Pregnancy in women with a history of Kawasaki disease: management and outcomes.

OBJECTIVE: To characterise the obstetrical management and outcomes in a series of women with a history of Kawasaki disease (KD) in childhood. DESIGN: Retrospective case series. SETTING: Tertiary healthcare setting in the USA. POPULATION: Women with a history of KD in childhood. METHODS: Women completed a detailed health questionnaire and participated in research imaging studies as part of the San Diego Adult KD Collaborative Study. MAIN OUTCOME MEASURES: Obstetrical management, complications during pregnancy and delivery, and infant outcomes. RESULTS: Ten women with a history of KD in childhood carried a total of 21 pregnancies to term. There were no cardiovascular complications during labour and delivery despite important cardiovascular abnormalities in four of the ten subjects. Pregnancy was complicated by pre-eclampsia and the post-partum course was complicated by haemorrhage in one subject each. Two of the 21 progeny subsequently developed KD. CONCLUSIONS: Women with important cardiovascular sequelae from KD in childhood should be managed by a team that includes both a maternal-fetal medicine specialist and a cardiologist. Pre-pregnancy counselling should include delineation of the woman's current functional and structural cardiovascular status and appropriate adjustment of medications, but excellent outcomes are possible with appropriate care. Review of the English and Japanese literature on KD and pregnancy revealed the occurrence of myocardial infarction during pregnancy in women with missed KD and aneurysms that were not diagnosed until their acute event. Our study highlights the need for counselling with regard to the increased genetic risk of KD in offspring born to these mothers.

Diagnostic value of ascitic fluid lactic dehydrogenase, protein, and WBC levels.

Three characteristics of an exudate, ie, an ascitic fluid lactic dehydrogenase (LDH) level of greater than 400 Sigma units (SU), an ascitic fluid-serum LDH ratio of greater than 0.6, and an ascitic fluid-serum protein ratio of greater than 0.5, were studied in a prospective fashion to determine their usefulness in the differential diagnosis of ascites. The ascitic fluid LDH level did not exceed 400 SU in any patient with uncomplicated chronic liver disease, whereas in patients with malignant, tuberculous, or pancreatic ascites it exceeded 500 SU in 12/19 patients. The finding of two of the three characteristics indicated a nonhepatic cause for the ascites whereas the absence of all three strongly suggested uncomplicated liver disease as the sole cause. The ascitic fluid WBC count was also useful in that values exceeded 500/cu mm in bacterial and tuberculous peritonitis whereas it was low (297 +/- 49/cu mm) in chronic liver disease.

Difference between human red blood cell Na+-Li+ countertransport and renal Na+-H+ exchange.

Several laboratories have reported that the activities of sodium-lithium countertransport are increased in red blood cells from patients with essential hypertension. Based on the many similarities between this transport system and the renal sodium-proton exchanger, a hypothesis has been put forth in the literature that increased red blood cell sodium-lithium countertransport activity may be a marker for increased sodium-proton exchange activity in the renal proximal tubule. The present studies were designed to test the hypothesis that sodium-lithium countertransport in red blood cells from humans or rabbits is mediated by the same transport mechanism that mediates sodium-proton exchange in the renal brush border from those species. Similar to what has been reported for the rabbit, the present studies show that an amiloride-sensitive sodium-proton exchanger is present in human renal brush border vesicles. However, Na+-Li+ countertransport in human and rabbit red blood cells, assayed under several different conditions, was not inhibited by amiloride. In agreement with what has been reported for humans, the present studies show that extracellular proton-stimulated sodium efflux is inhibited by amiloride in rabbit red blood cells. These data demonstrate a difference (amiloride sensitivity) between the red blood cell sodium-lithium countertransporter and the renal brush border sodium-proton exchanger in humans and rabbits. These experiments detract from the hypothesis that increased red blood cell sodium-lithium countertransport activity in patients with essential hypertension is a marker for increased sodium-proton exchange activity in the renal brush border.

Insulin inhibits migration of vascular smooth muscle cells with inducible nitric oxide synthase.

Vascular smooth muscle cell (VSMC) migration participates in atherosclerosis and arterial restenosis after balloon angioplasty. Because these processes are enhanced in insulin-resistant states, our goal was to determine whether insulin affects VSMC migration and, if so, how. The migration of primary cultured VSMCs from canine femoral artery was measured with the use of a wound migration assay and related to cGMP levels. Insulin (1 nmol/L) did not affect migration or cGMP production in control cells. When inducible nitric oxide synthase (iNOS) was induced by 24-hour preincubation with lipopolysaccharide and interleuken-1beta, basal migration decreased, cGMP production increased, and insulin inhibited migration by >90% and stimulated cGMP production by 3-fold. The nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine blocked the affect of insulin on the migration of VSMCs with iNOS. 8-Bromo-cGMP inhibited VSMC migration in control cells, and 1-H-1[1,2,4]oxadiazolo-[4, 3a]quinoxolin-1-one, a selective inhibitor of guanylate cyclase, blocked the inhibition by insulin of migration of cells with iNOS. We conclude that insulin does not normally affect cGMP production or the migration of these VSMCs. However, after the induction of iNOS, insulin stimulates cGMP production and inhibits migration via an NOS-and a cGMP-dependent mechanism.

Insulin acutely inhibits cultured vascular smooth muscle cell contraction by a nitric oxide synthase-dependent pathway.

Insulin acutely decreases contractile agonist-induced Ca2+ influx and contraction in endothelium-free cultured vascular smooth muscle (VSM) cells, but the mechanism is not known. Since it has been reported that insulin-induced vasodilation in humans is linked to nitric oxide synthase activity, we wished to determine whether insulin inhibits Ca2+ influx and contraction of cultured vascular smooth muscle cells by a nitric oxide synthase-dependent pathway. Primary cultures of endothelial cell-free VSM cells from canine femoral artery were preincubated with and without 1 nmol/L insulin for 30 minutes, and the 5-minute production of cGMP was measured. Insulin alone did not affect cGMP production, but in the presence of 10(-5) mol/L serotonin insulin stimulated cGMP production by 60%. N(G)-monomethyl-L-arginine (0.1 mmol/L), an inhibitor of nitric oxide synthase, inhibited the conversion of arginine to citrulline by these cells, blocked insulin-stimulated cGMP production, and blocked the inhibition by insulin of 5-hydroxytryptamine (5-HT)-stimulated Mn+2 (a Ca2+ surrogate) influx and contraction. Insulin did not affect contraction of VSM cells grown under conditions designed to deplete the cells of tetrahydrobiopterin, an essential cofactor of nitric oxide synthase. These studies demonstrate that insulin acutely inhibits 5-HT-stimulated Ca2+ influx and contraction of endothelium-free cultured VSM cells by a nitric oxide synthase-dependent mechanism.

Insulin reduces contraction and intracellular calcium concentration in vascular smooth muscle.

Resistance to insulin-induced glucose disposal is associated with hypertension, in accord with recent reports that insulin-induced vasodilation is impaired in men with resistance to insulin-induced glucose disposal. Nevertheless, the mechanism of insulin-induced vasodilation is not known. We wished to determine whether a physiological concentration of insulin inhibits agonist-induced contraction at the level of the individual vascular smooth muscle cell, and if so, how. Dispersed vascular smooth muscle cells from dog femoral artery were grown on collagen gels for 4 to 8 days. Contraction and intracellular Ca2+ concentration of individual cells were measured by photomicroscopy and fura 2 epifluorescence microscopy, respectively. Serotonin and angiotensin II contracted cells in a dose-dependent manner. Preincubation of cells for 20 minutes (short-term) or 7 days (long-term) with insulin (40 microU/mL) inhibited serotonin- and angiotensin II-induced contractions by approximately 50%. Insulin (10 microU/mL) acutely inhibited serotonin-induced contraction by 34%. The maximal effect of high extracellular K(+)-induced contraction was not affected by short-term insulin exposure, but the ED50 for extracellular K(+)-induced contraction was increased from 7.6 +/- 2.5 to 16.0 +/- 3.9 mmol/L (P < .05). Short-term insulin exposure also attenuated the peak rise of the serotonin-induced intracellular Ca2+ transient and increased the rate constant for intracellular Ca2+ decline. Verapamil and ouabain completely blocked the attenuation of agonist-induced contraction by short-term insulin exposure, indicating the importance of voltage-operated Ca2+ channels and the Na(+)-K+ pump for this effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Protein kinase C mediates insulin-inhibited Ca2+ transport and contraction of vascular smooth muscle.

Insulin acutely inhibits contraction of primary cultured vascular smooth muscle (VSM) cells from canine femoral artery by inhibiting contractile agonist-induced Ca2+ influx. Insulin also inhibits contraction at step(s) distal to intracellular Ca2+ concentration (Ca2+i) by stimulating cyclic guanosine monophosphate (GMP) production. We wished to see whether these effects of insulin are mediated by protein kinase C (PKC). Ca2+ influx was assessed by measuring the rate of fluorescence quenching of intracellular fura 2 by extracellular Mn2+. We found that 10 micromol/L serotonin (5-HT) stimulated Mn2+ influx 3-fold, and 1 nmol/L insulin inhibited the 5-HT-stimulated component of Mn2+ influx by 63% (P < .05), but insulin had no effect in the presence of 1 micromol/L staurosporine, an inhibitor of PKC. In the absence of insulin, preincubating cells with 0.1 micromol/L phorbol 12-myristate 13-acetate (PMA) for 5 min inhibited the 5-HT-stimulated component of Mn2+ influx by 69% (P < .05). Insulin inhibited cell contraction induced by raising Ca2+i to supraphysiologic levels with ionomycin by 75% (P < .05). We also noted that 10(-6) mol/L calphostin C, another PKC inhibitor, or 16-h preincubation with PMA completely blocked this effect of insulin. Finally, 10-min exposure to insulin or PMA increased cyclic GMP production in ionomycin-treated cells by 50% and 64%, respectively (both P < .05). We conclude that insulin inhibits VSM cell contraction by inhibiting 5-HT-stimulated Ca2+ influx and also at step(s) distal to Ca2+i by a PKC-dependent mechanism.

Feeding gastrostomy for the severely burned patient.

Twenty-two patients underwent feeding gastrostomy. Their ages ranged from 17 to 76 years. Their burn injuries were extensive, ranging from 31% to 88% total body surface area, with a mean of 60%. Nine gastrostomies were done through intact unburned skin, 12 were done through the burn wound itself, and one was done through a split-thickness skin graft donor site. No evidence of intraperitoneal or wound infection was observed. No intraoperative and only three postoperative complications were encountered. One patient had a wound dehiscence while in the hospital. Following discharge from the hospital, two other patients manifested incisional hernias. Initially, we were reluctant to consider this operative procedure for our patients because of anticipated intra-abdominal and wound complications. In view of our experience thus far, however, we are now more confident of the procedure.

Reasons for intracranial hypertension and hemodynamic instability during acute elevations of intra-abdominal pressure: observations in a large animal model.

In previous studies we reported that an acute elevation in intra-abdominal pressure (IAP) is responsible for the elevation in intracranial pressure (ICP) and mean blood pressure (MBP). Thus far, the reasons for the increased ICP during an acute elevation in IAP and the combined effects of increased IAP and ICP on hemodynamics have not been reported. Five large animals (swine) were studied. Each animal served as its own control. A subarachnoid screw was placed for ICP monitoring. The jugular vein, femoral vein, and femoral artery were cannulated. ICP, MBP, central venous pressure above (CVPA) and below (CVPB) the diaphragm, and PaC02 were monitored after a pneumoperitoneum with C02 was established at 5, 15, and 30 mm Hg of IAP. Cavography was performed to evaluate the morphology of the inferior vena cava at different increments of IAP. Measurements were obtained in reverse Trendelenburg (group 1), supine (group 2), and Trendelenburg (group 3) positions. Multiple regression analysis was used to examine the effects of IAP and positioning in separate models with different blood pressures as dependent variables. Increased IAP significantly increased CVPA, CVPB, ICP, and MBP. There were no changes in cerebral perfusion pressure. The change in position (from group 1 to group 3) significantly increased CVPA and decreased the CVPB. Cavograms performed on animals in the supine position with increased IAP showed a narrowing of the IVC at the level of the diaphragm. Increases in IAP will increase ICP and MBP without altering the cerebral perfusion pressure. A mechanical effect mediated by compression of the inferior vena cava at the level of the diaphragm with increased central venous pressure and decreased drainage from the lumbar plexus and central nervous system is responsible for this effect.

Herniography following indirect hernioplasty using the Marlex "mesh plug" technique.

In recent years, some surgeons have been performing indirect inguinal herniorrhaphies using a "mesh plug" technique without ligation or resection of the hernia sac. The authors have had an interest in herniography and questioned whether herniorrhaphy without ligation or resection of the indirect sac might result in a false positive herniogram or an abnormal filling defect within the peritoneal cavity. These questions were answered by the performance of herniography in five patients who had indirect hernias repaired by this method. No false positive herniograms were discovered, and the inverted sacs could not be identified within the peritoneal cavity. Therefore, herniography would still be a useful diagnostic tool in evaluating patients who have persistent or recurrent symptoms following operations wherein the hernia sac was left intact.

Herniography: a review of 333 herniograms.

We reviewed 333 consecutive herniographic studies in 306 patients for whom clinical data were available. Symptoms with either a negative or inconclusive physical examination (PE) were the most frequent reasons for requesting a herniogram. The herniogram was found to be more sensitive for the diagnosis of hernia, particularly inguinal, than PE. In 56 of 57 patients who came to operation the herniogram and the PE were concordant. In one patient, an incisional hernia was found at operation that had not been appreciated as such on the herniogram. We believe herniography should be used more frequently when the diagnosis of hernia is uncertain on PE, thereby reducing the incidence of unnecessary operative procedures.

The etiology of the adult indirect inguinal hernia: revisited.

It has generally been historically stated that indirect inguinal hernias develop only in patients who have a patient processus vaginalis that enlarges to become a hernia sac. Occasionally, this theory has been challenged but without any objective evidence. Herniography was performed by placing 50 mL of nonionic contrast material into the peritoneal cavity. The patient was then placed in a prone position with the head of the table elevated. Films of the inguinal fossae were obtained with the patient straining. The herniogram revealed a right indirect inguinal hernia. There was no left inguinal hernia, nor was there a patent processus vaginalis on the left side. Two years later, the patient developed left inguinal discomfort and swelling and was found to have a moderate-sized left inguinal hernia. At the time of operation, an indirect sac of moderate size was present. A mesh plug repair was performed. This case report is the first published objective evidence that, contrary to common thought, a patent processus vaginalis is not a necessary prerequisite to the development of an indirect inguinal hernia.

Molten metal burns: early treatment improves outcome.

Molten metal burns have received relatively little attention in the surgical literature. We performed a retrospective chart review of 150 patients who sustained molten metal burns between 1972 and 1997. The injuries all occurred in male foundry workers, most commonly from molten aluminum (60%). The typical accident was that of a splatter spill, creating a full-thickness burn. The mean burn size was 2.3 per cent of the body surface area (range, 0.25-25%). The lower extremities were the most commonly injured areas (85%), yet 37 per cent of patients had multiple sites burned. Patients were often initially treated nonoperatively and then referred to a surgeon when the wound failed to heal. Hospitalization was necessary in 89 patients at a mean of 16 days after the injury, and 92 patients required an operation, most commonly excision of the wound with skin grafting. The mean length of hospital stay was 11.2 days, and mean absence from work was 72.6 days. Fifty-one patients treated by the burn surgeon within 2 weeks of injury had a mean length of disability significantly shorter than those referred late (53.5 vs. 83.4 days; P < 0.05). We believe that an underestimation of the severity of these burns often leads to a delay in correct therapy and extends disability.

Treatment for depigmentation following burn injuries.

Partial-thickness burn injuries frequently heal with pigmentary changes. Occasionally, permanent depigmentation is observed, especially in areas such as the hands, fingers and wrists. This article reports our surgical technique and our success in using it to treat depigmentation after burn injuries. This technique consists of superficial dermabrasion of the depigmented region, followed by transplantation of melanocytes vie epithelial sheet grafts. With this technique, 30 separate surgical procedures have been performed on 21 patients. The follow-up period for these patients has ranged from 2 weeks to 94 months with an average of 17 months. The skin-graft take has been good to excellent in all patients. The colour match has been good or excellent in all but one patient. No complications have been observed. This procedure has consistently and reliably improved the disfigurement from depigmentation in all of the patients we have treated.

Management of burn injuries during pregnancy.

Burns suffered during pregnancy is rare and can be a devastating injury. The presence of a fetus creates many special maternal physiological changes, and the burn wound places additional great stress on systems that are already highly modified. Most of the literature has come from developing countries, and most reports from developed countries have come before 1980 and do not reflect the current standard of care. We have compiled a retrospective review of eight patients burned during pregnancy. The total body surface area (TBSA) burned ranged from 1 to 85% in these patients, and all survived the injury. All patients gave birth to healthy children except the most severely burned patient, whose child suffers from cerebral palsy. Based on our experience as well as a review of the literature, management recommendations are proposed. These include: (1) early pregnancy test for all female patients of childbearing age, (2) prompt and aggressive fluid resuscitation, (3) early supplemental oxygen and low threshold for mechanical ventilatory support, (4) early delivery of the fetus if the pregnancy is in the third trimester, and (5) high suspicion for venous thrombosis and sepsis, with early and aggressive treatment.

Treatment for depigmentation resulting from burn injuries.

A new surgical technique to "repigment" skin that has been depigmented by deep partial-thickness burn injuries has been developed and proven to be successful. Partial-thickness burn injuries frequently heal with pigmentary changes. Occasionally, permanent depigmentation is observed, especially in areas such as the hands and fingers. This article reports our surgical technique and our success in using it to treat depigmentation after burn injuries. This new technique consists of superficial dermabrasion of the depigmented region, followed by transplantation of melanocytes via epithelial grafts. With this technique, 15 separate surgical procedures have been performed on 11 patients. The follow-up period for these patients has ranged from 0.5 months to 94 months, with an average of 14 months. The skin-graft take has been excellent in all patients. The color match ranges from good to excellent. No complications have been observed, and this procedure has consistently and reliably improved the disfigurement from depigmentation after these burn injuries.

SENSIBILIZACIÓN A AEROALERGENOS EN PACIENTES CON RINITIS Y ASMA

Las enfermedades alérgicas han aumentado en las últimas décadas en todo el mundo. El asma y la rinitis alérgica podrían representar un espectro de la misma enfermedad, cuya patogénesis puede explicarse, entre otros factores, por la sensibilización a aeroalergenos. Los aeroalergenos más frecuentemente involucrados como sensibilizantes se hallan en el polvo del interior del hogar o lugar de trabajo (indoor). Dentro de los aeroalergenos indoor, los dermatophagoides son los más prevalentes. Este estudio demuestra que la prevalencia de sensibilidad a aeroalergenos indoor, en pacientes con rinitis y asma, es coincidente con la bibliografía. Es un área a investigar en el futuro, la prevalencia de sensibilidad a aeroalergenos outdoor

Allergic diseases have increased in recent decades worldwide. Asthma and allergic rhinitis could represent a spectrum of the same disease, whose pathogenesis can be explained, among other factors, by sensitization to aeroallergens. The aeroallergens most frequently involved as sensitizers are found in the dust inside the home or workplace (indoor). Within indoor aeroallergens, dermatophagoides are the most prevalent. This study demonstrates that the prevalence of sensitivity to indoor Aeroallergens, in patients with rhinitis and asthma, is consistent with the literature. It is an area to investigate in the future, the prevalence of sensitivity to outdoor aeroallergens.