LETTERS TO THE EDITOR electrophoresis and G6PD assay was also R.K. Mondal, normal. Methemoglobin assayed by S. Bandyapadhyay, spectroscopic method was 38% (normal Department of Pediatrics Medicine; <1%.). Erythrocyte NADH-dependent National Medical College, methemoglobin reductase level was low with 32, Gorachand Street, Kolkata 700 014, 30% of normal. HbM could not be estimated West Bengal, India. due to financial constraint. She was managed E-mail: [email protected] with oxygen inhalation, bronchodilator nebu- REFERENCES lisation, and oral antibiotics. The respiratory distress settled down after three days but 1. Lukens J. Methemoglobinemia and other cyanotic hue persisted even at discharge. She disorders accompanied by cyanosis. In: Lee GR, Foerster J, Lukens J, Paraskevas F, Greer was put on oral ascorbic acid and discharged. JP, Rodgers GM eds. Wintrobe’s Clinical Methemoglobin produces detectable Hematology. 10th Ed. Baltimore: Williams & Wilkins 1999; p. 1046-1055. cyanosis at concentration. Of 0.5 g/dL(1). In 1948 Horlein and Weber first described a 2. Mondal RK, Mann U, Sharma M. Cyanotic family of hereditary methemoglobinemia in Child-Can it be Methemoglobinemia? Indian J Pediatr 2002; 69: 989-990. Germany(l). Scott & Griffith in the following year described deficiency of NADH- 3. Kedar PS, Colah RB, Ghosh K, Mohanty D. cytochrome b5 reductase enzyme as the cause Congenital methemoglobinemia due to NADH-methemoglobin reductase deficiency of the disease(l). Our case is suffering from in three Indian families. Hematologia (Budap) hereditary methemoglobinemia (Type l) due 2002; 32: 543-549. to NADH-cytochrome b5 reductase defici- 4. Jaiswal RB, Khandelwal MK, Tiwaskar HV. ency. Hereditary methemoglobinemia patient Hereditary methaemoglobinaemia: case report generally maintains levels of methemoglobin of congenital cyanosis in a Rajput child. Indian between 15-30% of normal (1). Treatment is Pediatr 1968; 5: 226-229. rarely necessary except for cosmetic purpose 5. Mansouri A, Lurie AA. Concise review: or with coexisting G6PD deficiency causing Methemoglobinemia. Am J Hematol 1993; 42: superadded acquired methemoglobinemia(5). 7-12.

Meconeum Hydrocele Presenting only one case has been reported in the female as a Labial Mass neonate earlier ours being the second (1). A one-day-old female baby presented to us Meconeum peritonitis results from in utero at 7 hours after birth with a left labial mass of perforation of the bowel and subsequent 7 × 4 × 4 cm, soft, cystic, normal colour of spillage of meconeum into the peritoneal overlying stretched skin, no impulse on cavity. Meconeum hydrocele is caused by the crying, noncompressible, positive trans- free communication of the peritoneal space illumination in the upper 1/5th portion of the with the processus vaginalis during gestation. swelling and negative below that. The baby It has been reported often in male but passed stool and urine normally on first day of

INDIAN PEDIATRICS 1060 VOLUME 42__OCTOBER 17, 2005 LETTERS TO THE EDITOR life. On the second day of life, the swelling increased in size to 10 × 5 × 5 cm, turned yellowish in colour and there was impending perforation (Fig.1). The swelling ruptured spontaneously and the sloughed out skin was excised. The open cavity was dressed with povidone iodine and swelling never refilled. The baby passed stool normally. She was given intravenous antibiotics and discharged after 7 days. The wound healed up with granulation tissue. The baby is doing well at 3 months follow up. Fig. 1. Meconeum hydrocele of the . Meconeum peritonitis results from extrusion of sterile meconeum into the of the cases(5). The differential diagnosis of peritoneal cavity after fetal perforation. The meconeum hydrocele includes inguinal rich content of digestive enzymes of the hernia, ectopic ovary, labial lipoma, fibroma, meconeum leads to peritoneal irritation and leiomyoma or hemangioma, round ligament inflammatory response characterized by sarcoma, inguinal lymphadenopathy and foreign body granuloma formation and epidermal cyst(5). calcification. The majority of patients with meconeum peritonitis require surgical inter- If there is a labioscrotal swelling, this vention but many have spontaneous resolution remote possibility should always be kept by sealing of perforation. in mind otherwise it may lead to severe inflammation and spontaneous rupture. The processus vaginalis forms by 6 Shilpa Sharma, months of gestation as an evagination of A.N. Gangopadhyay, parietal and descends ventral to Department of Pediatric Surgery, the into or labium Institute of Medical Sciences, majus(2). In males, patency is maintained Banaras Hindu University, until birth or shortly thereafter with subse- Varanasi 221 005 (U.P.), India. quent proximal obliteration leaving the E-mail : [email protected] residual tunica vaginalis. REFERENCES In females, the processus vaginalis is small 1. Kizer JR, Bellah RD, Schnaufer L, Canning DA. and obliterated by 8 months of gestation. Meconium hydrocele in a female newborn: An Autopsy studies have proved that the female unusual cause of a labial mass. J Urol 1995; 153: gubernaculum or round ligament is different 188-190. from the male in ending just outside the 2. Moore KL, Persaud TVN. The developing external ring(3). If patency persists, hydro- Human: Clinically Oriented , 5th cele of the canal of Nuck has been described edn. Philadelphia: WB Saunders Co 1993; and ultrasound has been suggested as the best p. 294-300. mode of diagnosis(4). Delayed presentation 3. Attah AA, Hutson JM. The anatomy of the may lead to formation of infection. Associated female gubernaculums is different from the inguinal hernia has been reported in one-third male. Aust N Z J Surg 1991; 61: 380-384.

INDIAN PEDIATRICS 1061 VOLUME 42__OCTOBER 17, 2005 LETTERS TO THE EDITOR

4. Anderson CC, Broadie TA, Mackey JE, 5. Kucera PR, Glazer J. Hydrocele of the canal of Kopecky KK. Hydrocele of the canal of Nuck: Nuck. A report of four cases. J Repord. Med. Ultrasound appearance. Am Surg 1995; 61: 1985; 30: 439. 959-961.

What is Appropriate Post- immediate antibody-block to virus entry in Exposure Rabies Prophylaxis? fibroblasts, either in the first cycle itself or in subsequent cycles. Thus, virus entry into nerve endings is prevented, especially by the locally The report on rabies developing in a child injected immunoglobulin. Antibodies in body even after immunoprophylaxis has some fluids (from intramuscular injection) keep up lessons to teach us(1). Post-exposure prophy- this block. Active immunization ensures laxis consists of wound treatment and immuno- sustained high antibody levels. prophylaxis. In this child the wound should When the bite is at a site with sparse have been flushed with soap and water nerve endings (e.g., the leg), there is a window immediately after the bite. By taking the child period (of up to a few days) between the bite to the dispensary first aid was delayed, but even and virus entry into nerve endings. Only in then soap and water flushing should have such cases may active immunization alone preceded providone iodine application. Soap suffice. In the recommended vaccination disrupts rabies virus particles instantaneously schedule, antibody production would by dissolving the lipid coat, rendering them commence after the second dose, and will be non- infectious. Water disperses soap into the detectable by laboratory testing by day 7 wound and also mechanically removes un- (always before day 10). However, if the adsorbed virus particles. Since soap and water biting animal was rabid, passive immuniza- are available in every household, there should tion must be given irrespective of the site of be no delay in washing after animal bite. There bite. is actually no need of chemical treatment (which require longer contact time to kill virus) The window period is too short in case of after flushing with water and soap. bite on sites with high density of nerve endings (e.g., face, hand, genitalia), as in the reported Viruses deposited in the wound get child. Here, viruses may come directly into adsorbed on to local fibroblastic cells within a contact with nerve endings. Any delay, even of short period. Soap prevents virus adsorption or minutes, could make the difference between kills even adsorbed virus before cell entry. If life and death. In general, immune protection first aid was delayed or unsuccessful, then will not help once rabies virus has entered the virus enters and multiplies in the cells, and nerve cell. In the reported case there was huge numbers are released into the surrounding deficiency in first aid and delay in passive tissue. Eventually viruses meet with nerve immunization (of 6 hours). The fact that rabies endings and enter nerve cells. developed after a short incubation period (of 17 Each cell cycle of multiplication takes days) shows not only that virus travel to the several hours. Passive immunization provides brain was quick, but also that virus entered

INDIAN PEDIATRICS 1062 VOLUME 42__OCTOBER 17, 2005