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OBJECTIVE: To evaluate the endothelial cell loss and central corneal thickness in modified Blumenthal technique of MSICS and Phacoemulsification. METHOD: A prospective study in which 50 cases of nuclear sclerosis grade III (LOCS III) or more were randomized in two groups of 25 each. Group A underwent modified Blumenthal MSICS. Lens expression was facilitated by viscoelastic injection through ACM and scleral pressure by iris repositor. Group B underwent 2.8 mm phacoemulsification. Specular microscopy and pachymetry were done at 1(st) POD, 1(st), 3rd and 6th week. RESULTS: No significant difference in endothelial cell loss and central corneal thickness between group A and group B (p > 0.05) was found. CONCLUSION: This technique of MSICS is not inferior, an innovative, safe and highly effective in hard cataracts.

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Although acute compartment syndrome is considered a surgical emergency, controversies exist regarding diagnosis, surgical indications, and techniques of management. Acute compartment syndrome is associated with numerous causes, including fractures, crush injuries, burns, soft tissue injuries, and vascular trauma. Prolonged positioning of an extremity has not been previously described as a cause of compartment syndrome. The authors present a case of an acute compartment syndrome occurring because of prolonged extrication after a motor vehicle accident and without direct trauma to the involved extremity.

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In a series of 61 infants who had congenital diaphragmatic hernia (CDH) treated at our center from 1978 through 1996, 37 of 59 (61%) survived the perioperative period with two infants lost to follow-up. Nine (47%) of 19 infants survived before the introduction of extracorporeal membrane oxygenation (ECMO) into our region in 1986. Since 1986, 28 (70%) of 40 infants survived. Eighteen infants required ECMO, and 12 (75%) survived. A chart review was performed to determine whether infants surviving CDH are suffering from delays in neurological development, and, if so, whether this is attributable to ECMO. Of 12 ECMO survivors, 8 (67%) exhibited functional or anatomic evidence for neurological delay. Of 21 non-ECMO survivors, where adequate follow-up was available to make an assessment of neurological development, five (24%) exhibited evidence for delay. This difference was significant (P < .05, Fisher's Exact test). Of these five infants, three were premature, and one had DiGeorge syndrome. More ECMO survivors required diaphragmatic (67%) and abdominal (67%) patches at the time of diaphragmatic repair than non-ECMO survivors (4% and 12%, respectively; P < .05, Fisher's Exact test). In addition, more ECMO survivors required gastrostomy tube placement for feeding (50%) than non-ECMO survivors (16%; P < .05, Fisher's Exact test). A greater need for Nissen fundoplication in ECMO survivors (42%) than in non-ECMO survivors (12%) approached significance (P = .05, Fisher's Exact test). There were trends toward higher 1 and 5 minute APGAR scores and initial and best preoperative P(O2) in the non-ECMO survivors. A comparison between ECMO survivors who exhibited evidence of neurological delay with those who did not showed no differences in duration of ECMO, incidence of intracranial complications during ECMO, need for gastrostomy tube feeding or Nissen fundoplication, or incidence of carotid artery repair between the two groups. Infants surviving CDH who require ECMO have a greater incidence of neurological delay than those who do not. This is likely because of severity of the presenting illness as reflected by a greater need for diaphragmatic and abdominal patches during diaphragmatic repair, the need for Nissen fundoplication and gastrostomy tube feeding, and a trend toward poor APGAR scores and best preoperative P(O2) levels in these patients. However, there may be characteristics of ECMO, as yet unidentified, that may contribute to this outcome.

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BACKGROUND: Congenital diaphragmatic hernia continues to be a difficult management problem. Essentially all information on the condition has been compiled in a retrospective manner due to the individualized care that each infant must undergo. We contribute a review of our patients to add to the current fund of knowledge and to assess our experience before and since the introduction of extracorporeal membrane oxygenation in our institution. METHODS: This is a review of records of infants with congenital diaphragmatic hernia treated from 1978 through 1994. Repair has generally been accomplished early with only one repair being accomplished with an infant placed on extracorporeal membrane oxygenation preoperatively. RESULTS: Overall survival was 63%. Survival was 42% before extracorporeal membrane oxygenation becoming available in our region in 1986, and 75% afterward. Since 1986, 16 of 33 (48%) infants have required extracorporeal membrane oxygenation and 73% have survived. CONCLUSIONS: Overall survival in our series is comparable with that of other reported series. There appears to be an improvement in survival since the introduction of extracorporeal membrane oxygenation. Our present practice of early repair, and postrepair extracorporeal membrane oxygenation if needed, results in a survival rate comparable with that of currently available series reports regardless of the method of treatment reported.

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The mean age of 80 kala-azar cases was 20. 26 +/- 10.68 years, much higher than previously reported. This higher age incidence is probably related to fall of herd immunity particularly in the young adults resulting from less chance of natural infection during their childhood at such times when kala-azar in India had been largely controlled.

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The multicopy mini-exon-derived RNA (med RNA) locus of Leishmania donovani was enzymatically amplified by the polymerase chain reaction (PCR). The major 180 bp PCR product contained conserved med RNA gene sequences flanking the variable intergenic spacer from the med RNA gene tandem repeat. The oligonucleotide primers cross-reacted with other Leishmania species. In serial dilution experiments, positivity in the PCR assay was observed down to the genomic DNA equivalent of less than a single Leishmania cell. When the major PCR products from Indian L. donovani isolates were cloned and used as probes in dot hybridization analyses, they discriminated between L. donovani and L. amazonensis, L. major and L. infantum under high stringency conditions. DNA from spleen biopsies and blood samples of confirmed kala azar patients was positive, as were two skin biopsies from patients with post-kala azar dermal leishmaniasis (PKDL). These observations demonstrate that PCR amplification of med RNA intergenic spacers is sufficiently sensitive for clinical diagnosis of kala azar and PKDL, and furthermore, that cloned intergenic spacer probes may be useful for identification and classification of L. donovani.

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Indian kala-azar patients have normal numbers of peripheral blood NK cells but impaired functional activity due to decreased binding and lysis of target cells. This impairment of NK activity could not be corrected by exogenous recombinant human alpha or gamma interferon. However, recombinant human interleukin 2 was able to restore this activity by augmenting conjugate formation and lysis of target cells.

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Following sequence analysis of a Leishmania donovani kinetoplast DNA (kDNA) minicircle, we have developed synthetic oligonucleotides for use in the polymerase chain reaction (PCR). With these primers, we have amplified L. donovani kDNA from splenic aspirates and blood samples taken from kala-azar patients. Treatment of the samples for PCR requires only limited DNA purification by lysis in SDS, digestion with proteinase K, phenol extraction and ethanol precipitation of the resulting nucleic acid. We have obtained amplified product routinely with DNA prepared from the equivalent of 2.5-25 microliters of splenic aspirate or of 50-500 microliters of blood from infected patients. In dilution experiments a visible product has been obtained on amplification of DNA from the equivalent of 2.5 x 10(-7) microliters of splenic material. We therefore propose the amplification of L. donovani kDNA by PCR as a rapid and highly sensitive method for the diagnosis of kala-azar.

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