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Anaphylaxis
Clinical Significance.—The survival rate for teeth having orthograde retreatment after an initial conservative endodontic treatment was very good. It is likely that the high rate of tooth retention was accompanied by good tooth function and patient comfort. Clinicians can safely inform patients that about 89% of retreated teeth will be retained and will be functional for at least 5 years after the intervention.
Salehrabi R, Rotstein I: Epidemiologic evaluation of the outcomes of orthograde endodontic retreatment. J Endod 36:790-792, 2010 Reprints available from R Salehrabi, Univ of Southern California, Herman Ostrow School of Dentistry of USC, Room 310, Los Angeles, CA 90048-0641; e-mail: [email protected]
Oral Medicine Anaphylaxis Background.—Anaphylaxis is an alarming disorder in medicine. No universal approach to management or criteria for diagnosis has been developed. The latest concepts pertinent to defining and managing anaphylaxis from the field of emergency medicine were outlined. Definition, Etiology, and Pathophysiology.—The term anaphylaxis refers to a type I immune-mediated life-threatening systemic allergic reaction. It is an IgE-mediated response to an allergen that causes mast cell degradation and basophil activation. It is much more common in women, but is estimated to affect 1 in 10,000 persons in the general population. The term anaphylactoid reaction refers to the same clinical state and similar mediators but no IgE mediation. The mechanisms responsible are kinin generation with activation of coagulation or fibrinolysis, complement cascade activation, modulation of the metabolism of arachidonic acid, and direct histamine release. Many substances and conditions can trigger an anaphylactic (IgE) reaction, including food, drugs, local anesthetics that contain methyl paraben, vaccines, allergen extracts, foreign proteins, parasites, latex, hormones or enzymes, muscle relaxants, and exercise. Non-IgE reactions can be triggered by muscle relaxants, opioids, radiologic contrast media, immunoglobulins, aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs), dextran, and gelatin. Both IgE and nonimmune-mediated anaphylaxis involve the activation of mast cells and circulating basophils plus preformed mediator release. When the individual is exposed to an antigen, specific IgE antibodies are synthesized by lymphocytes and plasma cells. The Fc portions of these
antibodies attach themselves to mast cells and basophils. When the individual is exposed a second time, IgE antigen-antibody cross-binding and degranulation result. The preformed mediators are released and produce various reactions, such as vasodilatation and edema, bronchial smooth muscle contraction, and exacerbated inflammation and cell destruction. The clinical symptoms can range from sneezing to life-threatening compromise of the airway and cardiovascular system. In the early stages the patient often exhibits pruritus, rash, and tingling of the hands, feet, and axilla; generalized flushing; and a sinking sensation. These progress to urticaria, angioedema, or periorbital edema. Airway obstruction and cardiovascular collapse can follow, along with abdominal cramps, nausea, profuse vomiting, and diarrhea. Diagnosis.—When the patient meets three criteria there is a high likelihood that the diagnosis is anaphylaxis. These three are, specifically, (1) acute onset of an illness involving the skin, mucosal tissues, or both plus respiratory compromise or reduced blood pressure (BP) or other end-organ dysfunction; (2) rapid development after exposure of a likely allergen of at least two of the following: skin/mucosal tissue involvement, respiratory compromise, reduced BP or associated symptoms, and persistent gastrointestinal (GI) symptoms; and (3) reduced BP after exposure to a known allergen. For infants and children this reduction in BP consists of persistent low systolic BP or a decline of more than 30% in systolic BP. For adults the systolic BP falls below 90 mm Hg or shows a decline of more than 30% from baseline levels. Among the disorders that must be differentiated from anaphylaxis are cardiac arrhythmias or infarction, pulmonary embolism, and acute respiratory obstruction resulting from inhalation and vasovagal episodes.
Volume 56
Issue 2
2011
71
Once the patient has been resuscitated, 10 mL of clotted blood is obtained, then this step is repeated after 1 and 6 hours. These samples are analyzed for the presence of tryptase levels exceeding 15 mg/mL. Complement measurements are also obtained. These can confirm the diagnosis. Management and Follow-up.—The initial management of anaphylaxis focuses on basic life support, including rapid evaluation and maintenance of an airway, breathing, and circulation. Once the patient is diagnosed with anaphylaxis, epinephrine is administered immediately. Patients with questionable anaphylaxis may also be given epinephrine. Aqueous epinephrine, 0.01 mg/kg, maximum dose 0.5 mg, is preferentially delivered intramuscularly (IM) every 5 to 15 minutes as needed to control symptoms and maintain BP. Intravenous (IV) epinephrine may be used in cases where an IV line is in place or for patients who do not respond to the IM dose. However, lethal arrhythmias have occurred with IV drug, so continuous cardiac monitoring is recommended. Continuous low-dose epinephrine infusions may be the safest and most effective form of IV administration. Patients who are having respiratory symptoms or hypoxemia and those who are hemodynamically unstable can be given oxygen and adrenergic agonists. When the patient has bronchospasm refractory to the epinephrine, inhaled b2-agonists are useful. The next step in management will depend on the patient’s response to the epinephrine. All patients in anaphylactic shock should be placed in a recumbent position, lower extremities raised unless they complain of shortness of breath or vomiting. Patients who remain hypotensive despite epinephrine administration should receive aggressive fluid resuscitation, with large volumes of crystalloid needed during the first 5 or 10 minutes for patients with severe reactions plus hypotension. Fluid volume replacement is geared to the specific patient’s needs. If the patient’s systolic blood pressure remains below 90 mm Hg, potent vasopressors may be required. Antihistamines are considered a second-line treatment, used principally to manage urticaria/angioedema and pruritus. Corticosteroids are not helpful in the initial phases of anaphylaxis but may prevent a protracted or biphasic reaction, although evidence of this is lacking. Milder attacks may respond to oral prednisone 1 mg/kg.
as the epinephrine’s effects subside or a biphasic reaction may develop, usually within 72 hours. Severity of the initial reaction, reliability of the patient, and access to care are considered in determining how long the observation period should last, but 4 to 6 hours is reasonable for most cases, with longer times for patients who suffer severe or refractory symptoms. Outpatient follow-up may include prescribing self-injectable epinephrine; the clinical criteria for use of this measure remain undetermined. Patients who experience respiratory or cardiovascular symptoms after exposure to a known allergen are generally considered candidates for self-injectable epinephrine and should also have an emergency action plan for using this agent and obtaining follow-up management. All patients who experience an anaphylactic reaction should be educated about how to avoid the allergen, made aware of the availability of national organizations that can provide further information, and advised to follow up with an allergist and notify their primary care physician. Skin testing may be conducted to identify previously unknown allergens. Generally patients recover completely from an anaphylactic reaction with few longterm sequelae. A few patients suffer cardiac or neurologic damage from the episode. Discussion.—A multicenter prospective study is needed to determine if the diagnostic criteria that have been proposed will truly help the clinician identify patients with anaphylaxis and pinpoint the causative factors. Studies are also needed to provide evidence-based descriptions of the phenomenon and educate clinicians about ways to effectively prevent and intervene in such episodes. Sensitive and specific biomarkers of anaphylaxis and evolving anaphylaxis would be useful when a complete history is lacking or with atypical symptoms. Assays of these biomarkers could confirm the diagnosis and help to identify patients at risk for persistent or delayed reactions. An anaphylaxis registry would be helpful to researchers pursuing laboratory trials. Better understanding of the mechanisms of action and responses to treatment are also needed.
Clinical Significance.—Anaphylaxis is a critical problem for all areas of health care. We can often treat it effectively but we don’t know enough about it to say we have it mastered. It presents many topics for research studies that could improve our clinical interventions.
Patients taking b-blockers reportedly suffer more severe or treatment-refractory anaphylactic episodes because the b-blockers can blunt the response to epinephrine. If the patient does not respond to the epinephrine, glucagon 1 to 5 mg IV over 5 minutes plus an infusion of 5 to 15 mg/min titrated to response can be administered.
Sharma R, Sinba R, Menon PS, et al: Management protocol for anaphylaxis. J Oral Maxillofac Surg 68:855-862, 2010
Observation is an essential part of managing patients suffering an anaphylactic reaction. The reaction may recur
Reprints available from MAJ Sharma, Military Dental Ctr, Jalandhar, India
72
Dental Abstracts
Salehrabi R, Rotstein I: Epidemiologic evaluation of the outcomes of orthograde endodontic retreatment. J Endod 36:790-792, 2010 Reprints available from R Salehrabi, Univ of Southern California, Herman Ostrow School of Dentistry of USC, Room 310, Los Angeles, CA 90048-0641; e-mail: [email protected]
Oral Medicine Anaphylaxis Background.—Anaphylaxis is an alarming disorder in medicine. No universal approach to management or criteria for diagnosis has been developed. The latest concepts pertinent to defining and managing anaphylaxis from the field of emergency medicine were outlined. Definition, Etiology, and Pathophysiology.—The term anaphylaxis refers to a type I immune-mediated life-threatening systemic allergic reaction. It is an IgE-mediated response to an allergen that causes mast cell degradation and basophil activation. It is much more common in women, but is estimated to affect 1 in 10,000 persons in the general population. The term anaphylactoid reaction refers to the same clinical state and similar mediators but no IgE mediation. The mechanisms responsible are kinin generation with activation of coagulation or fibrinolysis, complement cascade activation, modulation of the metabolism of arachidonic acid, and direct histamine release. Many substances and conditions can trigger an anaphylactic (IgE) reaction, including food, drugs, local anesthetics that contain methyl paraben, vaccines, allergen extracts, foreign proteins, parasites, latex, hormones or enzymes, muscle relaxants, and exercise. Non-IgE reactions can be triggered by muscle relaxants, opioids, radiologic contrast media, immunoglobulins, aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs), dextran, and gelatin. Both IgE and nonimmune-mediated anaphylaxis involve the activation of mast cells and circulating basophils plus preformed mediator release. When the individual is exposed to an antigen, specific IgE antibodies are synthesized by lymphocytes and plasma cells. The Fc portions of these
antibodies attach themselves to mast cells and basophils. When the individual is exposed a second time, IgE antigen-antibody cross-binding and degranulation result. The preformed mediators are released and produce various reactions, such as vasodilatation and edema, bronchial smooth muscle contraction, and exacerbated inflammation and cell destruction. The clinical symptoms can range from sneezing to life-threatening compromise of the airway and cardiovascular system. In the early stages the patient often exhibits pruritus, rash, and tingling of the hands, feet, and axilla; generalized flushing; and a sinking sensation. These progress to urticaria, angioedema, or periorbital edema. Airway obstruction and cardiovascular collapse can follow, along with abdominal cramps, nausea, profuse vomiting, and diarrhea. Diagnosis.—When the patient meets three criteria there is a high likelihood that the diagnosis is anaphylaxis. These three are, specifically, (1) acute onset of an illness involving the skin, mucosal tissues, or both plus respiratory compromise or reduced blood pressure (BP) or other end-organ dysfunction; (2) rapid development after exposure of a likely allergen of at least two of the following: skin/mucosal tissue involvement, respiratory compromise, reduced BP or associated symptoms, and persistent gastrointestinal (GI) symptoms; and (3) reduced BP after exposure to a known allergen. For infants and children this reduction in BP consists of persistent low systolic BP or a decline of more than 30% in systolic BP. For adults the systolic BP falls below 90 mm Hg or shows a decline of more than 30% from baseline levels. Among the disorders that must be differentiated from anaphylaxis are cardiac arrhythmias or infarction, pulmonary embolism, and acute respiratory obstruction resulting from inhalation and vasovagal episodes.
Volume 56
Issue 2
2011
71
Once the patient has been resuscitated, 10 mL of clotted blood is obtained, then this step is repeated after 1 and 6 hours. These samples are analyzed for the presence of tryptase levels exceeding 15 mg/mL. Complement measurements are also obtained. These can confirm the diagnosis. Management and Follow-up.—The initial management of anaphylaxis focuses on basic life support, including rapid evaluation and maintenance of an airway, breathing, and circulation. Once the patient is diagnosed with anaphylaxis, epinephrine is administered immediately. Patients with questionable anaphylaxis may also be given epinephrine. Aqueous epinephrine, 0.01 mg/kg, maximum dose 0.5 mg, is preferentially delivered intramuscularly (IM) every 5 to 15 minutes as needed to control symptoms and maintain BP. Intravenous (IV) epinephrine may be used in cases where an IV line is in place or for patients who do not respond to the IM dose. However, lethal arrhythmias have occurred with IV drug, so continuous cardiac monitoring is recommended. Continuous low-dose epinephrine infusions may be the safest and most effective form of IV administration. Patients who are having respiratory symptoms or hypoxemia and those who are hemodynamically unstable can be given oxygen and adrenergic agonists. When the patient has bronchospasm refractory to the epinephrine, inhaled b2-agonists are useful. The next step in management will depend on the patient’s response to the epinephrine. All patients in anaphylactic shock should be placed in a recumbent position, lower extremities raised unless they complain of shortness of breath or vomiting. Patients who remain hypotensive despite epinephrine administration should receive aggressive fluid resuscitation, with large volumes of crystalloid needed during the first 5 or 10 minutes for patients with severe reactions plus hypotension. Fluid volume replacement is geared to the specific patient’s needs. If the patient’s systolic blood pressure remains below 90 mm Hg, potent vasopressors may be required. Antihistamines are considered a second-line treatment, used principally to manage urticaria/angioedema and pruritus. Corticosteroids are not helpful in the initial phases of anaphylaxis but may prevent a protracted or biphasic reaction, although evidence of this is lacking. Milder attacks may respond to oral prednisone 1 mg/kg.
as the epinephrine’s effects subside or a biphasic reaction may develop, usually within 72 hours. Severity of the initial reaction, reliability of the patient, and access to care are considered in determining how long the observation period should last, but 4 to 6 hours is reasonable for most cases, with longer times for patients who suffer severe or refractory symptoms. Outpatient follow-up may include prescribing self-injectable epinephrine; the clinical criteria for use of this measure remain undetermined. Patients who experience respiratory or cardiovascular symptoms after exposure to a known allergen are generally considered candidates for self-injectable epinephrine and should also have an emergency action plan for using this agent and obtaining follow-up management. All patients who experience an anaphylactic reaction should be educated about how to avoid the allergen, made aware of the availability of national organizations that can provide further information, and advised to follow up with an allergist and notify their primary care physician. Skin testing may be conducted to identify previously unknown allergens. Generally patients recover completely from an anaphylactic reaction with few longterm sequelae. A few patients suffer cardiac or neurologic damage from the episode. Discussion.—A multicenter prospective study is needed to determine if the diagnostic criteria that have been proposed will truly help the clinician identify patients with anaphylaxis and pinpoint the causative factors. Studies are also needed to provide evidence-based descriptions of the phenomenon and educate clinicians about ways to effectively prevent and intervene in such episodes. Sensitive and specific biomarkers of anaphylaxis and evolving anaphylaxis would be useful when a complete history is lacking or with atypical symptoms. Assays of these biomarkers could confirm the diagnosis and help to identify patients at risk for persistent or delayed reactions. An anaphylaxis registry would be helpful to researchers pursuing laboratory trials. Better understanding of the mechanisms of action and responses to treatment are also needed.
Clinical Significance.—Anaphylaxis is a critical problem for all areas of health care. We can often treat it effectively but we don’t know enough about it to say we have it mastered. It presents many topics for research studies that could improve our clinical interventions.
Patients taking b-blockers reportedly suffer more severe or treatment-refractory anaphylactic episodes because the b-blockers can blunt the response to epinephrine. If the patient does not respond to the epinephrine, glucagon 1 to 5 mg IV over 5 minutes plus an infusion of 5 to 15 mg/min titrated to response can be administered.
Sharma R, Sinba R, Menon PS, et al: Management protocol for anaphylaxis. J Oral Maxillofac Surg 68:855-862, 2010
Observation is an essential part of managing patients suffering an anaphylactic reaction. The reaction may recur
Reprints available from MAJ Sharma, Military Dental Ctr, Jalandhar, India
72
Dental Abstracts