gait but otherwise no signs of ataxia, normal speech, and a normal ophtalmoneurologic examination. based
Wernicke
Encephalopathy Following Prolonged Artificial Nutrition The necessity of vitamin supplementation during long-term artificial nutrition is well known. Nevertheless, it may be overlooked, particularly if the disorder causing the nutrition problems dominates the therapeutic measures. This was the situation in a case of Wernicke encephalopathy that developed after prolonged parenteral alimentation.
Comment.—Although Wernicke en¬ cephalopathy is associated with alco¬ holism, Wernicke pointed out in 1881 that it could appear after persisting vomiting.1 It has subsequently been reported in many different conditions involving defective nutrition.26 The role of thiamine deficiency was estab¬
Report of a Case.\p=m-\Thepatient is a 14\x=req-\ year-old boy, previously healthy, who was admitted to another hospital for treatment of esophageal aclasis. While the patient was undergoing therapeutic dilation with bougies, the abdominal part of the esophagus was accidentally perforated. The perforation was repaired and the boy was treated with antibiotics. During this time he was nourished only parenterally. After
companied by vomiting.7 Prolonged depletion leads to Wernicke encepha¬ lopathy characterized by various types of oculumotor palsies, nystag¬ mus, ataxia, tremor, disturbed con¬ sciousness varying from coma to mild confusion,8 and impaired vestibular
four weeks he became febrile and somnolent. Laboratory investigation disclosed severe acidosis (base excess, \m=-\12.5) and a low serum sodium level (124 mEq/liter). After glucose infusion and correction of the acid\x=req-\ base and electrolyte disturbances, there was transient improvement, but his condition soon deteriorated, and he had a brief epileptic seizure. On admittance to our hospital, the boy was somnolent, and exhibited paralysis of horizontal gaze and vertical nystagmus. The muscle reflexes were exaggerated; Babinski sign was absent. His voice was hoarse and his speech of a staccato type. The cerebrospinal fluid contained no bac¬ teria and no blood cells; total protein level was 66 mg/100 ml. Brain scanning and echoencephalography gave normal results. Conduction velocity of peripheral nerves was normal. The electroencephalogram showed a marked increase of slow waves. Parenteral nutrition was continued and the usual vitamin supplements were given. The neurological findings were first in¬ terpreted as due to a brain stem lesion caused by a septic embolus. It was then recognized that in several respects the con¬ dition fitted well with Wernicke disease. Checking of the patient's previous hospital record revealed that no vitamin supple¬ ments had been given during the month he had been totally deprived of perorai food intake. On the third day after admission, thiamine hydrochloride treatment was started; 20 mg/day for the first four days, 50 mg/day the following week. Two days later, there was a marked im¬ provement in the level of consciousness and in eye mobility. After one week the pa¬ tient could be mobilized. A transitory de¬ crease of the vestibular function and a slowly regressing ataxia were noted. The EEG gradually became normal. When he left the children's hospital after three weeks (for further treatment of the esoph¬ ageal aclasis) he had a slightly broad-
lished in the late 1930s.1 The earliest symptom of thiamine deficiency is anorexia sometimes ac¬
function.9 Cardiac symptoms in thiamine deficiency are seen almost entirely in infantile beriberi10; only two cases are on record with both car¬ diac and cerebral signs of thiamine deficiency.311 The cardiopathy in juvenile beriberi, and the polyneuropathy in that disease as well as in cases of Wernicke disease in alco¬ holics, are considered to have multifactorial origins.110 The clinical pic¬ ture in the present case—decreased consciousness, horizontal gaze palsy, nystagmus, and ataxia—thus fits well into the picture of Wernicke encepha¬
lopathy. The rapid improvement after vita¬ min supplementation is well in agree¬ ment with what would be expected in Wernicke encephalopathy. An im¬ provement has sometimes been
already within
seen
few hours after the start of thiamine treatment.1 The eye symptoms disappear first and usually completely. The ataxia regresses more slowly and not always com¬ a
pletely.
The present case stresses the need for vitamin supplementation in total parenteral alimentation. G\l=o"\staBLENNOW, MD Department of Pediatrics
University Hospital
S-221 85 Lund, Sweden M, Adams RD, Collins GH: The Wernicke-Korsakoff Syndrome. Oxford, England, Blackwell Scientific Publications, 1971. 1. Victor
2. Guerrero RM: Wernicke's syndrome due to vitamin B deficiency: Report of the disease in two infants. Am J Dis Child 78:88-96, 1949. 3. Davis RA, Wolf A: Infantile beriberi associated with Wernicke's encephalopathy. Pediatrics 3:409-420, 1958. 4. Cochrane WA, Collins-Williams C, Donohue WL: Superior hemorrhagic polioencephalitis (Wernicke's disease) occurring in an infant\p=m-\
Downloaded From: http://archpedi.jamanetwork.com/ by a New York University User on 06/17/2015
probably
due to thiamine deficiency from use of soya bean product. Pediatrics 28:771-777,1961. 5. Lopez RJ, Collins GH: Wernicke's encephalopathy: A complication of chronic hemodialysis. Arch Neurol 18:248-259, 1968. 6. Shah N, Wolff JA: Thiamine deficiency: Probable Wernicke's encephalopathy successfully treated in a child with acute lymphocytic leukemia. Pediatrics 51:750, 1973. 7. Guthrie HA: Introductory Nutrition. St Louis, CV Mosby Co, 1967, p 234. 8. Merritt HH: A Textbook of Neurology. Philadelphia, Lea & Febiger, 1967, p 653. 9. Ghez C: Vestibular paresis: A clinical feature of Wernicke's disease. J Neurol Neurosurg Psychiatry 32:134-139, 1969. 10. De Silva CC, Baptist NG: Tropical Nutritional Disorders of Infants and Children. Springfield, Ill, Charles C Thomas Publisher, 1969, p 117. 11. Cavazzuti GB, Gobbi U, Gullotta F, et al: Wernicke's encephalopathy in a child with congenital cardiomegaly. Helv Paediatr Acta 28:559-568, 1973. a
Seat Belt Buckle Burn
Seat belts and other child restrain-
ing devices remain underutilized immunizing agents that could greatly reduce the morbidity and mortality of automobile accidents. On rare occasions, they cause injury, and this report describes one such unusual case.
Report of a Case.\p=m-\A2\m=1/2\-year-oldgirl strapped in an adult seat belt in the middle front seat. Although her mother normally used a child safety harness in the
was
seat, the car was filled with adults and other children she was taking home. The car had been parked in the summer sun for several hours with the windows closed. As the mother fastened the belt around her daughter, the child cried and the mother noticed some reddening of the skin where it was in direct contact with the undersurface of the buckle. Only when arriving home did she notice the burns, which later vesiculated. The Figure shows three parallel second-degree burns on the right lower quadrant of the abdomen. The largest one, closest to the umbilicus, is the suspected initial position of the buckle. Apparently, the others were caused as the belt was tightened and the heat from the buckle dissipated. Three parallel scars remain. rear
Comment.—When exposed to the portions of seat belts become noticeably hot to adults. How¬ ever, they can cause thermal burns in sun, the metal
young children when in direct skin contact, as in this case. Burns can be produced experimentally by brief contact with a surface temperature of 70 C.1 Thus, the surface temperature of the underside of the buckle could be estimated to be around 70 C. Although a rare hazard, this injury could be prevented by covering or pushing the metal portions of seat belts under the seat back when park¬ ing in the hot sun. Newer cars with self-retracting belts and covered buckles should be less likely to cause this type of injury. Preferably, infants and young chil¬ dren should use special restraining devices, because of their body devel¬ opment and higher center of gravity. Several such restraints have been tested under simulated crash condi¬ tions and can be recommended to par¬ ents.2 However, some of the child safety chairs have a five-point har¬ ness system, with metal buckle parts that may be in contact with the child's thighs if he or she is wearing shorts. These parts could cause a burn similar to that reported here, and par¬ ents should check the buckles to make sure they are not too hot before fas¬ tening· them around the child. EDWARD W. SAITZ, MD Western Pennsylvania Regional Medical Program University of Pittsburgh 4200 Fifth Ave Pittsburgh, PA 15260 1. Moritz AR, Henriques FC Jr: Studies of thermal injury: II. The relative importance of time and surface temperature in the causation of cutaneous burns. Am J Pathol 23:695-720, 1947. 2. Shelness A, Charles C: Children as passengers in automobiles: The neglected minority on the nation's highways. Pediatrics: 56:271-284, 1975.
High
Fever
Sir.\p=m-\Inthe June 1975 issue of the Journal (129:693, 1975), I believe Dr Tomlinson has missed the point of the mothers' question, "aren't high fevers always serious?" What mothers are really asking is, "aren't high fevers
always harmful?"
A great many mothers (and some physicians) are concerned about high fevers because of their erroneous belief that the high fever in itself is harmful: "it can cook the brain," "it can damage the body," "it always causes convulsions." Too often we find mothers (and some physicians) vigorously and overzealously treating the temperature elevation and overlooking the cause of the fe-
iatrogenic anachronism left from the days when treatment of fever was the physician's main stock-in-trade. "Treat the child, not the thermometer" is advice we often ver—an over
give to apprehensive parents, empha¬ sizing that it is the underlying condi¬ tion that could be harmful and
re¬
quires treatment. The degree of fever
does not correlate with the serious¬ ness of the illness. It is not clear to me also why the author considers temperature eleva¬ tions to 40 C in the office or hospital to be more significant than a tempera¬ ture of 40 C noted by the mother at home. Further, I could not find confir¬ mation in the article itself for the conclusion that high fevers are "more likely to be associated with pneu¬ monia if they persist for 12 to 18 hours." I wonder if this has been the experience of others? In his conclusion, the author also states that "high fevers are some¬ times serious." I suspect that what he really means is that the cause of high fever and not the fever itself can sometimes (and sometimes not) be se¬ rious. With that modification of his conclusion I think we can all aeree. H. WILLIAM FINK, MD Department of Pediatrics Eastern Virginia Medical School 358 Mombray Arch Norfolk, VA 23501
In Reply.\p=m-\Iappreciate Dr Fink's careful reading and thoughtful comments on my article, "High Fever." I agree with everything Dr Fink says in his first paragraph (except for the phrase, "Dr Tomlinson has missed the point. .."!), and I agree with his last paragraph as well. Most practicing pediatricians have spent hundreds or thousands of hours trying to correct the erroneous beliefs Dr Fink mentions. In regard to Dr Fink's second paragraph, I did not mean to imply that high fever in the office or in the hospital is more significant than the same degree of fever in the home. But (I hope) its existence is more certain if a trained medical observer has read the thermometer. The basis for the conclusion that high fevers "are more likely to be associated with pneumonia if they persist for 12 to 18 hours" is the comparison of the two groups of patients shown in the Table. (Incidentally, the word "higher" in both footnotes to
Downloaded From: http://archpedi.jamanetwork.com/ by a New York University User on 06/17/2015
that Table should read "high.") The 12- to 18-hour figure may be mis¬ leading. This is a maximum or "out¬ side" figure, since I was inclined to see any child whose high fever did not come down in a few hours. A few ex¬ ceptions were made if the mother was deemed to be a good observer and the child did not seem very ill to her. These few exceptions did not extend beyond 18 hours in any case, but for most patients the time between the reporting by phone of the high fever and the time the child was examined was three to six hours. This interval was simply a result of my habits of
practice (telephone hour, hospital rounds, clinic chores, etc). The natural history of many pneu¬ monias as compared with nasopharyngitis, for example, might lead one to expect
a
difference in the duration of
high fever in these two diseases, but this probably varies with the type of infection and with other epidemio¬ logie factors. Perhaps a larger study a
would also show a correlation with the duration (or recurrence) of high fever and such diagnoses as urinary tract infection, roseola infantum, cer¬ vical adenitis, and shigellosis, but I would be neither greatly surprised nor disappointed if it did not. Con¬ versely, there is probably a correla¬ tion between the brevity of a high fe¬ ver and the unimportance of the causative disease, but I know of no data to support this. Perhaps this is considered obvious and is so widely believed, whether true or not, that no one wants to spend the time in veri¬ fying it. WILLIAM A. TOMLINSON, MD Department of Pediatrics Children's Memorial Hospital 2300 Children's Plaza Chicago, IL 60614 The "Otitis-Prone" Condition
Sir.\p=m-\Onreading the article by Howie et al, which appeared in the June issue of the Journal (129:676,1975), we were impressed that the only reference to allergy was that its incidence in the children studied was no greater than in the other patients. This has certainly not been the impression in the Otology Clinic at Children's Hospital in Buffalo, NY. We have found that many of the children with chronic secretory otitis have allergies. The parents, however, are often unaware that the nasal symptoms that a child manifests are due to allergy and
Wernicke
Encephalopathy Following Prolonged Artificial Nutrition The necessity of vitamin supplementation during long-term artificial nutrition is well known. Nevertheless, it may be overlooked, particularly if the disorder causing the nutrition problems dominates the therapeutic measures. This was the situation in a case of Wernicke encephalopathy that developed after prolonged parenteral alimentation.
Comment.—Although Wernicke en¬ cephalopathy is associated with alco¬ holism, Wernicke pointed out in 1881 that it could appear after persisting vomiting.1 It has subsequently been reported in many different conditions involving defective nutrition.26 The role of thiamine deficiency was estab¬
Report of a Case.\p=m-\Thepatient is a 14\x=req-\ year-old boy, previously healthy, who was admitted to another hospital for treatment of esophageal aclasis. While the patient was undergoing therapeutic dilation with bougies, the abdominal part of the esophagus was accidentally perforated. The perforation was repaired and the boy was treated with antibiotics. During this time he was nourished only parenterally. After
companied by vomiting.7 Prolonged depletion leads to Wernicke encepha¬ lopathy characterized by various types of oculumotor palsies, nystag¬ mus, ataxia, tremor, disturbed con¬ sciousness varying from coma to mild confusion,8 and impaired vestibular
four weeks he became febrile and somnolent. Laboratory investigation disclosed severe acidosis (base excess, \m=-\12.5) and a low serum sodium level (124 mEq/liter). After glucose infusion and correction of the acid\x=req-\ base and electrolyte disturbances, there was transient improvement, but his condition soon deteriorated, and he had a brief epileptic seizure. On admittance to our hospital, the boy was somnolent, and exhibited paralysis of horizontal gaze and vertical nystagmus. The muscle reflexes were exaggerated; Babinski sign was absent. His voice was hoarse and his speech of a staccato type. The cerebrospinal fluid contained no bac¬ teria and no blood cells; total protein level was 66 mg/100 ml. Brain scanning and echoencephalography gave normal results. Conduction velocity of peripheral nerves was normal. The electroencephalogram showed a marked increase of slow waves. Parenteral nutrition was continued and the usual vitamin supplements were given. The neurological findings were first in¬ terpreted as due to a brain stem lesion caused by a septic embolus. It was then recognized that in several respects the con¬ dition fitted well with Wernicke disease. Checking of the patient's previous hospital record revealed that no vitamin supple¬ ments had been given during the month he had been totally deprived of perorai food intake. On the third day after admission, thiamine hydrochloride treatment was started; 20 mg/day for the first four days, 50 mg/day the following week. Two days later, there was a marked im¬ provement in the level of consciousness and in eye mobility. After one week the pa¬ tient could be mobilized. A transitory de¬ crease of the vestibular function and a slowly regressing ataxia were noted. The EEG gradually became normal. When he left the children's hospital after three weeks (for further treatment of the esoph¬ ageal aclasis) he had a slightly broad-
lished in the late 1930s.1 The earliest symptom of thiamine deficiency is anorexia sometimes ac¬
function.9 Cardiac symptoms in thiamine deficiency are seen almost entirely in infantile beriberi10; only two cases are on record with both car¬ diac and cerebral signs of thiamine deficiency.311 The cardiopathy in juvenile beriberi, and the polyneuropathy in that disease as well as in cases of Wernicke disease in alco¬ holics, are considered to have multifactorial origins.110 The clinical pic¬ ture in the present case—decreased consciousness, horizontal gaze palsy, nystagmus, and ataxia—thus fits well into the picture of Wernicke encepha¬
lopathy. The rapid improvement after vita¬ min supplementation is well in agree¬ ment with what would be expected in Wernicke encephalopathy. An im¬ provement has sometimes been
already within
seen
few hours after the start of thiamine treatment.1 The eye symptoms disappear first and usually completely. The ataxia regresses more slowly and not always com¬ a
pletely.
The present case stresses the need for vitamin supplementation in total parenteral alimentation. G\l=o"\staBLENNOW, MD Department of Pediatrics
University Hospital
S-221 85 Lund, Sweden M, Adams RD, Collins GH: The Wernicke-Korsakoff Syndrome. Oxford, England, Blackwell Scientific Publications, 1971. 1. Victor
2. Guerrero RM: Wernicke's syndrome due to vitamin B deficiency: Report of the disease in two infants. Am J Dis Child 78:88-96, 1949. 3. Davis RA, Wolf A: Infantile beriberi associated with Wernicke's encephalopathy. Pediatrics 3:409-420, 1958. 4. Cochrane WA, Collins-Williams C, Donohue WL: Superior hemorrhagic polioencephalitis (Wernicke's disease) occurring in an infant\p=m-\
Downloaded From: http://archpedi.jamanetwork.com/ by a New York University User on 06/17/2015
probably
due to thiamine deficiency from use of soya bean product. Pediatrics 28:771-777,1961. 5. Lopez RJ, Collins GH: Wernicke's encephalopathy: A complication of chronic hemodialysis. Arch Neurol 18:248-259, 1968. 6. Shah N, Wolff JA: Thiamine deficiency: Probable Wernicke's encephalopathy successfully treated in a child with acute lymphocytic leukemia. Pediatrics 51:750, 1973. 7. Guthrie HA: Introductory Nutrition. St Louis, CV Mosby Co, 1967, p 234. 8. Merritt HH: A Textbook of Neurology. Philadelphia, Lea & Febiger, 1967, p 653. 9. Ghez C: Vestibular paresis: A clinical feature of Wernicke's disease. J Neurol Neurosurg Psychiatry 32:134-139, 1969. 10. De Silva CC, Baptist NG: Tropical Nutritional Disorders of Infants and Children. Springfield, Ill, Charles C Thomas Publisher, 1969, p 117. 11. Cavazzuti GB, Gobbi U, Gullotta F, et al: Wernicke's encephalopathy in a child with congenital cardiomegaly. Helv Paediatr Acta 28:559-568, 1973. a
Seat Belt Buckle Burn
Seat belts and other child restrain-
ing devices remain underutilized immunizing agents that could greatly reduce the morbidity and mortality of automobile accidents. On rare occasions, they cause injury, and this report describes one such unusual case.
Report of a Case.\p=m-\A2\m=1/2\-year-oldgirl strapped in an adult seat belt in the middle front seat. Although her mother normally used a child safety harness in the
was
seat, the car was filled with adults and other children she was taking home. The car had been parked in the summer sun for several hours with the windows closed. As the mother fastened the belt around her daughter, the child cried and the mother noticed some reddening of the skin where it was in direct contact with the undersurface of the buckle. Only when arriving home did she notice the burns, which later vesiculated. The Figure shows three parallel second-degree burns on the right lower quadrant of the abdomen. The largest one, closest to the umbilicus, is the suspected initial position of the buckle. Apparently, the others were caused as the belt was tightened and the heat from the buckle dissipated. Three parallel scars remain. rear
Comment.—When exposed to the portions of seat belts become noticeably hot to adults. How¬ ever, they can cause thermal burns in sun, the metal
young children when in direct skin contact, as in this case. Burns can be produced experimentally by brief contact with a surface temperature of 70 C.1 Thus, the surface temperature of the underside of the buckle could be estimated to be around 70 C. Although a rare hazard, this injury could be prevented by covering or pushing the metal portions of seat belts under the seat back when park¬ ing in the hot sun. Newer cars with self-retracting belts and covered buckles should be less likely to cause this type of injury. Preferably, infants and young chil¬ dren should use special restraining devices, because of their body devel¬ opment and higher center of gravity. Several such restraints have been tested under simulated crash condi¬ tions and can be recommended to par¬ ents.2 However, some of the child safety chairs have a five-point har¬ ness system, with metal buckle parts that may be in contact with the child's thighs if he or she is wearing shorts. These parts could cause a burn similar to that reported here, and par¬ ents should check the buckles to make sure they are not too hot before fas¬ tening· them around the child. EDWARD W. SAITZ, MD Western Pennsylvania Regional Medical Program University of Pittsburgh 4200 Fifth Ave Pittsburgh, PA 15260 1. Moritz AR, Henriques FC Jr: Studies of thermal injury: II. The relative importance of time and surface temperature in the causation of cutaneous burns. Am J Pathol 23:695-720, 1947. 2. Shelness A, Charles C: Children as passengers in automobiles: The neglected minority on the nation's highways. Pediatrics: 56:271-284, 1975.
High
Fever
Sir.\p=m-\Inthe June 1975 issue of the Journal (129:693, 1975), I believe Dr Tomlinson has missed the point of the mothers' question, "aren't high fevers always serious?" What mothers are really asking is, "aren't high fevers
always harmful?"
A great many mothers (and some physicians) are concerned about high fevers because of their erroneous belief that the high fever in itself is harmful: "it can cook the brain," "it can damage the body," "it always causes convulsions." Too often we find mothers (and some physicians) vigorously and overzealously treating the temperature elevation and overlooking the cause of the fe-
iatrogenic anachronism left from the days when treatment of fever was the physician's main stock-in-trade. "Treat the child, not the thermometer" is advice we often ver—an over
give to apprehensive parents, empha¬ sizing that it is the underlying condi¬ tion that could be harmful and
re¬
quires treatment. The degree of fever
does not correlate with the serious¬ ness of the illness. It is not clear to me also why the author considers temperature eleva¬ tions to 40 C in the office or hospital to be more significant than a tempera¬ ture of 40 C noted by the mother at home. Further, I could not find confir¬ mation in the article itself for the conclusion that high fevers are "more likely to be associated with pneu¬ monia if they persist for 12 to 18 hours." I wonder if this has been the experience of others? In his conclusion, the author also states that "high fevers are some¬ times serious." I suspect that what he really means is that the cause of high fever and not the fever itself can sometimes (and sometimes not) be se¬ rious. With that modification of his conclusion I think we can all aeree. H. WILLIAM FINK, MD Department of Pediatrics Eastern Virginia Medical School 358 Mombray Arch Norfolk, VA 23501
In Reply.\p=m-\Iappreciate Dr Fink's careful reading and thoughtful comments on my article, "High Fever." I agree with everything Dr Fink says in his first paragraph (except for the phrase, "Dr Tomlinson has missed the point. .."!), and I agree with his last paragraph as well. Most practicing pediatricians have spent hundreds or thousands of hours trying to correct the erroneous beliefs Dr Fink mentions. In regard to Dr Fink's second paragraph, I did not mean to imply that high fever in the office or in the hospital is more significant than the same degree of fever in the home. But (I hope) its existence is more certain if a trained medical observer has read the thermometer. The basis for the conclusion that high fevers "are more likely to be associated with pneumonia if they persist for 12 to 18 hours" is the comparison of the two groups of patients shown in the Table. (Incidentally, the word "higher" in both footnotes to
Downloaded From: http://archpedi.jamanetwork.com/ by a New York University User on 06/17/2015
that Table should read "high.") The 12- to 18-hour figure may be mis¬ leading. This is a maximum or "out¬ side" figure, since I was inclined to see any child whose high fever did not come down in a few hours. A few ex¬ ceptions were made if the mother was deemed to be a good observer and the child did not seem very ill to her. These few exceptions did not extend beyond 18 hours in any case, but for most patients the time between the reporting by phone of the high fever and the time the child was examined was three to six hours. This interval was simply a result of my habits of
practice (telephone hour, hospital rounds, clinic chores, etc). The natural history of many pneu¬ monias as compared with nasopharyngitis, for example, might lead one to expect
a
difference in the duration of
high fever in these two diseases, but this probably varies with the type of infection and with other epidemio¬ logie factors. Perhaps a larger study a
would also show a correlation with the duration (or recurrence) of high fever and such diagnoses as urinary tract infection, roseola infantum, cer¬ vical adenitis, and shigellosis, but I would be neither greatly surprised nor disappointed if it did not. Con¬ versely, there is probably a correla¬ tion between the brevity of a high fe¬ ver and the unimportance of the causative disease, but I know of no data to support this. Perhaps this is considered obvious and is so widely believed, whether true or not, that no one wants to spend the time in veri¬ fying it. WILLIAM A. TOMLINSON, MD Department of Pediatrics Children's Memorial Hospital 2300 Children's Plaza Chicago, IL 60614 The "Otitis-Prone" Condition
Sir.\p=m-\Onreading the article by Howie et al, which appeared in the June issue of the Journal (129:676,1975), we were impressed that the only reference to allergy was that its incidence in the children studied was no greater than in the other patients. This has certainly not been the impression in the Otology Clinic at Children's Hospital in Buffalo, NY. We have found that many of the children with chronic secretory otitis have allergies. The parents, however, are often unaware that the nasal symptoms that a child manifests are due to allergy and
