John P. Lichtenberger III, MD

• Department of Diagnostic Imaging
• David Grant USAF Medical Center
• Travis AFB, California

Surgical outcomes in human immunodeficiency virus-infected patients in the era of highly active antiretroviral therapy blood pressure chart to keep track of readings purchase lisinopril 10mg without prescription. Disseminated mucormycosis and necrotizing fasciitisin immune-compromised patients: Two case reports hypertension 40 years old generic lisinopril 2.5 mg amex. Carbon dioxide laser ablation of anogenital condyloma acuminata in pediatric patients blood pressure chart symptoms buy lisinopril 2.5 mg with visa. Variability of growth in children starting antiretroviral treatment in southern Africa heart attack quiz questions discount lisinopril 10 mg fast delivery. The management of surgery in infants and children with the acquired immune deficiency syndrome hypertension 33 weeks pregnant cheap 5 mg lisinopril amex. Anorectal surgery in patients infected with human immunodeficiency virus: Factors associated with delayed wound healing arteria gastroepiploica sinistra discount lisinopril 2.5mg with visa. Predictors of operative outcome in patients with human immunodeficiency virus infection and acquired immunodeficiency syndrome. The first ever human transplant was attempted in 1963 by Starzl1 on a 3-year-old child with biliary atresia. The infant did not survive the operation, and it was not until 4 years later that he obtained "success" in achieving survival for 400 days in an 18-month-old girl with a malignant liver tumor. Over the next decade, 1-year mortality remained high at around 50%, and it was not until cyclosporine was introduced in 1980 that survivals dramatically increased. In June 1983 at the National Institutes of Health Consensus Development Conference, liver transplantation was declared a valid treatment for end-stage liver disease. The introduction a decade later of tacrolimus, a more potent calcineurin inhibitor, pushed the boundaries of success even further. Technical advances included reduced-size liver transplantation,2 split-liver, transplants,3 and living related transplants. Current anxieties over organ donor scarcity militating against timely transplant, the long-term side effects of the immunosuppressive therapy, financial implications, and some ethical issues remain. The focus of attention has now shifted from an initial target of early posttransplant survival to quality of life in the long term. Shortage of donor organs has been tackled in an imaginative way with increasing use being made of size reduction of the donor liver even into a single segment, splitting the liver into two functioning units for two recipients, as well as the use of living related donors and non-heart-beating donors. This is probably because many liver conditions in children have led to rapid deterioration and death in the past. Pediatric liver transplantation is now established as routine treatment for children dying of end-stage chronic liver disease and acute/subacute liver failure in both developed and developing countries (Table 29. Acute and chronic hepatitis (a) Fulminant hepatic failure (viral, toxin, or drug induced) (b) Chronic hepatitis (B, C, etc. Obstructive biliary tract disease (a) Biliary atresia (b) Choledochal cyst with cirrhosis V. Nontransplant surgery may be required to facilitate full adaptation, but a >50% long-term survival can be expected. Parental substance abuse, severe psychiatric problems, and poor preoperative adherence with therapy are factors that need to be carefully examined. In developing countries, the socioeconomic factors such as poor sanitation and lack of access to adequate medical follow-up are often contraindications to transplantation. Adherence is more difficult to predict in families of children with acute liver failure, as time from presentation to can be complicated by hepatocellular failure. These include acute and subacute liver failure from metabolic, toxic, or viral insults, and chronic parenchymal disease of varying causes, of which biliary atresia, biliary hypoplasia, autoimmune hepatitis, viral hepatitis, and some metabolic diseases are the most common. Good adherence is one of the factors thought to contribute to the slightly better outcome after living-donor transplantation as the bond and responsibilities between donor and recipient are that much greater. As the outcome of the operation is so much better in recent years, indications for early transplant in patients with chronic liver disease would be evidence of impaired synthetic function, including prolonged prothrombin time, reduced serum cholesterol levels, and low serum albumin. Clinical indicators include presence of ascites, bleeding from esophageal varices not controlled by sclerotherapy/ banding, and poor response to nutritional resuscitation. Those with acute liver failure who develop encephalopathy, hypoglycemia, a prothrombin time of greater than 50 seconds, and a factor V level of less than 20% should be considered for transplant, as almost all of these children die without transplantation. All patients require initial confirmation of the diagnosis, intensive medical investigation, nutritional resuscitation, and active treatment of the complications of the liver disease, portal hypertension, and nutritional deprivation (Tables 29. Immunization status must Complete blood count, clotting profile Blood group and tissue typing Serum biochemistry and liver function tests Chest and abdominal x-ray X-ray wrists and long bones Ultrasound with Doppler for size and flow in the portal vein and unusual anatomy. Dental check Micronutrients: iron, zinc, selenium, manganese, and vitamin levels A and E J. Psycho-social assessment be reviewed and supplemented as required with hepatitis A and B, hemophilus influenza, pneumococcal, varicella, meningococcal, and human papilloma virus immunizations. It is important that live attenuated vaccines are given pretransplant, as these are contraindicated posttransplantation. Increasingly, marginal donors are being used with a surprisingly low incidence of primary poor function or nonfunction. However, stable donors aged under 45 years with a short intensive care unit stay (less than 3 days), little requirement for inotropic support and normal, or near-normal liver function are preferred, with an expected <5% incidence of impaired function after transplant. Greater than 50% fatty infiltration would preclude the use of the liver in most centers. Surgical techniques used for donor retrieval and recipient liver removal and engraftment have evolved over the last 40 years. The concept of cardiac death may be more acceptable to some and could increase the number of potential donors. Although there are considerable logistic problems to overcome, some success has been achieved with acceptable graft function even in segmental liver transplantation using a "super-rapid" technique and keeping both cold and warm ischemic times to a minimum. The recipient operation is commenced so that the estimated hepatic graft cold ischemic time is less than 12 hours. Much longer preservation times have been recorded, but this leads to an increased incidence of cholestasis and graft dysfunction. Careful dissection of the graft is required when splitliver transplantation is being used, that is, when the liver is divided into two functional units for two recipients, and decisions must be made as to which porta hepatis structures will go with which graft. It is advisable to perform a portable cholangiogram to confirm bile duct anatomy, as there are many variations in biliary anatomy. Depending on local preference, many centers opt to export the right-sided graft with the full complement of structures of bile duct, portal vein, and hepatic artery, keeping the left lateral segment as the graft for a pediatric recipient in much the same way as a living-donor transplant. Where a reduced-size liver 328 Liver transplantation is used, the caudate lobe is always excised. The division of liver tissue may be performed using the standard forceps clamp or bipolar diathermy technique with titanium clip and/or suture and ligation of vascular and biliary structures. The ultrasonic dissector (Cavitron Ultrasonic Surgical Aspirator), Ligasure or Harmonic Scalpel may also be used. If the recipient inferior vena cava is to be preserved, this is simply done by carefully excising the diseased liver clear of the cava and, when the liver has been removed, individually suturing closed all small areas of leakage from divided direct caudate lobe hepatic veins. Split grafts and living-donor segmental grafts may need to lie in an orthotopic anatomical position, and a number of techniques of stabilizing the graft have been used so as to avoid torsion at the hepatic vein-to-caval anastomosis and to facilitate vascular anastomoses without using interposition grafts. Prior to completion of the anastomosis, the liver is flushed of preservation solution via the portal vein with recipient blood, normal saline, or a colloid solution. It is important for the portal vein to be of adequate size and length, and it should lie without tension. If the recipient vein is too narrow and sclerotic, interposition of a donor iliac vein is indicated. The bile duct is trimmed back and spatulated in pediatric donors such that there is good bleeding from the cut edge and a wide anastomosis is obtained. With reduced- and variant-size grafts, a Roux-en-Y choledochojejunostomy is always performed using fine absorbable sutures. Stents or T tubes are optional but less used as there is some evidence of an increased incidence of biliary complications associated with their use. There are clear advantages in the planned nature of the procedure preferably before end-stage liver disease in the recipient, the excellent quality of the graft, and short ischemic time. The use of a living donor also increases the availability of donor organs in general for other patients on the waiting list. The only advantage to the donor is a psychological one, and there is a current morbidity of around 10% (wound sepsis, hernia, bile leak, and adhesive bowel obstruction). The donor should first undergo a thorough screening both clinical and psychological without coercion and be given an option to withdraw from the procedure at any time before the transplant. Cholangiography is essential as there is considerable variety in the intrahepatic biliary anatomy. Segments 2 and 3 are used for an infant and the right liver for an adult recipient. The graft can be further reduced in size by removing segment 2, or alternatively, segment 2 is used as the graft, and segment 3 is resected and discarded. Immunosuppressive regimens should, in addition to preventing acute and chronic rejection, promote good quality of life and be free of significant long-term side effects. Calcineurin inhibitors remain the cornerstone of immunosuppression, with tacrolimus being the preferred agent. Despite the long-term side effects, 55% of recipients were still on maintenance steroid therapy at 1 year. Other side effects include a delay in wound healing and hepatic artery thrombosis, and it is thus not recommended in the early postoperative period. Children with posttransplant lymphoproliferative disease or hepatoblastoma may benefit from immune suppression with sirolimus. Liver ultrasound with color flow Doppler is performed frequently to confirm vascular patency and the absence of biliary dilatation. Acute postoperative hypertension is almost universal in pediatric transplantation and persists in 25% of recipients. Aspirin 3 mg/kg given on alternate days is used as prophylaxis against arterial thrombosis, and a proton pump inhibitor is given for gastric mucosal protection. Early enteral feeding and vitamin supplementation is advised, and if delayed beyond 48 hours of surgery, parenteral nutrition should be commenced. Phosphate and magnesium deficiency is common and requires replacement therapy in nearly all patients. Liver biopsies are performed if indicated by increasing serum liver enzyme activity or by bilirubin levels, using the Menghini technique (Hepafix needle [Braun], diameter 1. Diagnosis of rejection can be made on the basis of clinical, biochemical, and histologic changes and usually presents in the first few weeks after transplant with fever, malaise, a tender graft, and loose stools. The grade of rejection is assessed according to established histological criteria (lymphocyte- predominant portal infiltrates, cholangiolar damage, and endotheliitis) according to the Banff schema. If there is ongoing rejection, pulsing with intravenous methylprednisone can be used, but this is seldom necessary with present-day immunosuppressive regimens. The patient should be given four doses of methyl prednisolone at 10 mg/kg, the first three doses on successive days and the fourth dose on the fifth day after commencing treatment. Biliary tract (a) Stenosis or stricture (b) Anastomotic leak-often associated with hepatic artery thrombosis (c) Cholangitis 2. Miscellaneous (a) Encephalopathy (cyclosporin, tacrolimus, hypertensive, metabolic) (b) Bowel perforation (steroid, diathermy, hypoxia) (c) Diaphragm paresis/paralysis (d) Gastrointestinal hemorrhage (peptic ulceration, variceal) (e) Obesity (steroids) (f) Other drug side effects Anti-infection agents Immunosuppression naturally leads to increased susceptibility to bacterial, fungal, protozoal, and viral infections. Antibiotics are given as prophylaxis and according to culture and sensitivity of blood, sputum, and body fluid. In infants, there is a low threshold for antifungal therapy with either amphotericin or fluconazole. Trimethoprim/sulfamethoxazole is routinely given for 6 months for pneumocystis jirovecci prophylaxis and can be restarted at times of increased immunosuppression. Antituberculosis prophylaxis is given only if the reason for transplant is a reaction to antituberculosis drugs with fulminant hepatic failure, where evidence of tuberculosis is found before surgery and if a close family contact has tuberculosis. First-line antituberculous therapy (isoniazid, rifampicin, ethambutol, and pyrazinamide) can be used in children with normal graft function, but regular monitoring of liver function tests is required as these drugs are potentially hepatotoxic. It is important to monitor tacrolimus/cyclosporin levels as rifampicin induces the cytochrome P450 system, resulting in increased drug metabolism. Tacrolimus or cyclosporin dosage should empirically be increased by 30% at the start of antituberculous therapy.

More recently blood pressure index chart buy lisinopril 5 mg low cost, a task force redefined sepsis in the Third International Consensus Definitions for Sepsis and Septic Shock blood pressure medication that starts with t buy lisinopril cheap. Sepsis is currently defined as "life-threatening organ dysfunction caused by a dysregulated host response to infection heart attack like symptoms order lisinopril 5 mg fast delivery," thus making the term "severe sepsis" redundant blood pressure medication used for hot flashes discount lisinopril 2.5mg with amex. Neonatal sepsis occurs within the first 28 days of life or up to 4 weeks beyond the expected delivery date in premature infants interleukin 6 arrhythmia discount 2.5mg lisinopril amex. Clinicians can apply these criteria to determine if sepsis is likely blood pressure medication quinapril buy lisinopril in india, guide subsequent workup and antibiotic therapy, or document the presence of sepsis for outcome analysis. However, the Rochester criteria neither effectively define sepsis nor assist in the management of complicated perinatal or preterm infants. This figure is not meant to be comprehensive but representative of several of the most well understood components of each phase. In addition, some criteria are strictly biochemical13 rather than clinical, in contrast to the more classic "Bone" criteria. Rates of infection vary by geographic region, available health care resources, and maternal and infant risk factors. Tachypnea (respiratory rate > 95th percentile for age) or increasing frequency of apneic events with bradycardia 4. Poor peripheral perfusion (delayed capillary refill or central-peripheral temperature disparity) 6. Thus, rate of sepsis for non-agematched birth weight has been reported as well (Tables 20. Unfortunately, birth weight does not capture an additional important variable-the trajectory of intrauterine weight gain. A trajectory of normal weight gain for a small for gestational age fetus is significantly less concerning Table 20. This includes transmission through hematogenous routes, chorioamnionitis, or during delivery through direct contact with or aspiration/ingestion of invasive organisms. The most commonly identified causative organisms are from the maternal vaginal flora. Additionally, widespread or prolonged use of broad spectrum antibiotics can lead to transmission of opportunistic or drug-resistant pathogens. Putative risk factors for such infections include low birth weight (<1500 g), parenteral nutrition, indwelling catheters, lack of enteral nutrition, mechanical ventilation, H-2 receptor antagonists, abdominal surgery, peritoneal dialysis, and exposure to broad spectrum or antenatal antibiotics. Microbial invasion depends on bacterial fimbriae or pili binding or adhering to host structural proteins or cellular integrins followed by internalization. The neonatal immune system is quite different from that of pediatric and adult patients. Cellular innate and adaptive defense mechanisms are present as early as 13 weeks gestation, but significant production of leukocytes does not occur until nearly the 30th week. Procalcitonin is produced by monocytes and hepatocytes 4 to 6 hours after infection. The guidelines were updated in 2012 and include "red flag" indicators that are strongly suggestive of sepsis as well as "non-red flag" risk factors (Table 20. Red flags include parenteral antibiotics given to the mother, suspected or confirmed infection in another baby if there is a multiparous pregnancy, respiratory distress starting more than 4 hours after birth, seizures, mechanical ventilation in a term infant, and signs of shock. While there are physiologic, laboratory, and biochemical criteria to aid in the diagnosis of sepsis (Table 20. Cultures One blood culture from a sterile site using at least 1 mL of blood in a single culture bottle is an adequate volume for bacterial detection. Up to 25% of infants with sepsis have low colony count bacteremia, and blood cultures with adequate volume are twice as likely to yield a positive result. Blood is most frequently drawn from a peripheral vein, but a sample from a recently placed umbilical artery catheter is also acceptable. Body surface cultures and gastric aspirates are of limited value in the evaluation of sepsis. Tracheal aspirates may be of value in intubated neonates shortly after birth and immediately after endotracheal tube placement. The first signs of infection in a preterm infant are often apnea, bradycardia, and cyanosis followed by lethargy and increased respiratory effort. Tachycardia is a nonspecific finding, and bradycardia is often a sign of more advanced sepsis. Meningitis may present with a high pitched cry, abnormal movements, arching of the back, and tense fontanels. The incidence of meningitis in healthy-appearing infants is low, but the incidence is up to 23% in bacteremic patients. Neonatal Infection: antibiotics for prevention and treatment 2012 [cited February 20, 2016]. Additionally, if analysis is delayed greater than 2 hours, values may change significantly. Abdominal x-ray can be used to evaluate intra-abdominal causes of sepsis, such as pneumatosis intestinalis in infants suspected of having necrotizing enterocolitis. Acute phase reactants and biomarkers Acute phase reactants and biomarkers can be measured in the evaluation of neonatal sepsis. There is no single biomarker that can be used to reliably diagnose neonatal sepsis. One study evaluated 13 clinical and laboratory signs of sepsis and found that the maximum positive predictive value of any sign studied was 31. Significant advances have been made in the prevention of sepsis in both the perinatal and peripartum period as well as in the early postpartum management of neonates. Alternatives for penicillin allergic mothers have not been measured in controlled trials for efficacy but include cefazolin, clindamycin, erythromycin, and vancomycin. Although aggressive skin care, including 3% hexachlorophene bathing, can significantly reduce S. Indeed, a recent randomized controlled trial investigating umbilical cord care demonstrated superiority and safety of chlorhexidine powder to dry care. Recommendations of space range from 36 to 100 square feet and nurse to patient ratio of 1:4 to1:1, depending on acuity. Although good outcome studies of individual interventions are not possible due to power restrictions, quality assurance and intervention bundle studies indicate that combined implementation of infection control techniques reduces the risk of nosocomial infections. This includes frequent hand hygiene, gowns and gloves, care of invasive devices, sterilization of equipment, and epidemic control techniques. The Surviving Sepsis Campaign guidelines now include pediatric considerations in the management of severe sepsis but do not distinguish between neonates and children. Resuscitation should include (1) maintaining the airway and attaining adequate oxygenation and ventilation, (2) maintaining circulation defined as normal perfusion and blood pressure, and (3) maintaining threshold heart rates. Therapeutic endpoints include capillary refill of less than 2 seconds, normal pulses with no difference in central and peripheral pulses, warm extremities, urine output of greater than 1 mL/kg/h, normal mental status, normal blood pressure for age, preductal and postductal oxygen saturation difference of less than 5%, and oxygen saturation of >95%. Significantly decreased tissue perfusion has several measurable laboratory and biochemical effects in the neonate. In particular, metabolic acidosis, base deficit, and serum lactate can be utilized as markers of poor perfusion. Fluid boluses of 10 mL/kg should be given up to 60 mL/kg in the first hour to attain normal perfusion and blood pressure. Vasoactive support may be required, but pulmonary vascular resistance should be considered when selecting a vasopressor and support for persistent pulmonary hypertension of the newborn should be initiated if needed. Due to the differing proportions of alpha- and beta-adrenergic receptors in the neonate, there has been significant skepticism regarding the utility of alpha-specific medications such as phenylephrine or norepinephrine, although they are used routinely in older patients. Nevertheless, a prospective trial evaluating norepinephrine demonstrated improved tissue perfusion and relative safety in the neonate with shock refractory to fluid and classic vasopressors. Nonetheless, current neonatal guidelines generally favor dopamine over dobutamine as an initial choice of vasopressor, and epinephrine as a rescue medication for dopamine-refractory shock, despite ongoing debate about the optimal pressor for different types of shock. Calcium chloride infusions, along with various other forms of calcium replacement, have been strongly advocated in the pediatric and anesthesia communities,75 but safety and intravenous access issues have not been studied in the setting of calcium infusion for septic shock. Nevertheless, most units prefer to add calcium to intravenous fluid and parenteral nutrition, as well as intravenous calcium boluses to maintain calcium in the normal range. Evidence supports endocrine replacement therapy in the setting of neonatal shock refractory to vasopressor treatment. Early nongenomic effects, on the other hand, are responsible for the efficacy of endocrine Management 227 Table 20. In particular, corticosteroids lead, in a nongenomic, rapid fashion, to the prevention of endocytosis of adrenergic receptors and downregulation of secondary messenger systems that lead to tachyphylaxis to both autologous and extrinsically infused adrenergic vasopressors. There are currently no evidence-based guidelines on weaning hydrocortisone in neonates. In the case of refractory shock, pericardial effusion, pneumothorax, blood loss, hypoadrenalism, hypothyroidism, inborn errors of metabolism, or heart disease should be evaluated and treated as discussed above. Patients should also be evaluated for other causes of infection, and aggressive source control should be initiated for infected or necrotic tissue. Blood cultures should be obtained, and empiric antibiotics should be administered within 1 hour of the identification of sepsis. Furthermore, decreasing Gram-negative and Gram-positive sepsis has led to a commensurate rise in anaerobic, fungal, and viral sepsis. The treatment duration varies from 10 to 14 days depending on the pathogen, while treatment for meningitis is usually longer. Duration should be adjusted based on response to therapy or complications including abscesses, osteomyelitis, or endocarditis. Trends in inflammatory biomarkers have been evaluated to determine response to antibiotic therapy and may allow for the early discontinuation of antibiotics in healthy appearing neonates. New therapies and preventive strategies Several new therapies have been proposed for the management of neonatal sepsis. Furthermore, neonates with birth weight between 401 and 750 g and the use of a third-generation cephalosporin were found to increase the risk of developing candidiasis, while enteral feeding appeared protective. These include cerebral palsy, visual impairment, delayed psychomotor development, low Bayley Scales of Infant Development scores, overall poor neurodevelopment, and impaired growth. Sepsis-induced endocarditis and thrombosis can cause rare complications such as pulmonary embolism, valvular damage, and infectious thromboembolism. As the prevention, identification, and therapy of sepsis advance, the epidemiology and bacteriology of the disease shift making optimal treatment of sepsis an evolving process. The World Health Organization Global Health Observatory Data Repository: World Health Organization; 2015 [cited 2015 February 24]. Neurodevelopmental and growth impairment among extremely low-birthweight infants with neonatal infection. Early goal-directed therapy in severe sepsis and septic shock revisited: Concepts, controversies, and contemporary findings. The influence of early hemodynamic optimization on biomarker patterns of severe sepsis and septic shock. Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock, 2012. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). Identification of infants unlikely to have serious bacterial infection although hospitalized for suspected sepsis. Febrile infants at low risk for serious bacterial infection-An appraisal of the Rochester criteria and implications for management. Predictive model for serious bacterial infections among infants younger than 3 months of age. International pediatric sepsis consensus conference: Definitions for sepsis and organ dysfunction in pediatrics. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Comparison of procalcitonin with C-reactive protein and serum amyloid for the early diagnosis of bacterial sepsis in critically ill neonates and children. Optimizing care and outcome for late-preterm (nearterm) infants: A summary of the workshop sponsored by the National Institute of Child Health and Human Development. Risk of early-onset neonatal infection with maternal infection or colonization: A global systematic review and meta-analysis. A practical guide to the diagnosis, treatment, and prevention of neonatal infections. Cortese F, Scicchitano P, Gesualdo M, Filaninno A, De Giorgi E, Schettini F et al. To tap or not to tap: High likelihood of meningitis without sepsis among very low birth weight infants. Early-onset sepsis and antibiotic exposure in term infants: A nationwide population-based study in Norway. Neonatal Infection: Antibiotics for prevention and treatment 2012 [cited 2016 February 20]. Reappraisal of guidelines for management of neonates with suspected early-onset sepsis. Pros and cons of using biomarkers versus clinical decisions in start and stop decisions for antibiotics in the critical care setting. Prevention of Perinatal Group B Streptococcal Disease Revised Guidelines Morbidity and Mortality Weekly Report2010 [cited 2016 February 20]. Higher rate of cord-related adverse events in neonates with dry umbilical cord care compared to chlorhexidine powder.

There are three main causes of acute shunt malfunction: obstruction of the proximal/ventricular catheter; obstruction distal to the proximal catheter heart attack full movie purchase lisinopril cheap, including the valve and distal catheter; and disconnection pulse pressure 82 generic lisinopril 10mg otc, breakage prehypertension meaning in urdu order lisinopril 2.5 mg visa, or migration of any component of the shunt system hypertension signs and symptoms lisinopril 2.5 mg on-line. A neurosurgical consult is often obtained while the child undergoes these studies heart attack medication purchase lisinopril pills in toronto. Important aspects to elucidate on history are reason for shunting pulse pressure difference discount lisinopril 5 mg mastercard, date of first shunt placement, number of revisions and reasons for revision, date of last revision and presenting signs or symptoms at that time, shunt type and setting and whether these were recently changed, and others. Common complaints related to shunt malfunction include nausea, vomiting, seizures, visual changes, malaise, and altered level of consciousness and depend upon factors such as age of the patient, severity of shunt malfunction, and etiology of hydrocephalus. Statements such as "this is what happens when his/her shunt malfunctions" or "this same thing happened before his/her last shunt revision" are often highly prognostic. The physical examination includes vital signs, which may demonstrate bradycardia or abnormalities in blood pressure and respiratory rate in severe cases. Other aspects of the physical examination include palpation of the shunt along its entire course. Fluid collections around the valve or ventricular insertion site often herald a shunt obstruction, as do abdominal ascites. During the neurologic examination, a funduscopic examination can be attempted to assess for papilledema. Other neurologic signs, such as ataxia, may also be indicators of shunt malfunction. Although some pediatric neurosurgeons do not believe that shunt pumping is useful in assessing shunt function,5 we believe that in certain cases, pumping the shunt can indicate shunt malfunction, particularly if the patient is well known to the practitioner. Furthermore, the results obtained from shunt pumping should never be used to definitively rule out a possible shunt malfunction. However, having a foreign body implanted into the human body still carries the risk for potential infection. Shunt malfunction is very common in the practice of pediatric neurosurgery, as shunt malfunction signs and symptoms are the most common presentation of shunt infection. Clinical trials have demonstrated that the failure rate of implanted shunts may be as high as 40% within the first year, with mechanical malfunctions constituting more than half of all failures. Thus, understanding the presentation of acute shunt malfunction and the management options that are available remains vitally important to the neurosurgeon. This article addresses the presentation, diagnosis, and management of acute shunt malfunction, excluding infectious causes and failures due to overdrainage, which are addressed in other chapters. We will specifically discuss the management protocols for acute shunt malfunctions at our institution. Multiple plain radiographs (shunt series) demonstrating continuous course of a ventriculoperitoneal shunt tubing from head to abdomen. A shunt series may also demonstrate disconnections, breaks, or kinks in the shunt system, which may lead directly to shunt malfunction. Comparison with prior films can also be of critical importance, for example, a fixed-position, coiled peritoneal catheter could serve as an etiology of shunt malfunction. In the majority of cases, even in cases of frank ventriculomegaly, brain imaging should be compared with prior scans with knowledge of the clinical history at each time point of previous imaging. Comparison with prior scans aids in the interpretation of current imaging in the setting of suspected shunt malfunction. An increase in the caliber of the ventricular system from a baseline examination obtained when the patient was asymptomatic, in addition to a clinical suspicion of shunt malfunction, warrants shunt exploration in the majority of cases. Additional imaging findings that may require attention include overdrainage signs such as subdural hygromas or slit ventricles, as well as a malpositioned proximal catheter. Radionuclide studies can be performed to identify the presence of a shunt obstruction but are rarely indicated in the acute setting. Ultrasound may be used in infants with a patent fontanelle and also to determine the presence of abdominal collections such as pseudocysts. For most shunt taps, we use a 23- or 25-gauge butterfly needle attached to a 25-cm length of tubing. The end of the butterfly tubing can then be placed below the level of the shunt valve to assess for proximal flow. Distal malfunction can sometimes be diagnosed by manually occluding the inlet portion of the valve and allowing the fluid column in the tubing to flow distally. Additionally, the trajectory of the existing proximal catheter can be used as a guide for the new trajectory. Postoperatively, patients are observed overnight and often sent home the following day. Postoperative imaging can be performed to confirm placement of the ventricular catheter and resolution of ventriculomegaly. In most cases, however, resolution of clinical symptoms and signs is a reliable indicator of reconstituted shunt function. Similarly the distal catheter can become occluded by debris, contents of the abdominal cavity, or even a blood clot in the case of atrial catheters. Less commonly, kinking of the distal catheter at its connection to the valve or entry site in the abdomen or chest can be the cause of distal obstruction and shunt malfunction. Replacement of the distal catheter or valve in the operating room is the treatment for distal shunt obstruction. In cases where numerous revisions have previously been performed, we often ask our colleagues from general surgery or thoracic surgery to assist us with placement of the distal catheter into an alternative site, such as the internal jugular vein, subclavian vein, or pleural space. Prior to closure, the proximal catheter should always be interrogated because a concomitant partial proximal obstruction may exist concurrently with a distal obstruction. In uncomplicated revisions, patients are monitored for 24 hours and then sent home. Proximal obstruction can sometimes be diagnosed solely by clinical examination when a fluid collection is palpated over the cranial burr hole. Occasionally, the diagnosis is not made until intraoperative interrogation of the shunt system is performed. The treatment of acute shunt malfunction due to proximal catheter obstruction is replacement of the ventricular catheter in the operating room. The procedure is scheduled as a level I emergency; thus, the patient should be taken expeditiously to the operating room. Removal of the proximal catheter can be difficult in cases of delayed shunt malfunction owing to the presence of adhesions and gliosis around the catheter. Gentle traction combined with cauterization of surface scar tissue is often sufficient to release the catheter. In some cases, a stylet may be placed down the proximal catheter and low intermittent monopolar cautery is applied to free the catheter. For most cases of proximal shunt obstruction, where catheter position is appropriate, we prefer to "soft-pass" a new catheter down the original shunt tract. In cases where new proximal catheter positioning is sought, the original burr hole should be 35. T2-weighted magnetic resonance images demonstrating baseline ventricular caliber (a) and ventricular caliber during shunt malfunction (b), aiding in the diagnosis of shunt malfunction. These may result from poorly assembled connections between the valve and catheters, or as the child grows, from excessive tension on one of the components of the shunt system. Intraoperative repair of disconnections should specifically address both of these issues. Fracture of the shunt catheter or valve can result acutely from local trauma or more often as a late complication of repeated biomechanical stress along with calcification and aging of the shunt components. Fractures often occur at sites where the shunt is in close contact with bony surfaces such as the clavicle or rib cage. The treatment of a fractured shunt catheter or valve is removal of the fractured pieces and replacement. Migration of the proximal catheter often results in shunt obstruction by occlusion of the inlet ports with brain tissue. Distal migrations are more common and have been described in a variety of locations, particularly with ventriculoperitoneal shunts. Plain skull radiographs demonstrating disconnection of the proximal catheter from the shunt reservoir (arrowhead) (a) and reconnection following surgical revision (b). These situations call for immediate action, often before any imaging studies can be obtained. An emergent shunt tap should be performed if it is found that the shunt does not pump properly. This, however, is rarely necessary in a patient with patent sutures because of the increased compliance of the calvarium. Following stabilization, the patient should be scheduled immediately for the operating room for shunt revision surgery. If the patient is sufficiently stabilized by appropriate measures, one may elect to proceed with imaging studies prior to the procedure, to identify the site of malfunction. This is commonly done for infected shunt systems that require removal and rarely necessary for mechanical malfunctions. Scenarios involving the investigation of multiple shunt systems, whether independent or T-connected, require special attention to ventricular asymmetry on imaging studies and can sometimes require shunt taps for each system. Replacement or revision of more than one system may be necessary and requires special attention to positioning in the operating room in order to replace multiple shunt parts in a single sitting. Axial noncontrast head computed tomography images demonstrating slitlike ventricles in a patient with shunted hydrocephalus presenting with symptoms of shunt malfunction. The diagnosis of shunt malfunction in the presence of slit ventricles can be challenging with standard techniques such as shunt tapping because of difficulty with result interpretation and often requires intraoperative exploration of the shunt system to confirm. Several treatment options have been proposed for slit ventricle syndrome, including subtemporal decompression, lumboperitoneal shunting, and even shunt removal. Recent clinical studies, though, have demonstrated high success rates in slit ventricle syndrome with use of a programmable valves. A multicenter prospective cohort study of the Strata valve for the management of hydrocephalus in pediatric patients. A randomized, controlled study of a programmable shunt valve versus a conventional valve for patients with hydrocephalus. Physical examination of patients with cerebrospinal fluid shunts: is there useful information in pumping the shunt Symptomatic pleural effusion without intrathoracic migration of ventriculoperitoneal shunt catheter. Bowel perforation and transanal protrusion of a ventriculoperitoneal shunt catheter. Migration of the distal catheter of a ventriculoperitoneal shunt into the heart: case report. Transoral protrusion of a peritoneal catheter: a case report and literature review. Thoracic complications of ventriculoperitoneal shunts: case report and review of the literature. Hydrocele of the canal of Nuck as a result of a rare ventriculoperitoneal shunt complication. Endoscopic third ventriculostomy: an outcome analysis of primary cases and procedures performed after ventriculoperitoneal shunt malfunction. Endoscopic third ventriculostomy in previously shunted children: a retrospective study. Intracranial pressure monitoring using a programmable pressure valve and a telemetric intracranial pressure sensor in a case of slit ventricle syndrome after multiple shunt revisions. The Perinatal Management of a Child Born with a Myelomeningocele 36 the Perinatal Management of a Child Born with a Myelomeningocele Kimberly A. This includes covering the defect with a sterile dressing, the initiation of broad-spectrum intravenous antibiotics, and rapid transport to a facility accustomed to caring for pediatric neurosurgical patients. Preoperative ultrasound assessment of the head, spine, kidneys, and, when indicated, the heart will alert the surgeon to associated abnormalities that may require additional attention. Double-blind randomized and nonrandomized studies have shown a 70% reduction in the recurrence rates for mothers of spina bifida children given folate supplements as compared with similar mothers given a placebo. Some neurosurgeons have attempted to look for elements within the disorder that might influence outcome as a means of determining which children should be treated aggressively and which children should be allowed to die. Of those who had no adverse criteria, one fourth died, half had severe sequelae, and 14% were mentally deficient. He surmised that treatment should be offered only to those patients who could "look forward to life without grave handicaps. Overall rates have declined because of improved nutrition, mandatory folate fortification, and elective termination. This article offers specific guidelines as to the perinatal management of these children based upon our current state of knowledge. Palpation of the lesion itself or probing with an instrument is neither helpful nor recommended. Stimulation, either by sound or by touch, may elicit reflex movements that give the parents a false sense of optimism. The orthopedic deformities, which result from the unopposed actions of certain muscle groups, may be of localizing value. All patients with spinal dysraphism are presumed to have some degree of neurogenic bladder dysfunction. Ten percent of children with spina bifida will have a chromosomal abnormality, and 15% will harbor other anomalies outside of the nervous system. Tandem abnormalities of the spinal cord such as diastematomyelia, syringomyelia, dermoid tumors, lipomas, or spinal arachnoid cysts are not uncommon. When the head is large, the scalp veins dilated, and the fontanelle full, the diagnosis of hydrocephalus is easily made; however, hydrocephalus may exist in the absence of clinical 36. Options include fetal surgery evaluation, early intervention postnatally, no intervention, and termination of the pregnancy, as discussed below. Progressive hydrocephalus is uncommon in the fetus and appears to be more likely to occur the higher the spinal level of the defect; however, if there is increasing ventriculomegaly, early intervention may take the form of cesarean section of the preterm infant once the lungs have reached maturity.

It is therefore not surprising that newborn anatomy differs from adults; some of these differences are particularly important for the pediatric surgeon (Table 3 blood pressure chart normal blood pressure range lisinopril 10mg cheap. This article summarizes the applied anatomy of the newborn pulse pressure change during exercise generic lisinopril 5 mg without a prescription, emphasizing aspects that are clinically relevant and different to adults blood pressure readings order lisinopril pills in toronto. Deoxygenated systemic blood returning from the fetal superior vena cava and coronary sinus is directed preferentially to the right ventricle hypertension over 55 lisinopril 2.5 mg line. However blood pressure chart daily purchase cheap lisinopril on-line, during late gestation heart attack pain in arm order generic lisinopril canada, only about 20% of the fetal cardiac output reaches the lungs4,5 because the ductus arteriosus shunts blood from the pulmonary trunk to the aortic arch, just distal to the origin of the left subclavian artery. In the fetus, ductal patency is maintained by locally produced prostaglandins, which inhibit muscle contraction in response to oxygen. At birth, the lungs inflate and, as a result of mechanical effects and oxygen-induced pulmonary vasodilatation, pulmonary vascular resistance falls. For example, the head of a full-term newborn infant accounts for about 25% of its body length and 20% of its body surface area. These changes in atrial pressure force the free lower edge of the primary atrial septum to flatten against and subsequently adhere to the margins of the fossa ovale, resulting in functional closure of the foramen ovale. Cardiovascular adaptation to neonatal life therefore requires the functional closure of three fetal conduits: l l Foramen ovale. Typically this has no consequences because of the flap-like arrangement of the opening and differential atrial pressures. In full-term neonates with no congenital heart disease, the ductus arteriosus starts to close immediately after birth. Smooth muscle contraction within the ductus produces an initial functional closure and is probably mediated by several mechanisms: an increased arterial oxygen concentration, suppression of endogenous prostaglandin E2 synthesis, plasma catecholamines, and neural signaling. In addition, ductal blood flow is reversed as a result of increased systemic vascular resistance (due to absence of the placental circulation) and decreased pulmonary vascular resistance. Persistent ductal shunting frequently occurs in preterm infants with respiratory distress. Spontaneous closure of the ductus venosus begins immediately after birth9 and is usually complete by about 17 days of age. In the adult, the remnant ligamentum venosum runs within the fissure separating the anatomic left lobe of the liver and the caudate lobe. Persistent patency of the ductus venosus is rare, is more common in boys, and may cause long-term problems such as hepatic encephalopathy. As the pulmonary circulation is established, the work of the right side of the heart decreases and the left increases, reflected by changes in ventricular muscle thickness; at birth, the mean wall thickness of both ventricles is about 5 mm, whereas in adults, the left ventricle is about three times as thick as the right. Congenital cardiac malformations account for up to a quarter of all developmental anomalies (8 per 1000 live births4) and include dextrocardia (isolated or part of situs inversus), isomerism, and structural defects (septal defects, abnormal atrioventricular or ventriculoarterial connections, and valvular anomalies). Ventriculoseptal defects are the most frequent, more often affecting the membranous than the muscular part of the interventricular septum. A true atrial septal defect occurs when there is a failure of normal development of the septum primum and/or atrioventricular endocardial cushions. Coarctation of the aorta is often included within the spectrum of congenital heart disease. Typically, there is narrowing or occlusion of the juxtaductal segment of aorta just distal to the origin of the left subclavian artery, although preductal (involving the aortic arch and its branches) and even postductal coarctation can occur. The presence of a single umbilical artery is associated with an increased risk of other congenital anomalies, particularly renal, vertebral, cardiovascular, and anorectal malformations,15 and an increased risk of prematurity, growth restriction, and perinatal mortality. Occlusion of the umbilical artery is facilitated by the "folds of Hoboken," constriction rings along the length of the umbilical artery produced by oblique or transverse bundles of myofibroblasts. Compared to an adult, the hemidiaphragms are relatively flat, the ribs are more horizontal, and the heart size is relatively large (although the transverse cardiothoracic ratio should still be less than 60%). After birth, the obliterated umbilical arteries become the paired medial umbilical ligaments usually visible under the peritoneum of the anterior abdominal wall below the umbilicus; the proximal parts of each umbilical artery remain patent as the superior vesical artery. The urachus has 32 Clinical anatomy of the newborn normally involuted before birth leaving the fibrous median umbilical ligament. The tip of an umbilical artery catheter is usually positioned above the diaphragm but below the ductus arteriosus ("high" position equivalent to T6-9 vertebral level). Sometimes, the catheter tip is sited below the origin of the renal and inferior mesenteric arteries but above the aortic bifurcation ("low" position at L3-4 vertebral level). Despite immature coordination of swallowing and breathing, the risk of aspiration is reduced by the high position of the larynx. The higher more anterior position of the larynx also means that it is easier to intubate the trachea with a straightbladed laryngoscope. As the infant grows, the larynx descends and the epiglottis loses contact with the soft palate. Gender differences in laryngeal shape and size only begin to appear at about 3 years of age. As in adults, the trachea starts at the level of the sixth cervical vertebra but bifurcates relatively higher at T3/4 (rather than T4/5 in adults). The right main bronchus is wider and steeper than the left, and the carina is more likely to lie to the left of the midline. Contrary to some reports, an aspirated foreign body is therefore more likely to enter the right lung. Most alveoli have been formed by 2 years of age and only increase in size thereafter. Neonates are obligate nose breathers and do not begin to breathe orally until about 4 months of age. Ingested liquids pass lateral to the epiglottis via the piriform Abdominal Wall and Gastrointestinal Tract 33 takes its first breath, the terminal bronchioles and alveoli are filled with fluid, mostly produced in the lung. There is more fluid in the lungs of a newborn infant delivered by cesarian section than after vaginal delivery. Surfactant also prevents alveolar collapse on expiration, which explains why very premature infants with inadequate surfactant production develop respiratory distress. Remodeling of the pulmonary vessels begins immediately after birth to reduce pulmonary vascular resistance. The peritoneal cavity is shallow anteroposteriorly because there is no lumbar lordosis and the paravertebral gutters are poorly developed. The greater omentum is delicate and membranous, rarely extending much below the level of the umbilicus. Indeed, the neonate has altogether less fat in the mesenteries and around the viscera. Diaphragmatic contraction tends to pull the ribs inward; concomitant outward movement of the abdomen (thoracoabdominal paradox) is a normal finding in newborns. The work of breathing is greater in a neonate than an adult and still greater in a preterm infant. The neonatal thymus is large (up to 5 cm wide and 1 cm thick) but variable in size at birth. The gland overlies the trachea, great vessels (especially the left brachiocephalic vein), and the upper anterior surface of the heart. After the first year of life, it becomes progressively less vascular, and the lymphoid tissue is increasingly replaced by fat. For these reasons, transverse supraumbilical incisions provide good surgical access. The rectus abdominis muscles may be relatively wide apart in the upper abdomen (divarication); this resolves with growth. Note the relative positions of the bladder (B) and uterus (U), the curvature of the sacrum (S), and the angle of the pelvis (dotted line between sacral promontory and pubic bone [P]). The narrowest part of the upper digestive tract is where the cricopharyngeus muscle blends with the upper esophagus, a potential site of esophageal perforation during the passage of a nasogastric tube. Gastric emptying is relatively slow and poorly coordinated in the first few weeks. The small bowel of the newborn is distributed more horizontally because of the shape of the abdominal cavity. The mean length of the small intestine from the duodenojejunal flexure to the ileocecal junction is around 160 cm when measured at term along its antimesenteric border in vivo39 but considerably longer when measured at autopsy. This vascular relationship is often abnormal in patients with intestinal malrotation, although abnormal orientation of these vessels can be seen in some healthy individuals and a normal relationship may sometimes exist in patients with intestinal malrotation. The cecum tapers to a proportionately large appendix with a relatively wide orifice. The anal canal has well-defined anal columns and prominent anal sinuses43; stasis within these sinuses is a putative cause of perianal sepsis, particularly in male infants. This makes it difficult to distinguish the small and large bowel on plain abdominal radiographs. Their relative position (central versus peripheral) and caliber are a guide, but a contrast study may be required to accurately differentiate small and large bowel pathology. The pancreatic tail is in contact with the spleen, usually at its hilum, in more than 90% of cases, which is a greater proportion than in adults. Individual nephrons consist of a renal corpuscle with (i) a central glomerulus concerned with plasma filtration and (ii) a renal tubule that produces urine by selective reabsorption of the filtrate. At birth, there are about 1 million renal corpuscles in the cortex of each kidney. Suprapubic aspiration and manual expression of urine are therefore relatively easy. The bladder does not achieve its adult pelvic position until about the sixth year. The neonatal Genitalia and reproductive tract By about the sixth month in utero, the testis lies adjacent to the deep inguinal ring connected to the developing scrotum by the gubernaculum. Although the testis originates as a retroperitoneal structure, it is suspended on a short mesentery (mesorchium) within the peritoneal Musculoskeletal system 35 cavity during abdominal "descent. At term, about 4% of boys have an undescended testis(es); the figure is considerably higher in premature infants. The penis and scrotum are relatively large, and the scrotum has a broad base and relatively thick walls. The prepuce begins to separate from the glans in utero but is usually only partially retractile at birth. In baby girls, the ovary lies in the lower part of the iliac fossa and only descends into the ovarian fossa within the true pelvis during early childhood as the pelvis deepens. At birth, the ovaries are relatively large and contain the full complement of primary oocytes, each surrounded by a single layer of follicular cells forming primordial follicles. Of the 7 million oocytes estimated to be present in the female fetus, only 1 million remain at birth, and this number decreases further to approximately 40,000 by puberty. Female newborns have a relatively prominent clitoris and labia, and the vagina, which is about 3 cm in length, is relatively thick-walled with a fleshy hymen. Premature fusion produces the elongated skull of sagittal craniosynostosis, the most common form of craniosynostosis. Premature babies have a tendency to develop a long thin head (dolichocephaly) secondary to postnatal gravitational molding, but this is not due to premature sutural fusion. The two most prominent are the anterior fontanel overlying the superior sagittal venous sinus at the junction of the metopic and sagittal sutures (bregma), and the posterior fontanel at the junction of the sagittal and lambdoid sutures (lambda). At birth, the bony external ear canal is not developed, and the mastoid process is absent. The facial nerve is therefore more at risk of injury where it emerges from the stylomastoid foramen. At birth, the two halves of the mandible are united by a fibrous symphysis that fuses in early childhood. The mandible subsequently changes shape as the teeth erupt and the muscles of mastication and chin develop. The maxillary and ethmoid sinuses are present at birth, but the sphenoid sinus is poorly developed and the frontal sinuses are absent. The hard palate is short, only slightly arched, and ridged by transverse folds, which assist with suckling. The nasolacrimal duct, which drains tear secretions from the conjunctival sac to the inferior meatus of the nasal cavity, is relatively short and wide at birth, but may be obstructed due to incomplete canalization. In the first 2 days of life, palpable overriding of the bones of the vault is common. Growth at the coronal suture is mostly responsible for fronto-occipital expansion of the skull; premature fusion causes brachycephaly if bilateral and plagiocephaly if unilateral. Growth at the metopic and Vertebral column, pelvis, and limbs the vertebral column in the neonate has no fixed curvatures other than a mild sacral curve. After birth, the thoracic curvature develops first and then, as the infant learns to control its head, sit, stand, and walk, curvatures in the lumbar and cervical spine develop, which help to maintain the center of gravity of the trunk when walking.

On irregularities of the pulmonary artery arrhythmia headaches buy lisinopril 10 mg on line, arch of the aorta and primary branches of the arch with an attempt to illustrate their mode of origin by a reference to development sinus arrhythmia buy discount lisinopril 10 mg online. Anomalous left pulmonary artery causing obstruction to right main bronchus: Report of a case pulse pressure points body cheap lisinopril online. Transformation of the aortic arch system during the development of the human embryo hypertension vs pulmonary hypertension purchase lisinopril 10 mg with amex. The roentgen diagnosis of double aortic arch and other anomalies of the great vessels blood pressure medication for sale safe 10 mg lisinopril. Diagnostic dilemma: Left aortic arch with right descending aorta- A rare vascular ring hypertension kidney failure order 2.5mg lisinopril with mastercard. Video-assisted thoracoscopic surgery: Is it a superior technique for the division of vascular rings in children Verlagerung durch eine abnorm verlaufende Arteria subclavia dextra (Arteria lusoria). Primary translocation of aberrant left subclavian artery for children with symptomatic vascular ring. Tracheoplasty with pericardial patch for extensive tracheal stenosis in infants and children. Variations in the technique of slide tracheoplasty to repair complex forms of longsegment congenital tracheal stenosis. Elliott M, Roebuck D, Noctor C, McLaren C, Hartley B, Mok Q, Dunne C, Pigott N, Patel C, Patel A, Wallis C. Outcomes of slide tracheoplasty in 101 children: A 17-year single-center experience. Compression of the trachea by an anomalous innominate artery; An operation for its relief. Cordovilla Zurdo G, Cabo Salvador J, Sanz Galeote E, Moreno Granados F, Alvarez Diaz F. Follow-up of surgical correction of vascular anomalies causing tracheobronchial compression. Follow-up of surgical correction of aortic arch anomalies causing tracheoesophageal compression: A 38-year single institution experience. Vascular tracheobronchial compression syndromes- Experience in surgical treatment and literature review. Vascular anomalies causing tracheoesophageal compression: A 20-year experience in diagnosis and management. Intermediate-term results of the free tracheal autograft for long segment congenital tracheal stenosis. The rupture of terminal air sacs causes air to escape into the pulmonary interstitium, resulting in pulmonary interstitial emphysema. The air tracks along the sheaths of pulmonary blood vessels to the lung hilum and air may then rupture into mediastinum, pleura, or pericardium. This approach has been shown to successfully remove interstitial gas, and after re-evacuation of the pneumothorax, ventilation could be discontinued shortly. The lesion represents air that has dissected along perivascular sheath within pulmonary interstitium. Also spontaneous pneumomediastinum without any history of mechanical ventilation or concomitant lung disease has been reported. The lungs are grossly hyperinflated with a diffuse cystic pattern in this film at 7 days of life. A shallow pneumothorax is present in the left upper zone and a left chest drain has been inserted. However, the survivors had a significantly lower maximal peak inspiratory pressure and FiO2 on the first day of ventilation. Treatment 427 It has also been described as having a crescentic configuration resembling a "spinnaker sail. It has been reported to be superior to x-ray under certain conditions and should be considered if a pneumomediastinum is clinically suspected and x-ray shows no typical findings. Tension pneumomediastinum has also been described to cause isolated left ventricular inflow obstruction. Symptomatic pneumomediastinum is managed by ultrasound-guided needle aspiration of the anterior mediastinal compartment. In asymptomatic cases, air is absorbed spontaneously and no treatment is indicated. A rare association of spontaneous pneumothorax with congenital cystic adenomatoid malformation35 and early spontaneous pneumothorax with common pulmonary vein atresia36 have been reported. The "surgical" cases of pneumothorax and/or pneumomediastinum at the Liverpool Neonatal Surgical Centre included infants with gross renal anomalies, large exomphalos, a rare type of vascular sling, and spontaneous perforation of esophagus. Tachypnea is a uniform finding and is often accompanied by grunting, chest retractions, and cyanosis. Physical findings in unilateral pneumothorax include a shift of the cardiac impulse to the unaffected side, diminished or absent breath sounds, and a hyperresonant percussion note on the affected side. In tension pneumothorax, arterial hypotension, apnea, and bradycardia are usually the initial signs. A large pneumothorax can be diagnosed by transillumination using a high-intensity light with fiber-optic probe. Other important observations in pneumothoraces are a mediastinal shift and absence of lung markings. Rarely, lobar emphysema, congenital cystic adenomatoid malformation, or congenital diaphragmatic hernia may resemble pneumothorax in the chest x-ray. Use of conventional chest drains is not free from complication as they can cause lung perforation41 or phrenic nerve injury related to abnormal location of the medial end of the chest tube. In the majority of cases, a properly sized ordinary chest drain with an underwater seal or with a vacuum-control unit should be adequate. The Heimlich flutter valve, though useful clinically, adds to the resistance of the system, especially if fluid accumulates in the valve. Aspiration is performed through the second intercostal space in the midclavicular line. The insertion of the needle is oblique through the muscle plane to avoid entry of air once the needle is removed. Occasionally a single aspiration may be enough, but all these babies must be closely observed and monitored clinically and radiologically as nearly all of them require a tube thoracostomy on follow-up. The tip of the chest tube should be placed anteriorly retrosternally for better drainage. The insertion site should be closed with a waterproof adhesive plastic film to avoid any air leak. A chest film after Pneumopericardium Pneumopericardium is the least frequent pulmonary air leak. However, recently, it has been occurring with increasing frequency as a complication of ventilatory therapy. Pneumopericardium can develop while the patients are on high-frequency ventilation respiratory support. The exact etiology of pneumopericardium is not known; it is probably interstitial pulmonary air, secondary to alveolar rupture, which dissects into the mediastinum and then enters the pericardial space at the reflection of the pericardium onto the great vessels. Simple needle pericardiocentesis is the appropriate therapy for most cases with cardiac tamponade. However, a few babies with pneumopericardium uncontrolled by needle aspiration require placement of a pericardial catheter for continuous drainage of air. Pneumopericardium can be masked by other pulmonary air leaks and should be considered if drainage of the primarily obvious site does not improve the cardiorespiratory status of the infant. Unsuccessful resuscitation of a preterm infant due to a pneumothorax and a masked tension pneumopericardium. Transport of air along sheaths of pulmonic blood vessels from alveoli to mediastinum, clinical applications. Pulmonary interstitial emphysema in low birth weight infants: Characteristics of survivors. Prophylactic protein free synthetic surfactant for preventing morbidity and mortality in preterm infants. Resolution of pulmonary interstitial emphysema following selective left main stem intubation in a premature newborn: An old procedure revisited. Unilateral pulmonary interstitial emphysema following pneumonia in a preterm infant successfully treated with prolonged selective bronchial intubation. Lateral decubitus position as therapy for persistent pulmonary interstitial emphysema in neonates: A preliminary report. Therapeutic lung puncture for diffuse unilateral pulmonary interstitial emphysema in preterm infants. Lung volume reduction surgery in lieu of pneumonectomy in an infant with severe unilateral pulmonary interstitial emphysema. Spontaneous pneumomediastinum in a child: Sonographic detection in a case with minimal findings on chest radiography. Ultrasound guided percutaneous relief of tension pneumomediastinum in a 1-day-old newborn. Collaborative quality improvement to promote evidence based surfactant for preterm infants: A cluster randomized trial. The factors affecting persistent pneumothorax and mortality in neonatal pneumothorax. Diagnosis of pneumothorax or pneumomediastinum in the neonate by transillumination. Neonatal phrenic nerve paralysis resulting from intercostal drainage of pneumothorax. Arterial blood gas and expiratory pressure monitoring in infants with pneumothorax: Prognostic predictability. In fetuses and neonates, the most common cause of congenital effusions is a chylothorax. A well-established entity, chylothorax results from leakage of chyle from the thoracic duct into the pleural cavity. The most common etiology of acquired pleural effusion in newborns is iatrogenic (result of cardiac or thoracic surgery). This article presents a basic description of the pathophysiology of pleural effusion and chyle, the anatomy and embryology of the pleura and lymphatic system, and an overview of key clinical aspects of neonatal pleural effusions, especially chylothorax, as well as fetal pleural effusion, hemothorax, and empyema, to provide the foundation for understanding this disorder. Fluid continuously moves from the parietal pleura though the pleural space to be absorbed by the visceral pleura. Recently, another hypothesis states that the amount of fluid can be controlled and absorbed via a metabolically active transport system in the parietal pleural mesothelial cells. Therefore, accumulation can occur when the balance between the rate of filtration and lymphatic clearance is altered. This can be seen in increased systemic capillary or venous pressure, increased capillary vessel permeability due to infection or inflammation, decreased plasma colloid osmotic pressure, increased negative intrapleural pressure, obstructed lymphatic flow, or abnormality or injury of the lymphatic system. Chylomicrons (emulsified fat globules) are absorbed from the small intestine, and are mixed with clear lymph from the pelvis and lower extremities, conducted centrally, and then drained into the venous system via the thoracic duct. At birth, chyle is clear and straw colored; soon after milk feeding begins, chylomicrons render it milky white. Lymph is collected in the cisterna chyli and reaches the venous system via the thoracic duct, which ascends in the posterior mediastinum between the azygos vein and the descending aorta. This duct crosses to the left at the level of the fifth thoracic vertebra, continues its ascent into the neck on the left of the esophagus, and opens into the venous system at the confluence of the internal jugular and subclavian veins. In the thorax, it receives lymph from the parietal pleura of both sides via several collecting trunks. Lymphatic branches from structures in the posterior mediastinum and from the left lung and its pleura join to form the left bronchomediastinal trunk; this trunk opens into the thoracic duct or directly into the great veins. While the thoracic duct is usually a singular structure, its embryology underscores the potential for anatomic variations and congenital anomalies. It may develop in different anatomical patterns with several lymphaticovenous anastomoses. Variation in lymphatic pathways and the presence of accessory lymphatic channels can account for chylous effusions resulting from surgical procedures that do not expose the main thoracic duct. Trauma to the duct in the posterior mediastinum can produce a unilateral or bilateral chylothorax. Rupture of the thoracic duct between the diaphragm and T5 usually produces a right-sided chylothorax, and above T5, a left-sided chylothorax. Rupture in the midline at T5 or as part of a more diffuse lymphatic condition causes bilateral chylothorax. Males are affected twice as frequently as females, and 60% of cases involve the right side of the chest. Congenital chylothorax can also be associated with other congenital malformations (76%), chromosomal anomalies (trisomy 21) (12%), and other syndromes (Noonan, Turner) (6%). Congenital pleural effusion with associated diseases Congenital pleural effusion is also associated with hydrops fetalis, other congenital anomalies, or genetic abnormalities.

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