LETTERS TO THE EDITOR THE JOURNAL devotes this section to comment by readers on topics of current interest to dentistry. T he editor reserves the right to edit all communications to fit available space and requires that all letters be signed. Printed comm unications do not necessarily reflect the opinion or official policy of the Association. Your participation in this section is invited.
Present shock □ The correspondence on ana phylaxis and vasoconstrictors (The journal, September) brought to light a major problem in all the health professions: communication. The term anaphylaxis indicates nothing more than an induced sensitivity characterized by contraction of smooth muscle and capillary dila tion. Anaphylactic shock is that state of circulatory insufficiency that re sults from a continual general cir culatory fluid loss created by gener alized capillary dilation. The treatment of anaphylaxis or anaphylactoid reactions, and the treatment of anaphylactic or anaphylactoid shock differ greatly, a fact that has not been generally ac cepted or understood. Anaphylaxis is the physiologic result of a noxious chemical reaction, and is usually caused by ingestion or injection of a chemical to which an individual has been sensitized. An anaphylactoid reaction is caused by endogenous histaminelike substances that also cause contrac tion of smooth muscle, in addition to generalized capillary dilation. . . . If there has been no uncompensated reduction in blood pressure, the pre ferred treatment for simple ana phylaxis has been the administra tion of epinephrine; this is usually followed by high doses of a steroid and an antihistamine with low som nolent effects. The bronchospasm and the edema can be treated as two entities. In anaphylactic or anaphylactoid shock the patient manifests pallor and hypotension in addition to
bronchospasm and edema. This hypotension will lead to loss of con sciousness, dilation of pupils, possi ble anoxic convulsions, and, if not successfully treated, to death. . . . Immediate restoration of functional circulation is necessary. The patient should be placed in the classic shock position and given oxygen by de mand or by positive pressure. . . . Circulating fluid volume can be re stored by the intravenous adminis tration of a lactated Ringer solution with an alpha-receptor stimulating drug. . . . To some extent the edema will be controlled by the capillary constriction caused by the latter. A massive intravenous dose of methylprednisolone sodium succinate should then be administered for its effect on stabilization of interstitial fluids, and for its antihistaminic and antiasthmatic actions. If a bronchodilator was not administered with the initial oxygen, it should be given intravenously; the preferred bronchodilator is aminophylline. Then an antihistamine should be admin istered. The patient should be taken to the hospital as soon as possi ble. . . .Control of fluid compart ments is the key to treatment of shock, no matter what the cause. ROBERT L. HAAS, DDS, MPH TAMPA, FLA
Microleakage □ We have been interested in the restoration of the cervical erosion lesion for some time and have read with interest the laboratory study on the microleakage of several Class V anterior restorative materials by Drs. Hembree and Andrews (The Journal, August). However, I ques
tion the validity of the use of their cervical erosion lesion model which is an area of gingival abrasion me chanically produced on anterior and premolar teeth. Artificially prepared Class V ero sion lesions have different surface and internal characteristics from those of naturally occurring Class V erosion lesions; this fact could af fect the leakage pattern seen in the laboratory. The cervical erosion lesion is formed by a loss of tooth structure. The erosion process is accompanied by the hypermineralization of the intertubular dentin, the deposition of inorganic substances within the dentinal tubules, and the formation of reparative dentin at the pulpdentinal interface. The cervical ero sion lesion contains hyperminer alized dentin whereas the mechan ically prepared lesion on an extrac ted tooth does not.1 The valid model for this type of laboratory study is the unaltered naturally occurring cervical erosion lesion. ROLAND F. BLEIHOLDER, PhD S. S. WHITE KING OF PRUSSIA, PA 1. Gwinnett, A.J., and Jendresen, M.D. Rela tion between resin and etched dentin in treatment of tooth erosion. J Dent Res (Special Issue A) 56:434 Feb 1977.
Author’s com m ent: Dr. Bleiholder’s criticism that a naturally occurring cervical abraded or eroded area was not used in our study is a valid one. We, too, have been concerned about this point. We initiated a study more than a year ago to evaluate the microleak (A D A , V o l. 9 7 , D ecem b er 1 9 7 8 ■ 9 4 1
Present shock □ The correspondence on ana phylaxis and vasoconstrictors (The journal, September) brought to light a major problem in all the health professions: communication. The term anaphylaxis indicates nothing more than an induced sensitivity characterized by contraction of smooth muscle and capillary dila tion. Anaphylactic shock is that state of circulatory insufficiency that re sults from a continual general cir culatory fluid loss created by gener alized capillary dilation. The treatment of anaphylaxis or anaphylactoid reactions, and the treatment of anaphylactic or anaphylactoid shock differ greatly, a fact that has not been generally ac cepted or understood. Anaphylaxis is the physiologic result of a noxious chemical reaction, and is usually caused by ingestion or injection of a chemical to which an individual has been sensitized. An anaphylactoid reaction is caused by endogenous histaminelike substances that also cause contrac tion of smooth muscle, in addition to generalized capillary dilation. . . . If there has been no uncompensated reduction in blood pressure, the pre ferred treatment for simple ana phylaxis has been the administra tion of epinephrine; this is usually followed by high doses of a steroid and an antihistamine with low som nolent effects. The bronchospasm and the edema can be treated as two entities. In anaphylactic or anaphylactoid shock the patient manifests pallor and hypotension in addition to
bronchospasm and edema. This hypotension will lead to loss of con sciousness, dilation of pupils, possi ble anoxic convulsions, and, if not successfully treated, to death. . . . Immediate restoration of functional circulation is necessary. The patient should be placed in the classic shock position and given oxygen by de mand or by positive pressure. . . . Circulating fluid volume can be re stored by the intravenous adminis tration of a lactated Ringer solution with an alpha-receptor stimulating drug. . . . To some extent the edema will be controlled by the capillary constriction caused by the latter. A massive intravenous dose of methylprednisolone sodium succinate should then be administered for its effect on stabilization of interstitial fluids, and for its antihistaminic and antiasthmatic actions. If a bronchodilator was not administered with the initial oxygen, it should be given intravenously; the preferred bronchodilator is aminophylline. Then an antihistamine should be admin istered. The patient should be taken to the hospital as soon as possi ble. . . .Control of fluid compart ments is the key to treatment of shock, no matter what the cause. ROBERT L. HAAS, DDS, MPH TAMPA, FLA
Microleakage □ We have been interested in the restoration of the cervical erosion lesion for some time and have read with interest the laboratory study on the microleakage of several Class V anterior restorative materials by Drs. Hembree and Andrews (The Journal, August). However, I ques
tion the validity of the use of their cervical erosion lesion model which is an area of gingival abrasion me chanically produced on anterior and premolar teeth. Artificially prepared Class V ero sion lesions have different surface and internal characteristics from those of naturally occurring Class V erosion lesions; this fact could af fect the leakage pattern seen in the laboratory. The cervical erosion lesion is formed by a loss of tooth structure. The erosion process is accompanied by the hypermineralization of the intertubular dentin, the deposition of inorganic substances within the dentinal tubules, and the formation of reparative dentin at the pulpdentinal interface. The cervical ero sion lesion contains hyperminer alized dentin whereas the mechan ically prepared lesion on an extrac ted tooth does not.1 The valid model for this type of laboratory study is the unaltered naturally occurring cervical erosion lesion. ROLAND F. BLEIHOLDER, PhD S. S. WHITE KING OF PRUSSIA, PA 1. Gwinnett, A.J., and Jendresen, M.D. Rela tion between resin and etched dentin in treatment of tooth erosion. J Dent Res (Special Issue A) 56:434 Feb 1977.
Author’s com m ent: Dr. Bleiholder’s criticism that a naturally occurring cervical abraded or eroded area was not used in our study is a valid one. We, too, have been concerned about this point. We initiated a study more than a year ago to evaluate the microleak (A D A , V o l. 9 7 , D ecem b er 1 9 7 8 ■ 9 4 1
