancer cavitated surfaces. Sugar-based medications given to chronically ill chil- best assess caries, to identify early lesions, and to provide a dren can increase their risk for dental caries, and baseline from which to assess future caries activity.

Documentation should be detailed to allow comparison Details on the interactions between pharmacology and and longitudinal assessment when the patient is reevalu- oral health status are discussed further in Chapter 7. The ated in future encounters. One assessment of past caries history is evident in the presence of existing restorations. Identifying the number of Dietary Screening existing restorations and cavities alone, however, is insuffi- cient information to determine overall caries risk status.

Evaluation of the dietary and nutritional issues associated Through an assessment of past and present caries and other with caries risk can be addressed in several ways. Dietary disease indicators, a current estimation of risk can be made. Assessment of fluoride exposure should be included in The individual questions were weighted for their impact. All potential sources of fluoride, such as A total score greater than three identifies persons likely community water fluoridation and personal patterns of to be at increased caries risk due to diet.

If so, a more use of toothpaste with fluoride and from other sources detailed dietary evaluation is indicated. A hour recall of should be included. Over-the-counter without confusing the patient. A more detailed assessment rinses and gels should be considered in the overall assess- of diet is discussed in Chapter 8. Responses to the dietary ment of past fluoride exposure, and frequency of profes- screening questions may be subsequently modified in light sional fluoride application in the past should be included.

Four validated questions are included in a caries risk Caries Status and History assessment see Figure as an indicator of low salivary function. If the patient Present and past caries is considered a central indicator of overall and future caries risk. The importance Modified from Fox PC, Busch KA, Baum BJ: Subjective reports of of measuring caries activity makes longitudinal measure- xerostomia and objective measures of salivary gland performance, ment of caries progression or stasis critical to the overall JADA , Although significant strides have Additional testing to ascertain salivary flow rates may be been made in addressing this disease, risk-based approaches initiated if the patient responds positively to any of the to address dental caries are necessary to identify those indi- screening questions.

The process for measuring unstimu- viduals at greatest risk and for efficient prevention. The dra- lated salivary flow rate is described in Chapter 9, as are matic reduction in disease among some segments of the several techniques to measure whole mouth levels of indi- population provides further opportunity to target and tailor cator cariogenic bacteria present in saliva.

Caries risk assessment provides a springboard to engage the patient in defining Tooth Morphology and achieving mutual disease prevention goals. Deep and retentive ease, the dental practitioner can better monitor the pits and fissures on occlusal tooth surfaces are at greater risk outcomes of care, and improve the quality of dental care. In adults, risk assessment activities should include an assessment of exposed root surfaces, caused by gingival recession, which may predispose a patient to root caries.

Krasse B: Caries risk: a practical guide for assessment and control, stable over time. The negative predictive value is superior to Chicago, , Quintessence Publishing Company. Veatch RM: Minority opinion: Dental sealants in the prevention help to identify individuals who are less likely to develop of tooth decay. Another major use is to assess dietary adher- Ed 48 Suppl 2 , With patient adherence to the , Hansen H: Caries prediction-state of the art review , Commun fall.

For these reasons and to identify those with high levels Dent Oral Epidemiol , Milne R, Gamble G, et al. Commercial kits are available to test indicator organisms. This assessment should be Niagara Falls, N. On the Ultimately, a caries risk assessment is a Kloch B, Krasse B: A comparison between different methods for systematic approach to identify all etiologic factors that prediction of caries activity, Scand J Dent Res , This leads to the specific and Kohler B, Bratthall D, Krasse B: Preventive measures in mothers individually tailored preventive interventions that are dis- influence the establishment of a bacterium streptococcus mutans cussed in Chapter For patients at low risk, this assess- in their infants, Arch Oral Biol , Kohler B, Andreen J, Jonsson B: The effect of caries-preventive ment will help confirm lack of etiological factors and basic measures in mothers on dental caries and the oral presence of the caries preventive behaviors and measures can be reinforced.

Pitts N: ICDAS—an international system for caries detection caries in young children: a systematic review of the literature, and assessment being developed to facilitiate caries, epidemiol- Community Dent Health , Acta Odont Scand , Lussi A: Validity of diagnostic and treatment decisions of future Slack GL: The technique of examination in clinical trials.

Dodds MWJ: Applications to current practice and need for National Council on Radiation Protection and Measurements Caries diagnosis and risk assessment: a review of preventive Loesche WJ: Clinical and microbiological aspects of chemother- risk assessment model for a multifactorial disease, Comm Dent apeutic agents used according to the specific plaque hypothesis, Oral Epidemiol , J Dent Res , Accessed November Scheie A, Peterson F: The biofilm concept: consequences for Chaffin JG: Dental population health measures: supporting future prophylaxis of oral diseases?

King BB: Revised dental population health metrics guidelines Air Force, January Disorientation in an elderly patient. Pacing 3. Head Injury or other central nervous system insult. Spitting 7. Alcohol or drug intoxication. Emotional lability 8. Has anti-secretory properties. Posture 1. Shrill 6. Expressions of anger. Coarse crackles beginning with inspiration may be heard. Relaxes bronchial smooth muscle by action on beta 2-receptors with little effect on cardiac muscle contractility.

Abusive 4. Excessive fidgeting 6. Strong consideration should be given to restraining all intubated patients. Look for potential etiologies and correct Do not yell at patient. Pharmacologic restraints may be used if physical restraints are not sufficient. Neuromuscular blocking agents never give without prior sedation in a conscious patient unless its an emergency.

Check distal extremities periodically q 15 minute pulses. All pharmacologic agents that can cause respiratory depression. If a Medical Crew Member has any doubt regarding the safety of transporting a potentially combative patient by ground or in the air. Protect airway from aspiration. Approach patient in a slow deliberate manner.

Rayon webbing strapped across chest and legs. Antipsychotics: Haldol may be used for acute psychosis. Speak softly and calmly around patients. Avoid compromising circulation by restraining too tightly. Restrain limbs at a comfortable angle. May be combined with a sedative agent for better overall effect.

Respiratory status must be carefully monitored if these agents are used. Excessive environmental stimulation. Air Traffic Control. Use of mechanical or pharmacologic restraints. Frequently complications involve ketoacidosis and hypoglycemia.

The complications of this disease are numerous. Diabetes Mellitus is characterized by decreased insulin secretion by the beta cells of the islets of Langerhans in the pancreas. Midazolam Versed. Law enforcement back up should be requested to assist in restraining after landing. En route considerations. If an unrestrained patient suddenly becomes combative in the air and cannot be controlled.

All 4 limbs a. Do not use any padding under restraints as this may reduce efficiency. Vercuronium Bromide Norcuron. The following physical restraints are authorized for use if a above does not work or apply. Morphine Sulfate. Diazepam Valium. All pharmacologic agents are used by protocol only. Be respectful of patients small personal space.

Safety must always take first priority in all transports. All combative patients will be transported by a two 2 person minimum medical crew. Lorazepam Ativan. Any unconscious patient who may awaken in flight should be restrained prophylactically. These patients must be restrained at all times. Use earplugs to reduce noise stimulation to patient. Micellaneous considerations. Sedative agents. Respiratory status must be carefully monitored. Should a patient become combative.

Give firm. Type 1 diabetes. Without insulin. The rate at which glucose can enter the cell is dependent upon insulin levels. The glucose level at which an individual becomes symptomatic is highly variable. In its early stages. The mainstay for hypoglycemia is glucose. Insulin acts as a messenger. Type 11 diabetes can often be controlled without using insulin and by adjusting diet. Kussmaul respirations may also occur deep.

Coma is not uncommon. Hypoglycemia is an urgent medical emergency as a prolonged episode can result in permanent brain injury. This results in osmotic diuresis. Glucose Supplement. When released by the pancreas. Dextrose is absorbed. Vitamin B1. Persons not previously diagnosed as diabetic will occasionally present in ketoacidosis. Ketoacidosis is often associated with infection or decreased insulin intake. The onset is slow. It may aid in minimizing liver glycogen depletion and exert a protein sparing action.

The patient may also experience a seizure or become comatose. Hypoglycemia can occur if a patient accidentally or intentionally takes too much insulin. In the early stages of hypoglycemia. Thiamine is indicated when giving E. If allowed to continue its progression. It provides a source of carbohydrate calories. Diabetic ketoacidosis is characterized by nausea. Deep respirations begin as the body tries to compensate for the metabolic acidosis as cellular glucose-depletion continues. The clinical signs and symptoms of hypoglycemia are many and varied.

Diabetes mellitus results from inadequate amounts of circulating insulin. This can result in serious brain damage or death. Type Once reaching its destination. The hyperglycemic patient ultimately needs insulin. Obtaining a blood sample for glucose check is performed in the case of infants and pediatrics as part of their baseline vital signs.

The breath may have a sweet or acetone-like character. In contrast to diabetic ketoacidosis. Treatment by emergency personnel should be geared toward rehydration via fluid administration. Patients who have Type 1 diabetes must take insulin. Hypoglycemia occurs when insulin levels are excessive. When hypoglycemia is found and treated in the diabetic patient. Thiamine may also be appropriate if alcohol abuse is suspected.

As cells become glucose-depleted. For the body to convert glucose to energy. The kidneys will excrete glucose in the urine taking water with it. In diabetes. This is evident on examination by dry. An abnormal mental status is the most important. As the blood sugar falls lower. Physical findings may include diaphoresis and tachycardia. It can occur in patients who fail to take their insulin or who take an inadequate amount over an extended period.

Morphine is also useful for its vasodilating effects. Massive hemorrhage can also occur with separation of arteriovenous fistulas. An arteriovenous shunt is a surgical connection between the arterial and venous systems. Complications may arise related to the venous access devices placed for chronic dialysis. The site should not be used for routine IV access. Treatment of renal failure takes on of two forms: hemodialysis or peritoneal dialysis. Nitrates are effective by all routes. Exerts effects opposite of insulin on blood glucose.

The internal fistula is located subcutaneous and will have a bruit that can be palpated. Useful when IV access is problematic. Pulmonary edema is frequent in renal failure and is usually due to volume overload. The best method to end the hemorrhage is by direct pressure and transport to the emergency department.

Lactated Ringers should not be used because of its potassium content. Consider pericardiocentesis if tamponade is suspected. Cardiac arrest may be due to hyperkalemia. Contact on line medical control for direction beyond immediate life threatening issues. These agents are used to reduce potassium levels.

IV Fluids 0. The two most common routes of access are external arteriovenous shunts or internal fistulae. Most medications used in pre-hospital care are used in the usual dosages. Complication of dialysis include hypotension. Antagonizes membrane effects of potassium. Another method for dialysis is via the peritoneum. It is utilized for fluid replacement because of its immediate expansion of the circulatory volume.

An electrolyte solution of sodium chloride in water. Adjustments may need to be made in dosage or frequency of subsequent treatments to account for changes in metabolism and excretion secondary to renal disease. Consider pericardial tamponade. When used. Loop diuretics Lasix may be effective at promoting diuresis in patients with residual renal function. Dysrhythmias produced in response to dialysis can be caused by potassium intoxication. This process helps remove toxic substances from the bloodstream.

Many people now have home dialysis units. Hemodialysis is a medical procedure whereby waste products. Redistributes extra cellular potassium into cells with minutes. Patients with renal failure must undergo dialysis two to three times a week. Glucose Elevating Agent. These agents can act in the pancreas or the peripheral tissues to increase blood glucose levels. Vascular access must exist to dialyze the patient. Clotting of the shunt offistula can occur spontaneously.

Hyperkalemia is the most common life-threatening emergency ion patients with ESRD. Hypotension due to dialysis is caused by dehydration. It can best be treated by hemodialysis. Its actions are two fold in vitamin depletion first. Elevates blood glucose levels by inhibiting glycogen synthesis and enhancing formation of glucose from noncarbohydrate sources. Pancreatic alpha cells of the islets of Langerhans produce this polypeptide hormone.

Fastest acting drug to treat hyperkalemia acts within Minutes. IV fluids should not be administered except for cases of frank shock. It can occur before. Disequilibrium syndrome is characterized by cerebral symptoms in patients with severe renal failure. These patients may present with headache. Toxicity is potentially increased because of delayed excretion and higher blood levels. They may also develop from transient myocardial ischemia. The form must be accessible to EMS personnel.

It occur in one percent or less of patients with hypertension. These include such things as pulmonary edema from left ventricular failure. Brady 3rd edition Paramedic Emergency Care. It states the kind of medical care an individual wants or does not want if unable to make his own decision regarding medical care.

The form must have an effective date. Treatment should be directed at the primary problem. It is important to note that in order to honor a DNRO it must be the properly completed original. A competent adult. The peak incidence in those aged years. A properly executed DNRO must be signed by a physician who has determined that the patient is in a terminal condition or vegetative state with very little probability of recovery.

Completion of this part of the form provides a convenient and rapid method for EMS personnel to determine that the form has been properly executed.. Patients with a true hypertensive emergency require careful titration of IV medications for good control and a smooth reduction of their BP. The signature of the patient on the DNRO form.

In some cases a patient may be wearing a white DNRO bracelet. Physicians Desk Reference and E-Medicine Site A hypertensive emergency is a life-threatening elevation of blood pressure. The most common hypertensive emergency is a rapid unexplained rise in BP in a patient with chronic essential hypertension. A pre—hospital DNRO may be revoked at any time by the patient or designated health care surrogate pursuant to section The DOH form is printed on yellow safety paper.

A living will may be executed by a perfectly healthy person or by one diagnosed with terminal condition. Once the patient or surrogate or proxy or guardian has properly completed the DNRO form. Hypertension is a related factor in other emergencies. Both of these forms are acceptable provided they are properly completed.

In these cases. Latex allergy is increased in populations with chronic occupational exposure to latex. Its use in hypertension is considered when the patient takes Lasix on a regular bases or is suffering with signs and symptoms of CHF. Latex is the milky fluid derived from the lactiferous cells of the rubber tree. Primarily inhibits the re-absorbption of sodium chloride Furosamide Lasix.

It also contains a large variety of sugars. The third. Labetalol Trandate. Potent diuretic. Symptoms usually develop within hours of cutaneous or mucous membrane exposure to latex in a sensitized person. Alpha and Beta-blocker. Patients with cerebral palsy. The administration of Lasix may avoid the administration necessity of more potent IV drugs.

Patients with spina bifida also may have a genetic predisposition for latex sensitization. Cross-reacting antigens have been found between these fruits and latex. The incidence of minor and serious allergic reactions to latex began to rise rapidly among patients and health care workers. Protein content varies with harvest location and manu-.

Type I allergy has been implicated clearly in intraoperative and intraprocedure anaphylaxis. Labetalol should only be administered with the patient in the supine position. The pressure that was placed on manufacturing companies resulted in hundreds of new. Other patients with a history of multiple surgeries or other latex. Symptoms generally begin within minutes of exposure.

It is a result of mechanical disruption of the skin due to the rubbing of gloves and accounts for the majority of latex-induced local skin rashes. It may be used alone or in combination with other antihypertensive agents. Labetelol should only be administered with the patient in a supine position. Latex proteins vary in their allergenic potential. Reinstitution of previously effective therapy in noncompliant patients may be all that is required.

Hypersensitivity symptoms may include: Pruritus of exposed skin and mucous membranes. Lowers BP. More than polypeptides have been isolated from latex. Because of alpha and beta blocking properties. Latex gloves were widely recommended to prevent transmission of blood-borne pathogens. The spectrum of clinical manifestations includes localized or generalized urticaria. Eight billion pairs of medical gloves were imported to the US in Latex exposure is associated with 3 clinical syndromes: The first syndrome is irritant dermatitis.

Latex sensitazation can occur after skin or mucosal contact. Decreases coronary vasospasm. These agents are used for exacerbations of hypertension. The second syndrome is a delayed Type IV hypersensitivity reaction. Also induces vessel dilation.

Potent agents with rapid onset. Common sources of latex exposure include but are not limited to tourniquets. Medical procedures may cause reactions in sensitized providers or patients. Abortions may be spontaneous or induced. Early notification is key to their preparation. For this discussion. Delivery between 20 and 38 weeks is considered pre—term birth.

Many viruses. Prehospital providers should be aware of the risk of latex allergy in patients and providers. Since a definitive placenta has begun to form with a more organized and larger blood supply. Major reactions in sensitized patients have been precipitated with latex medical equipment.

Latex-free resuscitation equipment must be available. Abortions per- RATIONALE Patients with known or suspected latex allergy who seek care for an unrelated medical condition or injury must be kept within a latex-safe environment to prevent serious complications. The complete suggested inventory list of supplies can be found on the following page. The receiving facility must be made aware of the need to completely avoid latex exposure to the patient during exams and procedures. This distinction is made because more difficulties are encountered in treating late abortions.

The importance of uterine fibroids or retroversion and impaired corpus luteum function appears to have been overestimated. Maternal factors that have been suggested as causes of spontaneous abortion include an incompetent. IV tubing. Search for and read Medical Alert-type bracelets. The National Institute for Occupational Safety and Health NIOSH recommends wherever feasible the selection of products and implementation of work practices that reduce the risk of allergic reactions.

The cornerstones of treatment are epinephrine and H1 antihistamines.. The history of latex allergy may be known or unknown. Systemic corticosteroids and H2 blockers may be useful. Spontaneous abortions occur without any instrumentation. A relationship to physical trauma has not been substantiated. An abortion is termed either early before 12 week of pregnancy or late between 12 and 20 weeks.

To rule out latex allergy that could worsen with further medical exposure. See allergic reaction and or anaphylactic reaction rationales. After 12 weeks of pregnancy. Individuals may be exposed to latex through their skin. Any woman with known obstetrical problems. This includes all patients with spina bifida. Fetal bones have also begun to form. BP cuffs. Patients presenting with frank symptoms of Type I latex allergy are treated as any other patients with systemic allergic reactions.

The Treasure Coast Guideline recommend providers carry a mobile container with complete latex free equipment. The patient is acutely ill. In ectopic pregnancy. Patients should be evaluated for unsuspected liver disease. The most common site of ectopic implantation is somewhere in a uterine tube. The incidence. If part of the products of conception is passed or if the membranes are ruptured. Interstitial cornual pregnancies have a somewhat longer course. Critically ill patients may evidence bacterial shock septic or endotoxic shock with vasomotor collapse.

Missed abortion occurs when the fetus has died but has been retained in utero 4 weeks or longer. Many pregnant women with morning sickness feel as though they are vomiting everything they ingest. Risk factors can be categorized as inherent. All pregnancies should be evaluated to determine whether there are or will be risk factors. After 6 weeks. The usual signs include cramping and spotting. Intrauterine devices do not prevent ectopic pregnancies.

Patients do not gain weight. Psychologic factors are prominent in this syndrome but do not lessen the danger. Untreated ectopic pregnancy is usually fatal. Classifying pregnancies as high risk is an effective way to ensure extra attention to patients who need medical care the most. Autopsies in such cases usually show severe necrosis in the central portion of the lobules or widespread fatty degeneration similar to that seen in starvation.

In the USA. Gradual hemorrhage from the tube causes pain and pressure. The symptoms are similar to those of threatened abortion. The incidence of septic abortion in the USA has fallen dramatically. Septic abortion develops when the contents of the uterus become infected before. If all of the products of conception are passed.

Cornual pregnancies rupture between 12 and 16 weeks. In the USA before legalization of abortion. Persistent hyperemesis gravidarum may be associated with serious liver damage. The incidence of high— risk pregnancy varies according to population. Weight loss. Its likelihood increases with previous tubal disease. Spontaneous abortions may be threatened. Most perinatal deaths not directly due to congenital anomalies are associated with prematurity often accompanied by abnormal presentation. The dead fetus syndrome usually occurs only when the loss is in the 2nd trimester or later.

The death rate for ectopic pregnancy has been falling. Threatened abortion is any bleeding or cramping of the uterus in the first 20 weeks of pregnancy. During labor. If this condition is allowed to progress eclampsia will follow. In a first pregnancy. This latent phase may be intermittent over several days or may last only a few hours. If the patient does not and if the fetus is at term. Labor usually begins within 2 weeks before or after of the estimated date of confinement.

Diagnosis of eclampsia or hypertension induced by pregnancy. A major complication of pre—eclampsia is abruptio placentae. Keep in mind that during pregnancy the blood pressure will drop. The stimulus for labor is unknown. Magnesium sulfate should be administered before a visual pelvic exam of a patient with eclampsia accompanied by any of the warning signs due to the possible induction of a seizure in the patient.

BUN and creatinine levels should also be obtained to rule out unsuspected kidney disease. Low— dose aspirin therapy has been tried as a preventive measure in high—risk patients. Signs of impending eclampsia in a severely pre— E. Both magnesium sulfate should be administered prophylactically if the patient is in labor. Criteria for Treatment: Headache. Bloody show a small amount of blood with mucous discharge from the cervix may precede the onset of labor by as much as 72 hours.

Circulating oxytocin secreted by the posterior pituitary gland may initiate labor. A latent phase. All routine laboratory tests CBC. Patients with eclampsia or severe preeclampsia should be transported rapidly but without the use of light or sirens due to the possibility of inducing a seizure.

Eclampsia is defined as the occurrence of grand mal seizures with severe pre—eclampsia and may occur anywhere from the fifth month of pregnancy to the end of the first week after delivery. Systolic blood pressure greater than mm Hg or a rise of 30 mm Hg above previous readings prenatal Diastolic blood pressure greater than 90 mm Hg or a rise of 15 mm Hg above previous readings prenatal NOTE: Blood pressures should be taken during resting state and not during contractions.

Delivery is the primary treatment for eclampsia. If untreated. Eclampsia develops in one out of two hundred pre—eclamptic patients and is usually fatal if untreated. Pre—eclampsia is defined as development of hypertension with albuminuria or edema between the 20th week of pregnancy and the end of the first week postpartum. The etiology of pre—eclampsia and eclampsia is unknown.

Mild preeclampsia develops as borderline hypertension. One attempt at replacing the uterus may be made. Retroplacental bleeding occurs. Placenta previa occurs in one out of two hundred deliveries. Abruptio placentae develops in 0. Administer high flow oxygen. Do not attempt to push to cord back into the vagina.

Treat for shock and place in the shock position with the uterus displaced to the left. Possible sources of bleeding include uterine atony. In severe cases. Symptoms and signs depend on the degree of separation and blood loss. The cause is unknown.

Vaginal bleeding may be minimal. Preexisting conditions such as previous uterine surgeries can predispose a patient to this condition. Place the mother in a knee— chest position or in a supine position the hips elevated and gently attempt to push the baby back up into the vagina to relieve pressure from the cord. Patients often report tearing sensation or constant area of specific pain.

To replace the uterus. Symptoms may include vaginal bleeding associated with pain. This condition requires rotation of the fetus within the uterus prior to delivery and can not be handled in the field. Maintain a high buttocks position to prevent further presentation and transport immediately.

Placenta previa frequently cannot be distinguished from abruptio placentae by clinical findings. Treat per the hypotension guideline. The baby is thereby in great danger of suffocation. Once the legs are clear. If head does not deliver within two or three minutes. Complete separation almost always results in death of the fetus. Separation can be either complete or partial. It is commonly caused by pulling on the umbilical cord while waiting on the placenta to deliver or from attempts to expel the placenta when the uterus is relaxed.

Noticeable contractions will cease and the uterus will be hard. Implantation of the placenta over or near the internal os of the cervix. Several factors may predispose a patient to this condition. Allow the buttocks and trunk of the baby to clear spontaneously. All degrees of placental separation. Profound shock usually accompanies this condition. The placenta may cover the internal os completely total previa or partially partial previa. Abruptio placentae may be confused with placenta previa.

The synergistic potential of benzodiazepines and narcotics or antiemetics is significant for respiratory depression. Paramedics must continue to monitor and assess patients during pain control and be prepared to intervene in the event of a complication. Proper pain medication can decrease heart rate. Elderly and pediatric patients in particular are at increased risk during analgesia. The medications used for moderate to severe pain control carry the potential for respiratory depression.

Pre-medication vital signs. Analgesia is used to minimize pain. Some patients perceive and verbalize pain differently. Opiates require careful titration to patient needs. When the placenta has dropped into the lower uterine segment and presents at the cervix. A brief history. Opiates are administered slowly and in small increments with adequate time for the sedative effects of the injected dose to be apparent before additional medication is given. The application of splints. If the uterus does not contract.

In addition to the usual stresses of life. Maximize non-pharmacological methods of pain control prior to administering medications. Pain and anxiety are common side effects associated with both acute and chronic medical and trauma patients. The use of pain medication requires continuous intravenous access until patient care is transferred to the emergency department.

Unrelieved acute and or moderate to severe chronic pain and poor symptom control can lead to anxiety and irritability. EKG and temperature are documented. Patients who are currently taking sedative or opioids may also be at a greater risk for over-sedation.

These methods can include transport in the position of comfort. The paramedic must have good access to the intravenous line and medication port throughout on-scene time transport. The perception. Paramedics are constantly challenged by having to move patients to stretchers from awkward positions. Comfort and compassion are mainstays of medical care and their importance cannot be overemphasized. Establishing pain levels will become the fourth vital sign. The inherent limitations of and over-reliance on pulse oximetry as monitors of respiration have become evident with reports of unrecognized hypercarbia and delayed recognition of respiratory depression.

The increase in carbon dioxide levels does not stimulate an increase in respiratory rate. Respiratory depression may occur when the pain is relieved and is no longer a stimulant. Patient observation and monitoring before. Respiratory depression becomes significant when intervention is needed. Promoting patient comfort and reducing or eliminating pain are the responsibilities of all pre-hospital clinicians.

When dealing with a patient experiencing a psychiatric emergency. Monitoring of respiration. Symptoms of withdrawal include agitation. Pulse oximeters do not detect apnea. While the risk of adverse events is low. Onset of action is usually within 2 minutes. Opioids interfere with carbon dioxide chemoreceptors in the medulla by retention of carbon dioxide.

Repeat boluses may be required to maintain adequate blood levels until the opioid agonist is eliminated. The potency and duration of action between different classes varies widely. Anxiety relief via pain control using pharmacological agents are critical elements to improving patient comfort both mentally and physically. The patient record should document any clinical or technical problems during administration of medications.

Capnography however. Hands-on monitoring should detect early signs of patient distress before compromises to vital functions occur. Patients at risk for respiratory depression. The paramedic must be diligent in recognizing early signs of distress and implement appropriate supportive or resuscitative measures. Opioids depress all phases of respiratory activity to some extent.

While pulse oximetry is usually an excellent and noninvasive technology for monitoring oxygen saturation. This narcotic antagonist can precipitate acute withdrawal symptoms in opioid-dependant or addicted patients. Keep stance as relaxed and neutral as possible. Empathize with the patient about their situation and ask the patient for suggestion to help improve it.

Remain calm and speak softly. Agree with the real aspects of their anger such as waiting a long line to see a doctor. If patient complains vehemently. Provide suicide patient with psychologically and physically protective environment. Perform a mental status examination. Be aware of both verbal and nonverbal communication as facial expressions. Assure safety of patient and others by removing any items they could use to harm themselves or others.

Typical signs and symptoms include feelings of worthlessness. Signs and symptoms of such an attack may include hyperactivity. Encourage the patient to express their concerns and to identify source of their anxiety. Keep in mind that suicidal thoughts represent an attempt to solve a problem.

Try to involve their family or friends in this planning process. Typical problems include job situation. A patient with an organic problem usually the result of metabolic or neurologic disorder may be disoriented or confused and have recent. Obtain background information to help determine nature and severity of problem. When assessing for suicide potential. Assist with diagnostic tests to help determine if an underlying physical condition is causing the psychiatric emergency.

To decrease patients anxiety. Then assess their mood their predominant emotion. Closely observe their body language. Find out what events led to this condition. Try to find out what the patient thinks their problem is. He may be demonstrating the behavior to obtain something he wants.

Is this a gesture—a way to manipulate others—or is it a real attempt at suicide? How upset or disturbed is the patient? If he attempted suicide. If their anger seems out of proportion to the situation. Help the patient set priorities. Let the patient know that the Team members are people. Attempt to establish rapport with the patient to gain their trust and cooperation.

Verbal abuse frequently precedes violent behavior. When in doubt. If the Team fears the patient may cause bodily harm. Speak to the patient firmly but calmly. A patient having a schizophrenic episode typically has delusions.

Move slowly and quietly. He typically believes that others are out to get him. Restraints may be used in response to dangerous behavior. Every effort should be made to utilize the least restrictive method of restraint. Their delusional system typically includes persecution feelings or excessive religious statements. Give medications. Use simple. Remain calm and authoritative. Obtain psychiatric consultation and arrange for hospital admission. Patients generally have a right to be free from restraints unless restraint is necessary to treat their medical symptoms or to prevent patients from harming themselves or others.

When dealing with an acute psychotic patient. Speak to the patient firmly to assure the patient that the Team is in control of the environment. Restraining a patient raises serious concerns. A patient suffering from paranoia a type of schizophrenia may have the following signs and symptoms. If possible. Monitoring must be performed by direct observation of and interaction with the patient. Their thought processes. Remove their clothing or any object that may conceal a weapon.

Situations arise in which restraints are not only appropriate and necessary. Restraint application is not a patient option. Patients may have injuries that result from being restrained. As soon as possible. Personnel injuries can occur from violent behavior.

Sedation could lead to drug interactions with adverse effects. Appearance of a team may convince a patient to permit application of restraints without resistance. For example. The fact that restraint will occur does not change. This recognition of the need to allow options.

A patient who vomits while in 4. Do not allow the patient to bargain with you. Pulse oximetry is helpful in measuring such patients. Uncooperative patients often provide inadequate histories. Once a clinician recognizes the need for restraint. At all times. Agencies currently utilizing leather restraints are encouraged to research and acquire soft. Most injuries are minor and include abrasions and bruises. Be on the lookout for patients with concealed weapons or dangerous objects ie. Oversedation could lead to loss of gag reflex.

Side rails are not considered restraints by themselves. Patients who are being restrained after an overdose pose particular problems because the ingested substances often are unknown. When was the last time you cleaned and treated your leather restraints? Would you prefer to be sitting up or lying down? Giving patients choices and options helps them to begin regaining a sense of selfcontrol.

Use caution whenever caring for patients in restraints. Emergency situations inflict an extremely frightening and threatening sense of loss of control upon the patients who experience them. This team approach minimizes risk of injury to the patient and the crew. A team of several members working together ie. Although physical restraints generally are the first method employed when restraints are necessary.

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