COMMUNICAnONS
LETTER TO THE EDITOR
TINNITUS AS A PRESENTING SYMPTOM IN PERNICIOUS ANEMIA
Dear Editor: In the March-April 1978 issue of the Annals there appeared an article by Karl H. Siedentop, MD et al' which makes a critical analysis of the "tympanometric method" for evaluation of eustachian tube function. As I introduced this method in 1969 I would like to make a few comments. The measurement technique which was used by Siedentop et al seems to differ from the one I presented in 1969. The equipment does not allow a variation of the nasopharyngeal air pressure levels. The device I am using allows a great variation of the nasopharyngeal air pressure. This means that the examiner has more possibilities to create negative air pressure in the nasopharynx, which then could be transmitted to the middle ear. This may explain one of the difficulties he had establishing negative middle ear pressure levels. As shown in Figure 2 in Siedentop's article the ear canal air pressure is continuously changed during the testing procedure. This may have influenced the patients' ability to create the middle ear pressure. Also, this influences the patients' ability to equilibrate the established middle ear pressure level. This may be another explanation for the differences between our results. I t is always difficult to compare materials, pathological and normal, between different populations. Also it may be difficult to select those in a normal group from those in a pathological group. This holds for my material as well as Siedentop's material. I can only say that my selection was based on a very thorough review of the history and otomicroscopic finding. As my normal material was limited in the original article, I investigated 70 medical students selected to represent normal individuals based on history, hearing and otomicroscopic examination. In only 10% of these it was impossible to create negative middle ear pressure. When it comes to establishing negative middle ear pressure I like to refer to Elner et al' who established negative middle ear pressure in 84% of normal individuals, using the same technique as I introduced. Elner et aI' examined 102 normal individuals and used an air flow technique in the ear canal to record the middle ear pressure change. They also used a pressure chamber for introducing negative middle ear pressure. Despite using only -100 mm H,O he found that 92% of his normal individuals could equilibrate the underpressure. Also, when using the testing technique similar to the one I introduced he noticed that all normals could equilibrate negative air pressure. Ingelstedt et al' also examined pilots and their ability to equilibrate negative middle ear pressure. They found that pilots with history of problems with air pressure equilibration really do have an inability to establish air pressure equilibration. T-his was reproduced in the air
JOHN
H.
PATRICK
COCHRAN, JR.,
W.
KOSMICKI,
MD MD
DENVER, COLORADO
The etiology of tinnitus includes a complicated differential diagnosis.' A comprehensive list as presented by Goodhill' includes many entities, but the physician's attention is usual, ly directed toward primary otologic pathologies. This patient presents a clear reminder of the need to be mindful of all the causes of tinnitus. CASE REPORT J.P. is a 64-year-old female referred for evaluation of pulsatile tinnitus in both ears for a few months. She had no history of ear infections, trauma, hearing loss, vertigo, noise exposure, exposure to ototoxic agents, or hypertension. On examination, her ear canals, tympanic membranes, and hearing were normal. She had bilateral carotid bruits and the intensity of the tinnitus could be decreased in either ear by even light pressure over the carotid for auscultation. In addition the patient appeared pale and did note some increased fatigability. A complete blood count revealed a hematocrit of 21% with macrocytic indices. Serum folate was normal, vitamin B12 was quite low, and bone marrow examination showed an increase in megaloblasts. A Schilling test was done which confirmed inadequate absorption of B12 and the diagnosis of pernicious anemia was made. She was treated with parenteral vitamin B12 and in three weeks her hematocrit was 38%. In addition, her tinnitus and bruits had completely resolved. SUMMARY An unusual case presenting to the otolaryngologist as pulsatile tinnitus is discussed. Fowler' points out that the circulatory response to anemia is increased cardiac output. There is associated tachycardia and increased arterial pulse pressure. Because of this increased flow state and turbulence, systolic bruits, venous hums, and "capillary" pulsations are found. This increased flow state is perceived in the ear as a transmitted pulsatile tinnitus. The successful treatment of this patient's pernicious anemia corrected the hyperdynamic circulatory state, and resulted in disappearance of her tinnitus. REFERENCES 1. Fowler EP: Head noises in normal and disordered ears. Arch Otolaryngol 39 :498, 1944 2. Goodhill V: A tinnitus Identification test. Ann Otol Rhlnol Laryngol 61 :778, 1952 3. Fowler NO: High cardiac output states in Hurst JW (ed) : The Heart, New York, Mc: Graw Hill, 1974
297
LETTER TO THE EDITOR
TINNITUS AS A PRESENTING SYMPTOM IN PERNICIOUS ANEMIA
Dear Editor: In the March-April 1978 issue of the Annals there appeared an article by Karl H. Siedentop, MD et al' which makes a critical analysis of the "tympanometric method" for evaluation of eustachian tube function. As I introduced this method in 1969 I would like to make a few comments. The measurement technique which was used by Siedentop et al seems to differ from the one I presented in 1969. The equipment does not allow a variation of the nasopharyngeal air pressure levels. The device I am using allows a great variation of the nasopharyngeal air pressure. This means that the examiner has more possibilities to create negative air pressure in the nasopharynx, which then could be transmitted to the middle ear. This may explain one of the difficulties he had establishing negative middle ear pressure levels. As shown in Figure 2 in Siedentop's article the ear canal air pressure is continuously changed during the testing procedure. This may have influenced the patients' ability to create the middle ear pressure. Also, this influences the patients' ability to equilibrate the established middle ear pressure level. This may be another explanation for the differences between our results. I t is always difficult to compare materials, pathological and normal, between different populations. Also it may be difficult to select those in a normal group from those in a pathological group. This holds for my material as well as Siedentop's material. I can only say that my selection was based on a very thorough review of the history and otomicroscopic finding. As my normal material was limited in the original article, I investigated 70 medical students selected to represent normal individuals based on history, hearing and otomicroscopic examination. In only 10% of these it was impossible to create negative middle ear pressure. When it comes to establishing negative middle ear pressure I like to refer to Elner et al' who established negative middle ear pressure in 84% of normal individuals, using the same technique as I introduced. Elner et aI' examined 102 normal individuals and used an air flow technique in the ear canal to record the middle ear pressure change. They also used a pressure chamber for introducing negative middle ear pressure. Despite using only -100 mm H,O he found that 92% of his normal individuals could equilibrate the underpressure. Also, when using the testing technique similar to the one I introduced he noticed that all normals could equilibrate negative air pressure. Ingelstedt et al' also examined pilots and their ability to equilibrate negative middle ear pressure. They found that pilots with history of problems with air pressure equilibration really do have an inability to establish air pressure equilibration. T-his was reproduced in the air
JOHN
H.
PATRICK
COCHRAN, JR.,
W.
KOSMICKI,
MD MD
DENVER, COLORADO
The etiology of tinnitus includes a complicated differential diagnosis.' A comprehensive list as presented by Goodhill' includes many entities, but the physician's attention is usual, ly directed toward primary otologic pathologies. This patient presents a clear reminder of the need to be mindful of all the causes of tinnitus. CASE REPORT J.P. is a 64-year-old female referred for evaluation of pulsatile tinnitus in both ears for a few months. She had no history of ear infections, trauma, hearing loss, vertigo, noise exposure, exposure to ototoxic agents, or hypertension. On examination, her ear canals, tympanic membranes, and hearing were normal. She had bilateral carotid bruits and the intensity of the tinnitus could be decreased in either ear by even light pressure over the carotid for auscultation. In addition the patient appeared pale and did note some increased fatigability. A complete blood count revealed a hematocrit of 21% with macrocytic indices. Serum folate was normal, vitamin B12 was quite low, and bone marrow examination showed an increase in megaloblasts. A Schilling test was done which confirmed inadequate absorption of B12 and the diagnosis of pernicious anemia was made. She was treated with parenteral vitamin B12 and in three weeks her hematocrit was 38%. In addition, her tinnitus and bruits had completely resolved. SUMMARY An unusual case presenting to the otolaryngologist as pulsatile tinnitus is discussed. Fowler' points out that the circulatory response to anemia is increased cardiac output. There is associated tachycardia and increased arterial pulse pressure. Because of this increased flow state and turbulence, systolic bruits, venous hums, and "capillary" pulsations are found. This increased flow state is perceived in the ear as a transmitted pulsatile tinnitus. The successful treatment of this patient's pernicious anemia corrected the hyperdynamic circulatory state, and resulted in disappearance of her tinnitus. REFERENCES 1. Fowler EP: Head noises in normal and disordered ears. Arch Otolaryngol 39 :498, 1944 2. Goodhill V: A tinnitus Identification test. Ann Otol Rhlnol Laryngol 61 :778, 1952 3. Fowler NO: High cardiac output states in Hurst JW (ed) : The Heart, New York, Mc: Graw Hill, 1974
297
