patient is exaggerated. The moth¬ showed a prolonged TSH response. With substitution therapy the thyroid
our er
enlargement slowly disappeared. Thy¬ roid dysfunction in the newborn after lithium therapy of the mother during pregnancy seems to be a rare compli¬ cation. However, lithium therapy should
be
avoided
in
pregnant
women.
PER W. NARS, MD J\l=U"\RGGIRARD, MD University Children's CH-4005 Basel, Switzerland
Hospital
A, Eskjaer JS, Olsen T: Occurrence of goiter during lithium treatment. Br Med J 3:710, 1968. 2. Lepp\l=a"\luotoJ, M\l=a"\nnist\l=o"\PT, Virkkunen P: On the mechanism of goitre formation during 1. Amdisen
lithium treatment in the rat. Acta Endocrinol 74:296-306, 1973. 3. Berens SC, Bernstein RS, Robbins J, et al: Antithyroid effects of lithium. J Clin Invest
49:1357-1367, 1970.
4. Fries H: Lithium in pregnancy. Lancet
1:1233, 1970.
5. Wright TL, Hoffmann LH, Davies J: Lithium teratogenicity. Lancet 2:876, 1970. 6. Bennie EH, Lazarus JH: Lithium-induced
thyroid dysfunction. Lancet 2:44-45, 1972. 7. Burrow GN, Burke WR, Himmelhoch JM, et al: Effect of lithium on thyroid function. J Clin Endocrinol Metab 32:647-652, 1971. 8. Kirkegaard C, Birk LU, Nerup J: Lithium and the thyroid. Lancet 2:1210, 1973. 9. Wilbanks GD, Bressler B, Peete CH, et al: Toxic effects of lithium carbonate in a mother and newborn infant. JAMA 213:865-867, 1970. 10. Tunnessen WW, Herzt CG: Toxic effects of lithium in newborn infants: A commentary. J Pediatr 81:804-807, 1972. 11. Schou M, Amdisen A: Lithium in pregnancy. Lancet 1:1391, 1970. 12. Lemarchand-B\l=e'\raudT, Gemazzani AR, Bagnoli F, et al: Thyroid function in the premature and the full term newborn. Acta endocrinol 70:445-453, 1972. 13. Brock Jacobsen B, Andersen H, DigePetersen H, et al: Thyrotropin response to thyrotropin-releasing hormone in fullterm, euthyroid and hypothyroid newborns. Acta Paediatr Scand 65:433-438, 1976.
Tetany and Renal Failure Chemotherapy in Acute Lymphocytic Leukemia
Hyperuricemia
Prior to
and hypocalcemia metabolic complications occurring during induction of remission in acute lymphocytic leukemia (ALL) especially in patients with a large mediastinal mass, high WBC count, and massive organomegaly. Recently, we encountered a girl with ALL who developed tetany and renal failure prior to any chemotherapy. To our knowledge, there is no previous are common
report of tetany prior
to chemotherafor of ALL. treatment py
Report of a Case.\p=m-\A13-year-old girl developed nasal bleeding, easy bruising, malaise, and mild fever about one week prior to admission. On admission, she had a temperature of 39.4 C, a pulse rate of 140 beats per minute, respirations 28 per min, and blood pressure of 98/50 mm Hg. She was alert, but restless. Extensive petechiae and bruises were noted. Liver and spleen were felt 4 and 3 cm below their respective costal margins, but no lymphadenopathy noted. Fundi were normal. Both Chvostek's and Trousseau's signs were
was
negative. The hemoglobin level was 7.5 gm/100 ml;
WBC count, 217,000/cu mm with 84% lymphoblasts; and platelets, 25,000/eu mm. Roentgenogram of the chest showed a large anterior mediastinal mass. Bone marrow examination revealed replacement by lymphoblasts. Intravenously adminis¬ tered fluid, antibiotics (gentamicin sulfate and carbenicillin disodium) and allopurinol were given. Only 5 ml of grossly bloody urine was passed during the initial five hours. Blood chemistry values were as follows: uric acid, 46 mg/100 ml; BUN, 49 mg/100 ml; calcium, 6.6 mg/100 ml; phos¬
phorus, 6.8 mg/100 ml; creatinine, 2.6 mg/ 100 ml; total protein, 5.6 gm/100 ml; and albumin, 3.1 gm/100 ml. Six hours after admission she developed an attack of tetany with trismus that was only partially relieved by intravenous infusion of calcium chloride. Apnea and cardiac arrest ensued and the patient died 7.5 hours after admis¬ sion. No autopsy was permitted. Two blood cultures grew Diplococcus pneumoniae. Cell surface marker studies of peripheral WBCs performed according to Jondal et al1 and Pernis et al2 showed only 2% of the
mononuclear cells had surface immuno-
globulin, while 79% had receptors for three or more sheep erythrocytes (E-rosette formation) indicating thymus-derived lym¬ phocyte origin of the lymphoblasts. The
cortisol levels obtained at 10 am and 720 µg/l and 840 µg/l, respec¬ tively, by the radioimmunoassay method of Foster and Dunn (normal range, 70 to 270 µg/liter at 9 am). serum
2
pm were
'
Comment.—Hypocalcemia is usually as a late complication or in patients undergoing remission induc¬ tion chemotherapy.4-5 This patient had no chemotherapy, but still developed severe hyperuricemia and hypocal¬ cemia leading to renal failure and tetany. The mechanism of hypocal¬
but also at 2 PM. With such high cortisol levels and abolition of the regular diurnal decrease in the after¬ noon, the patient most likely secreted a large amount of endogenous corticosteroid. Since response to corticosteroid is frequently very dramatic, massive lysis of leukemic cells may have occurred, with subsequent devel¬ opment of hyperuricemia. Because the patient was anurie and there was no
am
hyperphosphatemia, hypocalcemia could not be explained simply as a consequence of massive cell lysis. The mechanism of hypocalcemia remains unclear. From the study of Jaffe et al,5 renal failure, sepsis, corticosteroid, or hormonal dysfunction may all contrib¬ ute to the development of hypocal¬ cemia.
JEN-YIH CHU, MD, PHD DENNIS M. O'CONNOR, MD STANFORD T. ROODMAN, PHD RICHARD C. AHRENS, MD Department of Pediatrics and Pathology St Louis University School of Medicine, and Cardinal Glennon Memorial Hospital for Children 1465 S Grand Blvd St Louis, MO 63104 Helen Gagen gave laboratory assistance, and Catherine Camp gave secretarial assistance. 1. Jondal M, Holm G, Wigzell H: Surface markers on human T and B lymphocytes. J Exp Med 136:207-215, 1972. 2. Pernis B, Forni L, Amante L: Immunoglobulin spots on the surface of rabbit lymphocytes. J Exp Med 132:1001-1018, 1970. 3. Foster LB, Dunn RT: Single-antibody technique for radioimmunoassay of cortisol in unextracted serum or plasma. Clin Chem 20:365\x=req-\ 368, 1974. 4. Zusman J, Brown DM, Nesbit ME: Hyperphosphatemia, hyperphosphaturia and hypocalcemia in acute lymphoblastic leukemia. N Engl J Med 289:1335-1340, 1973. 5. Jaffe N, Paed D, Kim BS, et al: Hypocalcemia\p=m-\acomplication of childhood leukemia. Cancer 29:392-398, 1972.
seen
cemia is still not well understood. Some believe that the high phosphate load liberated from leukemic cells during chemotherapy is the cause,1 while others consider renal shutdown also responsible.5 Serum cortisol levels in our patient were markedly elevated not only at 10
Downloaded From: http://archpedi.jamanetwork.com/ by a New York University User on 06/05/2015
Cervical Lymphadenitis Caused by Haemophilus influenzae Type B We report a case of cervical
lymphadenitis caused by Haemophilus influenzae type b, an organism with a steadily increasing prevalence in childhood infections.
Report of a Case.\p=m-\A4-year-old boy was admitted to Colorado General Hospital on Sept 24,1976. He had been seen on Sept 20, 1976 because of complaints of pharyngitis and mild right-sided cervical adenitis. He was
prescribed
a
penicillin pending
a
throat culture; the medication was discontinued after three doses when the culture proved negative for group A \g=b\-hemolytic streptococcus. In the meantime, all his symptoms had abated. On Sept 23,1976, the right-sided swelling reappeared and spread to the left side. He was seen again and hospitalized. Physical examination showed him to be a distressed, obviously ill child. His rectal temperature was 38.7 C. He had three by five centimeter nonindurated, erythematous nodes in both anterior cervical regions. There were no other important physical findings. The WBC count was 18,500 cu mm with 40% segmented neutrophils and 41% band cell forms. Saline injection and aspiration of the right node yielded a few drops of fluid that were divided between a supplemented peptone broth tube and a chocolate agar plate. Blood cultures were obtained and he was given treatment with intravenous sodium penicillin G, 50,000 units/kg/day and oxacillin sodium, 100 mg/kg/day. À Tine test subsequently proved negative. He rapidly defervesced and appeared more comfortable. On Sept 25, 1976, a pure culture of Haemophilus influenzae type b grew on the chocolate agar; all other cultures were negative. Therapy was changed to intravenous ampicillin sodium, 150 mg/kg/day for a total of 72 hours followed by oral ampicillin for seven more days. He was discharged from the hospital on Sept 28, 1976 with greatly diminished swelling, which subsequently resolved com¬
pletely.
Comment—Haemophilus influen¬ is not usually discussed as a cause of cervical lymphadenitis. Powers and
the etiologic agent in lymphadenitis may necessi¬ use of penicillinase-resistant penicillin or cephalosporin as initial therapy for this disease.2 In addition, the use of techniques to recover anaer¬ obic bacteria has been emphasized.2-7 However, H influenzae type b may also be an important pathogen, and it is logical to look for it, using appro¬ priate media, when a lymph node is to be aspirated. aureus
as
cervical tate the
JACK MARK FISHAUT, MD STEFAN T. MOKROHISKY, MD
Department of Pediatrics, C 227 University of Colorado Medical Center
4200 E Ninth Ave Denver, CO 80262 1. Powers GF, Boisvert PL: Age as a factor in streptococcosis. J Pediatr 25:481-504, 1944. 2. Barton LL, Feigin RD: Childhood cervical lymphadenitis: A reappraisal. J Pediatr 84:846\x=req-\
852, 1974. 3. Dajani AS, Garcia RE, Wolinsky E: Etiology
of cervical lymphadenitis in children. N Engl J Med 268:1329-1333, 1963. 4. Smith EWP, Haynes RE: Changing incidence of Haemophilus influenzae meningitis. Pediatrics 50:723-727, 1972. 5. Todd JK, Bruhn FW: Severe Haemophilus influenzae infections: Spectrum of disease. Am J Dis Child 129:607-611, 1975. 6. Garrod LP, O'Grady F: Antibiotic and Chemotherapy, ed 3. Baltimore, Williams & Wilkins Co, 1971, p 267. 7. Bradford BJ, Plotkin SA: Cervical adenitis caused by anaerobic bacteria. J Pediatr 88:1060, 1976.
Acute Leukemia With Heart Block
Complete
Arrhythmias directly attributable
to the leukemic process per
Comment.—The relevant autopsy were an extensive infiltra¬ tion of the atria as well as ventricles with leukemic cells, and gross enlarge¬ ment of the heart. It is believed that this case of acute leukemia with complete heart block would be of considerable interest to other workers. SURAJ GUPTE, MD Department of Pediatrics Government Medical College and Associated Hospitals Jammu 180 001, Kashmir, India
findings
zae
Boisvert1 never recovered this orga¬ nism. Barton and Feigin,2 although including thioglycolate broth and anaerobic media, did not use chocolate agar; 15% of their cultures of aspi¬ rated nodes were negative. Only Dajani and co-workers3 cultured rou¬ tinely on this medium but did not recover H influenzae. Their study antedates the rise in the incidence of infections due to H influenzae*; there¬ fore it is not surprising that cervical lymphadenitis should now be included among the many illnesses caused by this organism.5 Haemophilus influenzae infections are best treated with ampicillin or chloramphenicol, but this organism is often sensitive to obtainable serum levels of penicillin G." Thus, it is not unexpected that this patient's lym¬ phadenitis seemed to respond to the initial oral penicillin, nor that other infections due to H influenzae some¬ times are cured by this drug. Some authors believe that the increased frequency of Staphylococcus
costal margin and was tender. Mild pedal edema was present. Bilateral hemorrhages were also present. Laboratory investigations showed the following levels: hemoglobin, 3.5 gm/100 ml; total WBC count, 12,000/cu mm; lymphocytes 66%; blast cells, 32% eosinophils, 2%; and only few platelets were seen. The bone marrow was full of primitive blast cells. A chest roentgenogram re¬ vealed an enlarged heart and an ECG showed atrial beats that were completely blocked. The patient died about six hours after hospitalization, while she was being treated symptomatically; antileukemic treatment with prednisone and mercaptopurine had just been initiated.
se are
unusual in pediatric practice.1.2 An extensive review of literature has revealed just one such case, reported by Habel in 1974.3 The present communication documents the occurrence of complete heart block in an 8-year-old girl under author's care at the Snowdon Hospital, Simla, India.
Report of a Case\p=m-\Thisyoung girl had a of severe epistaxis and progressively increasing respiratory difficulty. Physical examination revealed a well-nourished child (weight, 25.5 kg; height, 126 cm) with severe pallor and dyspnea. There were widespread petechial spots. Her pulse was irregular, with a rate
two-day history
of 56 beats per minute, and blood pressure was 90/50 mm Hg. The apex beat was displaced about 2 cm outside the midclavicular line and a soft systolic hemic murmur could be heard all over the precordium, with maximum intensity over the mitral area. The spleen was just palpable. The liver was palpable 4 cm below the right
Downloaded From: http://archpedi.jamanetwork.com/ by a New York University User on 06/05/2015
1. Roberts WC, Bodey GP, Wertlake PT: The heart in acute leukemia: A study of 420 autopsy cases. Am J Cardiol 21:388-412, 1968. 2. Gupte S: Newer horizons in pediatrics. Part III. Med Surg 13:36-45, 1973. 3. Habel A: Symptomatic disorders of cardiac conduction in childhood leukemia. Am J Dis Child 128:841-843, 1974.
Starch Eater's Anemia
Ferguson and Keaton1 reported that 39% of 361 pregnant women in rural Mississippi ate a varying amount of laundry starch. Merkatz2 described parotid enlargements in a 36-year-old black housewife from the ingestion of a full box of starch daily over the period of a year. Gastric obstruction and subsequent partial obstruction of a small bowel was described as due to the excessive ingestion of laundry starch.3 Severe hypochromic anemia has been observed in black women whose diets have consisted chiefly of corn starch as used for laundering clothes,4 and there is one report of anemia in a 16\x=req-\ month-old black boy.5 Starch-eating appears to be confined almost to black women (particularly during pregnancy). This particular dietary aberration is more common among blacks of the South. Report of a Case.\p=m-\A13-year-old black was brought to the Matthew Walker
girl
our er
enlargement slowly disappeared. Thy¬ roid dysfunction in the newborn after lithium therapy of the mother during pregnancy seems to be a rare compli¬ cation. However, lithium therapy should
be
avoided
in
pregnant
women.
PER W. NARS, MD J\l=U"\RGGIRARD, MD University Children's CH-4005 Basel, Switzerland
Hospital
A, Eskjaer JS, Olsen T: Occurrence of goiter during lithium treatment. Br Med J 3:710, 1968. 2. Lepp\l=a"\luotoJ, M\l=a"\nnist\l=o"\PT, Virkkunen P: On the mechanism of goitre formation during 1. Amdisen
lithium treatment in the rat. Acta Endocrinol 74:296-306, 1973. 3. Berens SC, Bernstein RS, Robbins J, et al: Antithyroid effects of lithium. J Clin Invest
49:1357-1367, 1970.
4. Fries H: Lithium in pregnancy. Lancet
1:1233, 1970.
5. Wright TL, Hoffmann LH, Davies J: Lithium teratogenicity. Lancet 2:876, 1970. 6. Bennie EH, Lazarus JH: Lithium-induced
thyroid dysfunction. Lancet 2:44-45, 1972. 7. Burrow GN, Burke WR, Himmelhoch JM, et al: Effect of lithium on thyroid function. J Clin Endocrinol Metab 32:647-652, 1971. 8. Kirkegaard C, Birk LU, Nerup J: Lithium and the thyroid. Lancet 2:1210, 1973. 9. Wilbanks GD, Bressler B, Peete CH, et al: Toxic effects of lithium carbonate in a mother and newborn infant. JAMA 213:865-867, 1970. 10. Tunnessen WW, Herzt CG: Toxic effects of lithium in newborn infants: A commentary. J Pediatr 81:804-807, 1972. 11. Schou M, Amdisen A: Lithium in pregnancy. Lancet 1:1391, 1970. 12. Lemarchand-B\l=e'\raudT, Gemazzani AR, Bagnoli F, et al: Thyroid function in the premature and the full term newborn. Acta endocrinol 70:445-453, 1972. 13. Brock Jacobsen B, Andersen H, DigePetersen H, et al: Thyrotropin response to thyrotropin-releasing hormone in fullterm, euthyroid and hypothyroid newborns. Acta Paediatr Scand 65:433-438, 1976.
Tetany and Renal Failure Chemotherapy in Acute Lymphocytic Leukemia
Hyperuricemia
Prior to
and hypocalcemia metabolic complications occurring during induction of remission in acute lymphocytic leukemia (ALL) especially in patients with a large mediastinal mass, high WBC count, and massive organomegaly. Recently, we encountered a girl with ALL who developed tetany and renal failure prior to any chemotherapy. To our knowledge, there is no previous are common
report of tetany prior
to chemotherafor of ALL. treatment py
Report of a Case.\p=m-\A13-year-old girl developed nasal bleeding, easy bruising, malaise, and mild fever about one week prior to admission. On admission, she had a temperature of 39.4 C, a pulse rate of 140 beats per minute, respirations 28 per min, and blood pressure of 98/50 mm Hg. She was alert, but restless. Extensive petechiae and bruises were noted. Liver and spleen were felt 4 and 3 cm below their respective costal margins, but no lymphadenopathy noted. Fundi were normal. Both Chvostek's and Trousseau's signs were
was
negative. The hemoglobin level was 7.5 gm/100 ml;
WBC count, 217,000/cu mm with 84% lymphoblasts; and platelets, 25,000/eu mm. Roentgenogram of the chest showed a large anterior mediastinal mass. Bone marrow examination revealed replacement by lymphoblasts. Intravenously adminis¬ tered fluid, antibiotics (gentamicin sulfate and carbenicillin disodium) and allopurinol were given. Only 5 ml of grossly bloody urine was passed during the initial five hours. Blood chemistry values were as follows: uric acid, 46 mg/100 ml; BUN, 49 mg/100 ml; calcium, 6.6 mg/100 ml; phos¬
phorus, 6.8 mg/100 ml; creatinine, 2.6 mg/ 100 ml; total protein, 5.6 gm/100 ml; and albumin, 3.1 gm/100 ml. Six hours after admission she developed an attack of tetany with trismus that was only partially relieved by intravenous infusion of calcium chloride. Apnea and cardiac arrest ensued and the patient died 7.5 hours after admis¬ sion. No autopsy was permitted. Two blood cultures grew Diplococcus pneumoniae. Cell surface marker studies of peripheral WBCs performed according to Jondal et al1 and Pernis et al2 showed only 2% of the
mononuclear cells had surface immuno-
globulin, while 79% had receptors for three or more sheep erythrocytes (E-rosette formation) indicating thymus-derived lym¬ phocyte origin of the lymphoblasts. The
cortisol levels obtained at 10 am and 720 µg/l and 840 µg/l, respec¬ tively, by the radioimmunoassay method of Foster and Dunn (normal range, 70 to 270 µg/liter at 9 am). serum
2
pm were
'
Comment.—Hypocalcemia is usually as a late complication or in patients undergoing remission induc¬ tion chemotherapy.4-5 This patient had no chemotherapy, but still developed severe hyperuricemia and hypocal¬ cemia leading to renal failure and tetany. The mechanism of hypocal¬
but also at 2 PM. With such high cortisol levels and abolition of the regular diurnal decrease in the after¬ noon, the patient most likely secreted a large amount of endogenous corticosteroid. Since response to corticosteroid is frequently very dramatic, massive lysis of leukemic cells may have occurred, with subsequent devel¬ opment of hyperuricemia. Because the patient was anurie and there was no
am
hyperphosphatemia, hypocalcemia could not be explained simply as a consequence of massive cell lysis. The mechanism of hypocalcemia remains unclear. From the study of Jaffe et al,5 renal failure, sepsis, corticosteroid, or hormonal dysfunction may all contrib¬ ute to the development of hypocal¬ cemia.
JEN-YIH CHU, MD, PHD DENNIS M. O'CONNOR, MD STANFORD T. ROODMAN, PHD RICHARD C. AHRENS, MD Department of Pediatrics and Pathology St Louis University School of Medicine, and Cardinal Glennon Memorial Hospital for Children 1465 S Grand Blvd St Louis, MO 63104 Helen Gagen gave laboratory assistance, and Catherine Camp gave secretarial assistance. 1. Jondal M, Holm G, Wigzell H: Surface markers on human T and B lymphocytes. J Exp Med 136:207-215, 1972. 2. Pernis B, Forni L, Amante L: Immunoglobulin spots on the surface of rabbit lymphocytes. J Exp Med 132:1001-1018, 1970. 3. Foster LB, Dunn RT: Single-antibody technique for radioimmunoassay of cortisol in unextracted serum or plasma. Clin Chem 20:365\x=req-\ 368, 1974. 4. Zusman J, Brown DM, Nesbit ME: Hyperphosphatemia, hyperphosphaturia and hypocalcemia in acute lymphoblastic leukemia. N Engl J Med 289:1335-1340, 1973. 5. Jaffe N, Paed D, Kim BS, et al: Hypocalcemia\p=m-\acomplication of childhood leukemia. Cancer 29:392-398, 1972.
seen
cemia is still not well understood. Some believe that the high phosphate load liberated from leukemic cells during chemotherapy is the cause,1 while others consider renal shutdown also responsible.5 Serum cortisol levels in our patient were markedly elevated not only at 10
Downloaded From: http://archpedi.jamanetwork.com/ by a New York University User on 06/05/2015
Cervical Lymphadenitis Caused by Haemophilus influenzae Type B We report a case of cervical
lymphadenitis caused by Haemophilus influenzae type b, an organism with a steadily increasing prevalence in childhood infections.
Report of a Case.\p=m-\A4-year-old boy was admitted to Colorado General Hospital on Sept 24,1976. He had been seen on Sept 20, 1976 because of complaints of pharyngitis and mild right-sided cervical adenitis. He was
prescribed
a
penicillin pending
a
throat culture; the medication was discontinued after three doses when the culture proved negative for group A \g=b\-hemolytic streptococcus. In the meantime, all his symptoms had abated. On Sept 23,1976, the right-sided swelling reappeared and spread to the left side. He was seen again and hospitalized. Physical examination showed him to be a distressed, obviously ill child. His rectal temperature was 38.7 C. He had three by five centimeter nonindurated, erythematous nodes in both anterior cervical regions. There were no other important physical findings. The WBC count was 18,500 cu mm with 40% segmented neutrophils and 41% band cell forms. Saline injection and aspiration of the right node yielded a few drops of fluid that were divided between a supplemented peptone broth tube and a chocolate agar plate. Blood cultures were obtained and he was given treatment with intravenous sodium penicillin G, 50,000 units/kg/day and oxacillin sodium, 100 mg/kg/day. À Tine test subsequently proved negative. He rapidly defervesced and appeared more comfortable. On Sept 25, 1976, a pure culture of Haemophilus influenzae type b grew on the chocolate agar; all other cultures were negative. Therapy was changed to intravenous ampicillin sodium, 150 mg/kg/day for a total of 72 hours followed by oral ampicillin for seven more days. He was discharged from the hospital on Sept 28, 1976 with greatly diminished swelling, which subsequently resolved com¬
pletely.
Comment—Haemophilus influen¬ is not usually discussed as a cause of cervical lymphadenitis. Powers and
the etiologic agent in lymphadenitis may necessi¬ use of penicillinase-resistant penicillin or cephalosporin as initial therapy for this disease.2 In addition, the use of techniques to recover anaer¬ obic bacteria has been emphasized.2-7 However, H influenzae type b may also be an important pathogen, and it is logical to look for it, using appro¬ priate media, when a lymph node is to be aspirated. aureus
as
cervical tate the
JACK MARK FISHAUT, MD STEFAN T. MOKROHISKY, MD
Department of Pediatrics, C 227 University of Colorado Medical Center
4200 E Ninth Ave Denver, CO 80262 1. Powers GF, Boisvert PL: Age as a factor in streptococcosis. J Pediatr 25:481-504, 1944. 2. Barton LL, Feigin RD: Childhood cervical lymphadenitis: A reappraisal. J Pediatr 84:846\x=req-\
852, 1974. 3. Dajani AS, Garcia RE, Wolinsky E: Etiology
of cervical lymphadenitis in children. N Engl J Med 268:1329-1333, 1963. 4. Smith EWP, Haynes RE: Changing incidence of Haemophilus influenzae meningitis. Pediatrics 50:723-727, 1972. 5. Todd JK, Bruhn FW: Severe Haemophilus influenzae infections: Spectrum of disease. Am J Dis Child 129:607-611, 1975. 6. Garrod LP, O'Grady F: Antibiotic and Chemotherapy, ed 3. Baltimore, Williams & Wilkins Co, 1971, p 267. 7. Bradford BJ, Plotkin SA: Cervical adenitis caused by anaerobic bacteria. J Pediatr 88:1060, 1976.
Acute Leukemia With Heart Block
Complete
Arrhythmias directly attributable
to the leukemic process per
Comment.—The relevant autopsy were an extensive infiltra¬ tion of the atria as well as ventricles with leukemic cells, and gross enlarge¬ ment of the heart. It is believed that this case of acute leukemia with complete heart block would be of considerable interest to other workers. SURAJ GUPTE, MD Department of Pediatrics Government Medical College and Associated Hospitals Jammu 180 001, Kashmir, India
findings
zae
Boisvert1 never recovered this orga¬ nism. Barton and Feigin,2 although including thioglycolate broth and anaerobic media, did not use chocolate agar; 15% of their cultures of aspi¬ rated nodes were negative. Only Dajani and co-workers3 cultured rou¬ tinely on this medium but did not recover H influenzae. Their study antedates the rise in the incidence of infections due to H influenzae*; there¬ fore it is not surprising that cervical lymphadenitis should now be included among the many illnesses caused by this organism.5 Haemophilus influenzae infections are best treated with ampicillin or chloramphenicol, but this organism is often sensitive to obtainable serum levels of penicillin G." Thus, it is not unexpected that this patient's lym¬ phadenitis seemed to respond to the initial oral penicillin, nor that other infections due to H influenzae some¬ times are cured by this drug. Some authors believe that the increased frequency of Staphylococcus
costal margin and was tender. Mild pedal edema was present. Bilateral hemorrhages were also present. Laboratory investigations showed the following levels: hemoglobin, 3.5 gm/100 ml; total WBC count, 12,000/cu mm; lymphocytes 66%; blast cells, 32% eosinophils, 2%; and only few platelets were seen. The bone marrow was full of primitive blast cells. A chest roentgenogram re¬ vealed an enlarged heart and an ECG showed atrial beats that were completely blocked. The patient died about six hours after hospitalization, while she was being treated symptomatically; antileukemic treatment with prednisone and mercaptopurine had just been initiated.
se are
unusual in pediatric practice.1.2 An extensive review of literature has revealed just one such case, reported by Habel in 1974.3 The present communication documents the occurrence of complete heart block in an 8-year-old girl under author's care at the Snowdon Hospital, Simla, India.
Report of a Case\p=m-\Thisyoung girl had a of severe epistaxis and progressively increasing respiratory difficulty. Physical examination revealed a well-nourished child (weight, 25.5 kg; height, 126 cm) with severe pallor and dyspnea. There were widespread petechial spots. Her pulse was irregular, with a rate
two-day history
of 56 beats per minute, and blood pressure was 90/50 mm Hg. The apex beat was displaced about 2 cm outside the midclavicular line and a soft systolic hemic murmur could be heard all over the precordium, with maximum intensity over the mitral area. The spleen was just palpable. The liver was palpable 4 cm below the right
Downloaded From: http://archpedi.jamanetwork.com/ by a New York University User on 06/05/2015
1. Roberts WC, Bodey GP, Wertlake PT: The heart in acute leukemia: A study of 420 autopsy cases. Am J Cardiol 21:388-412, 1968. 2. Gupte S: Newer horizons in pediatrics. Part III. Med Surg 13:36-45, 1973. 3. Habel A: Symptomatic disorders of cardiac conduction in childhood leukemia. Am J Dis Child 128:841-843, 1974.
Starch Eater's Anemia
Ferguson and Keaton1 reported that 39% of 361 pregnant women in rural Mississippi ate a varying amount of laundry starch. Merkatz2 described parotid enlargements in a 36-year-old black housewife from the ingestion of a full box of starch daily over the period of a year. Gastric obstruction and subsequent partial obstruction of a small bowel was described as due to the excessive ingestion of laundry starch.3 Severe hypochromic anemia has been observed in black women whose diets have consisted chiefly of corn starch as used for laundering clothes,4 and there is one report of anemia in a 16\x=req-\ month-old black boy.5 Starch-eating appears to be confined almost to black women (particularly during pregnancy). This particular dietary aberration is more common among blacks of the South. Report of a Case.\p=m-\A13-year-old black was brought to the Matthew Walker
girl
