Prostaglandin E1 Infusion Research Articles

Risk factors of mortality and recoarctation after coarctation repair in infancy

The main challenge of aortic coarctation repair in infants is to obtain durable results without morbidity. We aimed to describe predictors of mortality and of arch aortic re-intervention after aortic coarctation repair. Between January 2000 and March 2014, we retrospectively included consecutive infants with isolated coarctation or coarctation with ventricular septal defect (CoA + VSD) who had surgical repair of the aortic arch before three months of age. Five hundred and thirty patients were included: 308 (58%) patients had isolated coarctation and 222 (42%) had CoA + VSD. Three hundred and eighty-five patients (72.6%) only had coarctation repair, 51 patients (9.6%) had coarctation repair with closure of VSD, and 94 patients (17.8%) had coarctation repair and pulmonary artery banding. Mean age at operation was 13 ± 1.6 days, with 294 patients (55.5%) operated before 2 weeks. Mean weight at repair was 3.2 ± 0.75 kg. Median follow-up was 7.57 [0.25–15.98] years. Sixty-one patients (11.5%) needed reintervention on the aortic arch (surgery or endovascular interventions). Freedom from aortic arch reintervention was 90% at one year, and 88.5% at five years. Rates of aortic arch reintervention were similar in the different surgical strategy groups ( P = 0.80). However, in patients receiving prostaglandin E1 (PGE1), the end-to-end repair was at higher risk of re-coarctation compared to the extended end-to-side repair ( P = 0.0081). The risk factors of aortic arch reintervention were age at repair < 15 days ( P = 0.032), and the need for PGE1 infusion at surgery ( P = 0.0072). Overall mortality was 3.6% (19 patients) without significant difference between surgical strategies ( P = 0.078). In multivariate analysis, the risk factors of death were the presence of VSD ( P = 0.037), and low weight at surgery ( P = 0.001). Coarctation repair in young infants has an overall good outcome. The use of PGE1 may modify the aortic arch anatomy and mask the boundaries of the resection to be performed. Strategies to improve the surgical strategy preoperatively should be developed.

Experience of medical treatment of neonates with Ebstein anomaly in the intensive care unit

Background: Neonates with Ebstein anomaly may remain a challenge for neonatal intensive care units due to continuously changing clinical manifestations. Maintaining an adequate cardiac output in the presence of cardiomegaly, severe cyanosis, high pulmonary vascular resistance, and rhythm disorders is a difficult task. Aim: To demonstrate the possibility of conservative management, as well as clinical and instrumental criteria of assessment of neonates with Ebstein anomaly and arterial hypoxemia and cardiomegaly. Materials and methods : Four neonates aged from 3 to 8 days of life were admitted to the neonate intensive care unit due to persistent arterial hypoxemia (SaO 2 ≤ 90%) and O2-dependence. Their cardiothoracic ratios ranged from 55 to 75% and were higher in the neonate with initial severe tricuspidal insufficiency (stage 3–4). Great Ormond Street Echocardiography (GOSE) score > 1 was found in 2 neonates with clinical manifestation of severe heart failure, arterial hypoxemia and cardiomegaly. Results : During the following 3 to 4 days, two neonates (aged 5 and 6 days) were transferred to the 2 nd stage of care due to the absence of clinical manifestations of heart failure and severe hypoxemia. In the other two cases, intensive management was necessary, with catecholamine support, oxygen therapy, infusion of prostaglandin E1, anti-arrhythmic agents, with no surgical intervention. Conclusion: The majority of symptomatic neonates with Ebstein anomaly can be stabilized in the settings of adequate conservative management. However, some of them would require transition from conservative treatment to surgical intervention. Such clinical and instrumental criteria, as SaO 2 , cardiothoracic ratio, and GOSE are the main benchmarks to choose between conservative and surgical strategy.

Abstract P-327: OUTCOMES OF BABIES WITH CONGENITAL DIAPHRAGMATIC HERNIA IN A NON ECMO PEADIATRIC INTENSIVE CARE UNIT IN SOUTH AUSTRALIA. A RETROSPECTIVE OBSERVATIONAL STUDY OVER 16 YEARS.

Aims & Objectives: Introduction: Congenital diaphragmatic hernia (CDH) is a common birth defect which is associated with high morbidity and mortality. The cause for mortality is usually severe persistent pulmonary hypertension (PPHN) resulting from pulmonary hypoplasia. With Advances in intensive care and ECMO, mortality has reduced to < 20% in many centres. We report outcomes from Non ECMO tertiary PICU.1,2,3 Methods This retrospective observational study done over 16 years in a tertiary PICU without ECMO in South Australia. Results 62 babies born or referred to us with CDH had survival rate of 87%comparable to many ECMO centres. We noted severe PPHN in 30% (19/62) managed with inhaled Nitric oxide (iNO) of whom 36%(7/62) expired. Prostaglandin infusion was given to avoid right heart failure in 27 %(17/62) of which 50% received nitric and Prostaglandin infusion (8/62). Conclusions The outcome of CDH has improved with survival rates of 70–90% in centres even without ECMO. We report a survival rate of 87% with conventional management NO and PGE1 infusion. PGE1 results in ductal patency with reduction of right ventricular strain to manage transitional PPHN. We report increasing use of PGE1 over the past decade with improved outcomes.

Abstract P-535: A CASE OF HYPOPLASTIC LEFT HEART SYNDROME AND ATRESIA OF THE CENTRAL PULMONARY VEINS

Aims & Objectives: We present a case of a female neonate with hypoplastic left heart syndrome (HLHS) associated with complete atresia of the pulmonary veins. Methods After an uneventful pregnancy, spontaneous delivery at 40 + 5 weeks of gestation, and seemingly normal initial adaptation, the patient rapidly developed signs of cardiopulmonary failure within the first hour of life. Echocardiography established the diagnosis of HLHS with restricted interatrial communication and possible pulmonary venous abnormality. On clinical exam, marked hepatomegaly was noted and a chest X-ray showed diffuse, bilateral ground glass opacifications consistent with pulmonary venous congestion. The patient was subsequently intubated, started on a prostaglandin infusion, and transferred for further diagnostics and potential intervention. Results Angiocardiography was remarkable for the following findings: Marked delay in contrast filling of normal caliber mean and peripheral pulmonary arteries; bilateral absence of discernable pulmonary veins; late, diffuse capillary contrast filling; only faint contrast drainage at the atrial level; normal systemic venous return. This condition of bilateral central pulmonary venous atresia was deemed not amenable to surgical or interventional therapies. Comfort care measures were instituted, and the patient passed away shortly after discontinuation of prostaglandin. Conclusions Abnormalities of pulmonary venous return constitute a spectrum of disease. The presented case represents the most severe form of this challenging entity of congenital heart diseases. It has only been reported a few times before.

Arch Augmentation via Median Sternotomy for Coarctation of Aorta With Proximal Arch Hypoplasia

Coarctation of the aorta can be associated with hypoplasia of the proximal transverse aortic arch. One approach to manage this condition is via left thoracotomy and extended end-to-end anastomosis with the expectation that the proximal arch will grow over time. Our preferred approach is to augment the aorta via midline sternotomy. We hypothesized that this approach is safe, durable, and allows reliable growth of the aorta. We identified the records of patients with biventricular anatomy who had coarctation of the aorta, hypoplasia of the proximal transverse arch, and no other cardiac lesion that would mandate cardiopulmonary bypass use and midline sternotomy. The records of 62 such patients operated on between 2005 and 2016 were retrospectively reviewed. Patient demographics, clinical variables and outcome data were collected and analyzed using SAS 9.4. Data are presented as median (interquartile range [IQR]). Sixty-two patients (23 girls [37%]) underwent repair at 10 (IQR, 5 to 21) days of life. Forty-nine (79%) patients were on prostaglandin infusion to maintain ductal patency. Fifteen (24%) patients presented in shock with end organ dysfunction, 17 (27%) were on inotropes, and 26 (42%) were mechanically ventilated. The proximal transverse arch was 41% (IQR, 34% to 47%) of the size of ascending aorta as measured by echocardiography (z-score, -5 [IQR, -5.8 to -4.3]). Following median sternotomy, repair was carried out on cardiopulmonary bypass (41 [IQR, 37 to 47] minutes). The arch was reconstructed with (n= 26 [42%]) or without (n= 36 [58%]) coarctectomy usually using homograft patch aortoplasty (n= 58 [94%]). In all but 2 patients, repair was undertaken with circulatory arrest (27 [IQR, 22 to 31] minutes). Patients were extubated 4 (IQR, 3 to 5) days later and discharged home in 12 (IQR, 8 to 18) days. There was no mortality, and 8 morbidity events (3 recurrent nerve injury, 2 chylothorax, 1 phrenic nerve injury, 1seizure, and 1 superficial wound infection) in 7 (11%) patients. All patients are alive at 41 (IQR, 11 to 64) months of follow-up. Reintervention was required in 6 (10%) patients (5 catheter based and 3 surgical) for recurrent distal coarctation. Reintervention-free survival at 1, 3, and 5 years was 87%. Only 1 child was currently on antihypertensive therapy, and all were in New York Heart Association functional class I symptoms. At last echocardiogram, the proximal transverse arch was 97% (IQR, 84% to 103%) of the diameter of the ascending aorta (z-score, 0.8 (IQR, 0.3 to 1.3]), ejection fraction was 70% (IQR, 60% to 76%), and only 2 patients had significant left ventricular hypertrophy. Arch augmentation via median sternotomy is a safe and effective procedure that can be accomplished with low morbidity and mortality. The reconstructed arch retains excellent growth potential resulting in a very favorable physiologic outcome.

Preoperative Physiology, Imaging, and Management of Interrupted Aortic Arch.

Interrupted aortic arch (IAA) is a rare form of critical neonatal heart disease in which there is lack of continuity between the ascending aorta and the descending thoracic aorta. In the absence of prenatal diagnosis, patients with IAA present in shock when the patent ductus arteriosus closes. Diagnosis can generally be made by echocardiography, and initiation of prostaglandin E1 infusion allows for adequate lower body perfusion prior to surgical repair. Full neonatal repair can be achieved with good outcomes in most cases. However, there is often underdevelopment of the left ventricular outflow tract and risk for later surgical re-intervention. Many patients with IAA, particularly those with type B, have DiGeorge syndrome, which has important development implications.

Perioperative management with phosphodiesterase type 5 inhibitor and prostaglandin E1 for moderate portopulmonary hypertension following adult-to-adult living-donor liver transplantation: a case report

BackgroundPortopulmonary hypertension (PPH) is a relatively rare but well-recognized complication of end-stage liver disease. Moderate or severe PPH (mean pulmonary artery pressure [mPAP] ≥ 35 mmHg) is usually a contraindication for liver transplantation due to high operation-related mortality. Here, we report on a patient with moderate PPH whose condition was successfully managed with a phosphodiesterase type 5 (PDE5) inhibitor (tadalafil) and prostaglandin E1, who experienced rapid improvement of PPH after living-donor liver transplantation (LDLT).Case presentationA 63-year-old woman with alcoholic decompensated cirrhosis was referred to our hospital for LDLT. She had mild dyspnea on exertion as well as fatigue. Echocardiography and subsequent cardiac catheterization revealed a high mPAP (35 mmHg), and she was diagnosed with moderate PPH. We commenced treatment with oral tadalafil for the PPH. A second preoperative echocardiography demonstrated improved PPH, and she underwent LDLT. An intravenous infusion of prostaglandin E1 was introduced instead of tadalafil during and after the operation.The mPAP value showed a rapid decrease in mPAP value to 22 mmHg in 2 days. After discontinuation of the prostaglandin E1, the mPAP value remained 23 mmHg. Postoperative catheterization 2 months after LDLT showed no exacerbation of PPH. She was discharged on foot 70 days after LDLT in good condition and has shown a good clinical condition more than 2 years after LDLT.ConclusionLDLT could be a radical treatment for PPH with careful management and adequate patient selection. PDE5 inhibitor and PGE1 is effective and feasible for perioperative management of the patient with moderate portopulmonary hypertension in LDLT.

Enteral Feeding Practices in Infants With Congenital Heart Disease Across European PICUs: A European Society of Pediatric and Neonatal Intensive Care Survey.

To describe enteral feeding practices in pre and postoperative infants with congenital heart disease in European PICUs. Cross-sectional electronic survey. European PICUs that admit infants with congenital heart disease pre- and postoperatively. One senior PICU physician or designated person per unit. None. Fifty-nine PICUs from 18 European countries responded to the survey. PICU physicians were involved in the nutritional care of children with congenital heart disease in most (76%) PICUs, but less than 60% of units had a dedicated dietician. Infants with congenital heart disease were routinely fed preoperatively in only 63% of the PICUs, due to ongoing concerns around prostaglandin E1 infusion, the presence of umbilical venous and/or arterial catheters, and the use of vasoactive drugs. In three quarters of the PICUs (76%), infants were routinely fed during the first 24 hours postoperatively. Units cited, the most common feeding method, both pre and postoperatively, was intermittent bolus feeds via the gastric route. Importantly, 69% of European PICUs still did not have written guidelines for feeding, but this varied for pre and postoperative patients. Wide variations in practices exist in the nutritional care between European PICUs, which reflects the absence of local protocols and scientific society-endorsed guidelines. This is likely to contribute to suboptimal energy delivery in this particularly vulnerable group.

Endotoxin Activity in Neonates Undergoing Cardiac Surgery: Cohort Study.

Endotoxemia in pediatric cardiac surgical patients is poorly understood. The endotoxin activity assay (EAA) levels were examined in neonates undergoing cardiac surgery in order to assess their reference levels and their association with other pre-, intra-, and postoperative risk factors for gut hypoperfusion. We finally observed if refeeding was associated with modification of endotoxin levels. In a prospective cohort study, neonates undergoing surgery for correction or palliation were enrolled. Preterm birth, weight below 1.5 kg, the need for extracorporeal membrane oxygenation, and urgent surgery were exclusion criteria. Among the 26 enrolled neonates, 12 underwent on-pump and 14 off-pump surgery, 22 received a preoperative infusion of prostaglandin E2. Overall, 11 patients were surgically corrected and 15 received a palliation. Endotoxin activity assay baseline levels were inversely correlated with age at surgery ( r = -.50, P = .006) and they increased to postoperative day2 ( P = .002). On-pump versus off-pump surgery ( P =.36) and surgical palliation with a Blalock-Taussig shunt versus correction ( P = .45) did not predict increase in EAA levels. Aortic clamping for coarctation repair was associated with the lowest levels ( P = .04). Systolic, mean, and diastolic pressures were associated with EAA levels ( r = -.55, P = .01; r = -.45, P = .02; r = -.37, P = .04, respectively). Endotoxin activity assay levels after refeeding were similar to baseline levels. Patients with abdominal distension and feeding intolerance showed higher median peak EAA levels (0.7, 0.66-1.11) than asymptomatic patients (0.53, 0.35-0.64; P = .01). Endotoxin activity assay levels increase after elective neonatal surgery and are not modified by refeeding. High postoperative levels may predict feeding intolerance.

OAB without an overactive bladder in the acute prostaglandin E2 rat model.

Intravesical prostaglandin E2 (PGE2) was previously used to induce overactive bladder (OAB) symptoms, as it reduces bladder capacity in rats and causes a "strong urgency sensation" in healthy women. However, the mechanism by which this occurs is unclear. To clarify how PGE2 reduces bladder capacity, 100 µM PGE2 was administered intravesically during open, single-fill cystometry with simultaneous measurement of sphincter EMG in the urethane-anesthetized female Wistar rat. PGE2 was also applied to the urethra or bladder selectively by use of a ligature at the bladder neck before (urethra) or during (bladder) closed-outlet, single-fill cystometry. Additional tests of urethral perfusion with PGE2 were made. PGE2 decreased bladder capacity, increased voiding efficiency, and increased sphincter EMG during open cystometry compared with saline controls. The number of nonvoiding contractions did not change with PGE2; however, bladder compliance decreased. During closed-outlet cystometry, PGE2 applied only to the bladder or the urethra did not decrease bladder capacity. Urethral infusion of PGE2 decreased urethral perfusion pressure. Taken together, these results suggest that intravesical PGE2 may decrease bladder capacity by targeting afferents in the proximal urethra. This may occur through urethral relaxation and decreased bladder compliance, both of which may increase activation of proximal urethra afferents from distension of the proximal urethra. This hypothesis stands in contrast to many hypotheses of urgency that focus on bladder dysfunction as the primary cause of OAB symptoms. Targeting the urethra, particularly urethral smooth muscle, may be a promising avenue for the design of drugs and devices to treat OAB.

Stimulation of the pelvic nerve increases bladder capacity in the prostaglandin E2 rat model of overactive bladder.

Overactive bladder (OAB) syndrome is a highly prevalent condition that may lead to medical complications and decreased quality of life. Emerging therapies focusing on selective electrical stimulation of peripheral nerves associated with lower urinary tract function may provide improved efficacy and reduced side effects compared with sacral neuromodulation for the treatment of OAB symptoms. Prior studies investigating the effects of pelvic nerve (PelN) stimulation on lower urinary tract function were focused on promoting bladder contractions, and it is unclear whether selective stimulation of the PelN would be beneficial for the treatment of OAB. Therefore our motivation was to test the hypothesis that PelN stimulation would increase bladder capacity in the prostaglandin E2 (PGE2) rat model of OAB. Cystometry experiments were conducted in 17 urethane-anesthetized female Sprague-Dawley rats. The effects of intravesical PGE2 vs. vehicle and PelN stimulation after intravesical PGE2 on cystometric parameters were quantified. Intravesical infusion of PGE2 resulted in decreased bladder capacity and increased voiding efficiency without a change in bladder contraction area under the curve, maximum contraction pressure, or contraction duration. Bladder capacity was also significantly decreased compared with vehicle (1% ethanol in saline) confirming that the change in bladder capacity was mediated by PGE2 PelN stimulation reversed the PGE2-induced change in bladder capacity and increased the external urethral sphincter electromyogram activity at a specific stimulation condition (amplitude of 1.0 times threshold at 10 Hz). These results confirm that the urodynamic changes reported in conscious rats are also observed under urethane anesthesia and that PelN stimulation is a novel and promising approach for the treatment of the symptoms of OAB.

Evaluation of prostaglandin E1 infusion on urinary calcium excretion in neonates with congenital heart disease

Evaluation of prostaglandin E1 infusion on urinary calcium excretion in neonates with congenital heart disease

Presentation of coarctation of the aorta in the neonates and the infant with short and long term implications

Abstract Coarctation of the aorta (CoA) can present with acute circulatory collapse during the neonatal period or in early infancy. This review article aims to cover the presentation and management of CoA; including the common signs and symptoms, pathophysiology, medical and surgical management. We will not cover the features of the disease presentation in older children or adults. A high index of suspicion of CoA is extremely important in infants presenting with circulatory collapse in the first 6–8 weeks of life. Decreased femoral arterial pulse volume as compared to the right brachial artery, raised upper limb blood pressure as compared to lower limb and differential cyanosis should raise suspicion of coarctation in an infant presenting with circulatory collapse. Prostaglandin (PGE1 or PGE2) infusions should be started as soon as possible to restore forward circulation.

Lecture 7: Management of Critical CHD Neonates: Focus on PDA Stenting

Duct-dependent pulmonary circulation is one of the most common form of critical congenital heart disease in neonates. Cyanosis is the predominant presentation symptom. Infusion of Prostaglandin E1 is helpful in maintaining short-term ductal patency. An urgent systemic-to-pulmonary artery shunt is required to maintain the blood flow supply to pulmonary arteries. But the complications related to placing a shunt to pulmonary arteries were not infrequent in neonates. With the advent of transcatheter techniques, stenting of patent ductus arteriosus (PDA) can be an alternative to systemic-to-pulmonary artery shunts. Recently, bare coronary stents have been successfully used to stent PDA. The vascular access to stent PDA can be either from a prograde route (femoral vein) or retrograde route (axillary artery). Sometimes, more than one stent is required to covert the whole length of ductus. Generally, a 3.5 mm or 4.0 mm coronary stent was used. Neonates with a non-restrictive large ductus (narrowest diameter ≥ 2.5 mm) or juxta-ductal branch pulmonary artery stenosis should be excluded. Anti-platelet agents should be given to prevent thrombosis within the stent. Although stenting PDA is a safe procedure and can be an alternative to shunt placement, complications such as stent migration, thrombus and heart failure were not uncommon.

A Case of Hepatic Artery Thrombosis after Liver Transplantation

Introduction: Hepatic artery thrombosis (HAT) is the most serious vascular complication after liver transplantation. The most common presentation is elevation of liver function tests. When the diagnosis of hepatic arterial thrombosis is established, prompt intervention should be performed.Case Presentation: In this case report, we present a 37-year-old male with Chronic Hepatitis B infection who underwent a successful liver transplantation, and later developed multiple complications. The most significant of which is hepatic artery thrombosis. He underwent revascularization, supported by heparin and prostaglandin infusion. Succeeding doppler ultrasound surveillance showed patency of right hepatic artery flow. Conclusion: Early identification of hepatic artery thrombosis should be paid attention after liver transplantation to prevent its complications. Once the diagnosis is established, prompt intervention such as retransplantation or revascularization should be performed.

Impact of prenatal diagnosis of transposition of the great arteries on postnatal outcome

Objective: To assess the impact of prenatal diagnosis of transposition of the great arteries (TGA) on postnatal outcome.Methods: Hundred and fifty-four patients with either simple (n = 101) or complex forms (n = 53) of TGA, diagnosed prenatally (G1, n = 88) or postnatally (G2, n = 66), who were admitted and underwent surgical correction in our centre between 1998 and 2014, were analysed.Results: Prostaglandin E1 (PgE1) infusion and balloon atrial septostomy (BAS) were performed in the first 48 h after birth more commonly in G1. The hospital mortality rate for the whole group was 7.1%, higher for complex forms (13.2%) than for simple TGA (3.9%), (p = 0.034). The overall mortality rate was similar in G1 and G2. The mortality for simple TGA was higher when PgE1 infusion and BAS were implemented after the first 48 h (p = 0.001). All deaths in G2 occurred in patients first receiving PgE1 and BAS beyond 48 h. PgE1 was initiated in the first 48 h in most patients (83%) with simple TGA postnatally diagnosed.Conclusions: Adequate measures in the first 48 h after birth are essential to reduce the early mortality in TGA, especially in the simple form. This can be provided by prenatal diagnosis or by early neonatal clinical suspicion and prompt measures.

Case 1: Absent Lower Limb Pulses in a Neonate

A 3-kg term male infant is born to a 26-year-old primigravida woman after 5 years of primary infertility secondary to polycystic ovary syndrome. Vacuum extraction is performed for fetal distress, and the infant is resuscitated with positive pressure ventilation and chest compressions for 60 seconds. In the NICU, mechanical ventilation is initiated. The first blood gas measurement 10 minutes after birth reveals a pH of 6.6, partial pressure of carbon dioxide of 64 mm Hg (8.5 kPa), partial pressure of oxygen of 100.8 mm Hg (13.4 kPa), and bicarbonate of 5.4 mEq/L (5.4 mmol/L). Systemic hypothermia is initiated for perinatal asphyxia with moderate encephalopathy. He develops features of poor perfusion 6 hours after birth and is resuscitated with 2 normal saline boluses. A dobutamine infusion is started, followed by epinephrine infusion for refractory shock. Packed red blood cells are transfused, because the hematocrit is only 35% (0.35) and the infant has a subgaleal hemorrhage. He is given phenobarbitone, phenytoin, and levetiracetam, and later midazolam infusion for refractory seizures. In view of the refractory shock, systemic hypothermia is discontinued and the infant is rewarmed over a period of 8 hours. As his perfusion improves, it is noted that the femoral pulses are weaker than the brachial pulses, with systolic blood pressures 20 mm Hg higher in the upper limbs. The infant is suspected to have critical coarctation of the aorta and a prostaglandin infusion is started. However, an echocardiography at the bedside shows a normal thoracic aorta and aortic arch. A computed …

Evaluation of the Cyanotic Newborn: Part 2—A Cardiologist’s Perspective

Congenital heart disease is a major cause of cyanosis in the newborn, which should be considered and recognized promptly. Careful history and meticulous physical examination along with appropriate investigations are essential for the diagnosis of cyanotic congenital heart diseases. Although cardiac echocardiography is the diagnostic choice for congenital cardiac lesions, many centers may not have it readily available. In such cases, use of pulse oximetry, the hyperoxia test, chest radiography, and electrocardiograpy will usually differentiate heart disease from other causes of cyanosis. If a ductal-dependent lesion is suspected, the immediate initiation of prostaglandin E1 infusion may be life-saving. Understanding the pathophysiology of cyanotic congenital heart diseases is crucial in the initial management in such settings. A high index of suspicion must be maintained for the appropriate management and institution after birth-saving measures.

Threatened limb from stingray injury

We present the case of a 43-year-old female who suffered a stingray injury to her left ankle. The sting caused occlusion of the dorsalis pedis artery, causing dry gangrene of the medial forefoot. A below knee amputation was recommended but she was transferred for a second opinion. A Prostaglandin E1 infusion was commenced, resulting in alleviation of pain and improvement in perfusion. Amputation of great and second toes was performed, with the head of the first metatarsal preserved and covered via a cross-over skin flap raised from the contralateral leg. Achilles tendon lengthening was then performed to return the foot to a functional position. This case serves to highlight the utility of prostaglandin infusion, and the requirement for a multidisciplinary approach to critical limb ischemia in order to avoid major amputation.

Perioperative prostaglandin e1 infusion in living donor liver transplantation: A double-blind, placebo-controlled randomized trial.

The role of prostaglandin E1 (PGE1) infusion in improving early graft function has not been well defined, especially in the scenario of living donor liver transplantation (LDLT). We designed a randomized, double-blind, placebo-controlled trial to evaluate the role of perioperative PGE1 infusion in LDLT. Patients in the study arm received PGE1 (alprostadil) at the rate of 0.25 μg/kg/hour, starting at 1 hour after portal venous reperfusion, and continued for 96 hours. The primary endpoint was early allograft dysfunction (EAD). We analyzed multiple secondary endpoints including postoperative liver function and renal function parameters, acute kidney injury (AKI), hepatic artery thrombosis (HAT), postoperative bleeding, overall mortality, and posttransplant hospital stay. The incidence of EAD was lower in the PGE1 arm, although the difference did not reach statistical significance (22.4% versus 36%; P = 0.21). Among the secondary endpoints, the incidence of AKI was significantly lower in the PGE1 arm (8.2% versus 28%; P = 0.02), as were the peak and mean postoperative creatinine levels. The need for renal replacement therapy was similar between the 2 groups. Among the postoperative graft function parameters, postoperative alanine aminotransferase level was significantly lower in the PGE1 arm (P = 0.04), whereas the remaining parameters including serum bilirubin, aspartate aminotransferase, and international normalized ratio were similar between the 2 arms. There was no difference in the incidence of HAT and postoperative bleeding, in-hospital mortality, and posttransplant hospital stay between the 2 arms. Perioperative PGE1 infusion reduces the incidence of posttransplant renal dysfunction in patients undergoing LDLT. Liver Transplantation 22 1067-1074 2016 AASLD.