The major finding of this study was there was no significant difference between NAC and placebo in the prevention of contrast nephropathy. Human immunodeficiency virus; LDH: A report of this meeting can be found in Related Products. This report presents the case of a year-old woman who developed acute pancreatitis after the onset of herpes zoster.
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In 2 RCTs the N-acetylcysteine was administered intravenously Koc, ; Kotlyar, with total doses varying between 0. The follow-up time for laboratory parameters in the studies varied between 2 days and 30 days. To answer our clinical question a systematic literature analysis was performed for the following research question:. Can prophylactic N-acetylcysteine in addition to hydration reduce the incidence of CI-AKI in patients receiving intravascular contrast?
Can prophylactic N-acetylcysteine in addition to hydration reduce the incidence of CI-AKI in patients receiving intravascular contrast in certain subgroups of patient For example, patients with reduced kidney function? P patient category adult patients undergoing radiological examinations receiving intravascular contrast;. O outcome post-contrast acute kidney injury PC-AKI , start dialysis, decrease in residual kidney function, adverse effects of hydration congestion, intensive care unit admittance, and mortality , cost-effectiveness.
The working group considered PC-AKI, mortality and start dialysis critical outcome measures for the decision making process and the intensive care admission important outcome measures for the decision-making process. Thus the number needed to treat would be , ergo: This search was updated on 1 May A total of studies were found. The initial literature search produced hits and the update produced 39 hits.
The following search criteria were applied:. Based on title and abstract a total of 91 studies were selected. After examination of full texts a total of 67 studies were excluded and 24 studies definitely included in the literature summary.
Reasons for exclusion are described in the exclusion table. The evidence tables and assessment of individual study quality are included under the tab Onderbouwing. Not specifically patients with normal or abnormal kidney function mix of impaired kidney function and diabetics.
Not specifically patients with normal or abnormal kieny function mix of impaired kidney function and diabetics. Bias due to inadequate blinding of participants to treatment allocation? Bias due to inadequate blinding of care providers to treatment allocation? Bias due to inadequate blinding of outcome assessors to treatment allocation?
Evidence table for intervention studies randomized controlled trials and non-randomized observational studies [cohort studies, case-control studies, case series] 1. This table is also suitable for diagnostic studies screening studies that compare the effectiveness of two or more tests.
This only applies if the test is included as part of a test-and-treat strategy — otherwise the evidence table for studies of diagnostic test accuracy should be used. However it does not improve mortality rate or the need for dialysis. On the basis of the serum creatinine concentration, iv administration of NAC appears protective against the nephrotoxicity of contrast medium.
An ultra-high dose of intravenous NAC is ineffective at preventing nephrotoxicity in patients with renal impairment undergoing emergency contrast CT. Acetylcycsteine orally mg twice daily on the day before and on the day of administration of the contrast agent.
Increase of at least 0. Prophylactic administration of the antioxidant acetylcysteine, along with hydration, prevents the reduction in renal function induced by iopromide, a non-ionic, low-osmolality contrast agent, in patients with chronic renal insufficiency.
Or they had received thrombolytic therapy with failed recanalization so the cardiac catheterisation was an emergency procedure. The prophylactic administration of intravenous NAC provides no additional benefit to saline in high-risk coronary patients with normal renal function.
These results suggest that both prophylactic NAC and aminophylline administration are effective in preventing CIN, but not with hydration alone. NAC pre-contrast and post-contrast does not confer any benefit in preventing radiocontrast induced nephropathy in vascular patients. No major adverse events death, acute renal failure requiring temporary replacement therapy, need for mechanical ventilation occurred in either group during the in-hospital follow-up period.
Hydration with intravenous 0. High-dose iv NAC does not provide additional clinical benefit to placebo with respect to CIN in non-selected patients undergoing angioplasty with moderate doses of contrast medium and optimal hydration.
In this large randomized trial we found that acetylcysteine does not reduce the risk of contrast-induced acute kidney injury or other clinically relevant outcomes in at-risk patients undergoing coronary or peripheral vascular angiography. Our findings suggest that the addition of NAC does not add further benefit in CIN prevention, compared to standard hydration with isotonic saline infusion.
In our experience, NAC did not prevent CIN in patients receiving iso-osmolar iodixanol contrast media and adequate hydration. Our results show that oral acetylcysteine does not reduce the risk of contrast nephropathy when used before elective diagnostic CAG in patients with renal dysfunction.
Our study indicates that high doses of NAC plus hydration provide better protection against CIN than combination therapy of NAC and ascorbic acid plus hydration, or hydration alone. Addition of NAC to standard hydration therapy is not associated with reduction in incidence of CIN in patients with mild to moderate renal impairment undergoing elective CAG.
NAC mg intravenously, once hours before procedure and once hours after procedure total dose mg. NACmg intravenously, once hours before procedure and once hours after procedure total dose mg. Patients with acute renal failure, endstage renal disease requiring dialysis, intravascular administration of contrast material within previous 6 days, pregnancy, lactation, emergent coronary angiography, history of hypersensitivity reaction to contrast media, cardiogenic shock, pulmonary edema, mechanical ventilator, parenteral use of diuretics, recent use of NAC, recent use of ascorbic acid, and use of metformin or NSAIDS within 48 h of procedure were excluded from the study.
The major finding of this study was there was no significant difference between NAC and placebo in the prevention of contrast nephropathy. These results suggest that this cohort gained no added protection to renal function with the use of NAC.
The evidence regarding NAC benefit for prevention of PC-AKI in patients with an impaired renal function is weak due to the quality of the trials and the heterogeneity of the results.
For example, follow-up time was only 2 to 5 days in the majority of included studies; thus meaningful conclusions could not be drawn about the consequences of NAC use for mid and long term morbidity and mortality. Furthermore, the studies were not powered to draw conclusions about morbidity and mortality, only for the short-term PC-AKI laboratory diagnosis.
Another meta-analysis concluded that NAC may help to prevent PC-AKI in patients undergoing coronary angiography, but does not have any impact on clinical outcomes such as dialysis or mortality Submaramiam, Furthermore, the dose and route of administration of NAC differed between studies. Of note, only studies that described hydration strategies representative to those used in the Netherlands were included in this analysis.
No studies were found that compared oral to intravenous N-acetylcysteine route of administration in patients undergoing intravascular contrast administration. Despite the theoretically potential kidney protection arguments, we do not recommend adding NAC to hydration routinely in patients with an impaired kidney function. Reason is that the level of evidence is weak and the demonstrated benefit is small at best, and clinically not proven relevant.
Moreover, the low costs of NAC itself is offset by extra handling time and a more complex AKI preventive protocol, which are unnecessary confounding and cost enhancing factors.
The board of the Radiological Society of the Netherlands will determine at the latest in if this guideline per module is still valid and applicable. If necessary, a new working group will be formed to revise the guideline. The validity of a guideline can be shorter than 5 years, if new scientific or healthcare structure developments arise, that could be seen as a reason to commence revisions. The Radiological Society of the Netherlands is considered the keeper of this guideline and thus primarily responsible for the actuality of the guideline.
The other scientific societies that have participated in the guideline development share the responsibility to inform the primarily responsible scientific society about relevant developments in their field. The guideline development was assisted by the Knowledge Institute of Medical Specialists www.
The aim of the Part 1 of Safe Use of Iodine-containing Contrast Media guidelines is to critically review the present recent evidence with the above trend in mind, and try to formulate new practical guidelines for all hospital physicians to provide the safe use of contrast media in diagnostic and interventional studies.
The ultimate goal of this guideline is to increase the quality of care, by providing efficient and expedient healthcare to the specific patient populations that may benefit from this healthcare and simultaneously guard patients from ineffective care.
Furthermore, such a guideline should ideally be able to save money and reduce day-hospital waiting lists. This guideline is intended for all hospital physicians that request or perform diagnostic or interventional radiologic or cardiologic studies for their patients in which CM are involved.
A multidisciplinary working group was formed for the development of the guideline in The working group consisted of representatives from all relevant medical specialization fields that are involved with intravascular contrast administration. All working group members have been officially delegated for participation in the working group by their scientific societies.
The working group has developed a guideline in the period from October until July The working group members have provided written statements about financially supported relations with commercial companies, organisations or institutions that are related to the subject matter of the guideline.
Furthermore, inquiries have been made regarding personal financial interests, interests due to personal relationships, interests related to reputation management, interest related to externally financed research and interests related to knowledge valorisation.
The statements on conflict of interest can be requested at the administrative office of the Knowledge Institute of Medical Specialists and are summarised below. Secretary section of Abdominal Radiology; Radiological Society of the Netherlands until spring of Receives Royalties for books: Has been a public speaker during symposia organised by GE Healthcare about contrast agents most recently in June At this time, the patient was admitted to the emergency department of our hospital.
She had no significant past medical history, and denied any alcohol, drug or smoke consumption. Moderate tenderness in the upper abdomen was observed with no rebound tenderness, a rectal examination was normal, and heart and chest auscultation did not reveal any findings.
No jaundice was seen in the skin and sclera. The combined results indicated moderately severe acute pancreatitis according to the revised Atlanta classification[ 7 ] and a Ranson score of 4[ 8 ]. The decreased serum calcium concentration and elevated blood glucose also indicated significant impairment of the pancreas with a poor prognosis. Serum calcium concentration; CRP: Erythrocyte sedimentation rate; FBG: Fasting blood glucose; HbA1C: Hepatitis C virus antibody; HIV: Human immunodeficiency virus; LDH: Presentation of characteristic rash.
Image showing a punctiform low signal intensity in the gallbladder arrowhead and peri-pancreatic exudation arrows. Image showing the swelling of the pancreas with peri-pancreatic exudation and liquid collection arrows.
Grade E acute pancreatitis was diagnosed based on the computed tomography severity index. The patient was fasted upon admission and received passive gastric decompression along with mask oxygen inhalation, fluid resuscitation, and total parenteral nutrition. She was administered octreotide 0. Vomiting ceased on the first day of admission, abdominal pain gradually improved, and the rash progressively regressed. The herpes zoster rash was determined by a dermatologist to be in the recovering phase and locally treated with acyclovir ointment.
The patient began enteral nutrition on the tenth day after amylase levels decreased to normal and C-reactive protein levels had decreased noticeably. She was permitted a fluid diet after 20 d, and discharged 27 d after admission with normal serum chemistry work-up results. The patient remained well during the one-month follow-up.
Acute pancreatitis is an inflammatory disease of the pancreas that may also involve peri-pancreatic tissues. The most common symptom of acute pancreatitis is acute abdominal pain, especially in the epigastrium, as well as gastrointestinal symptoms such as nausea and vomiting. Of the few cases of herpes zoster-associated acute pancreatitis that have been reported, most involve immunocompromised individuals, such as those in intensive care[ 11 ], AIDS patients[ 12 ], or receiving long-term immunosuppression, such as recipients of stem cell[ 13 - 15 ], renal[ 16 , 17 ] or liver[ 18 ] transplants.
Three studies reported acute pancreatitis associated with VZV in children with chickenpox[ 19 - 21 ] and one study reported an elderly patient with herpes zoster suffering from systemic complications including pancreatitis and encephalitis[ 22 ]. The case presented here is the first report of acute pancreatitis in an immunocompetent adult without comorbidity.
Although the mechanism of pancreatitis with herpes zoster is still unknown, VZV may remain latent in posterior sensory nerve roots that contain fibers from both skin and abdominal viscera, including the pancreas[ 23 ]. Although the location and the quality of the pain changed several days later, it could have easily been attributed to neuralgia caused by herpes zoster and ignored by mistake. The severity of the nausea and vomiting prompted the patient to seek additional treatment.
At this time, the diagnosis of acute pancreatitis was not difficult to confirm, based on serum amylase elevation and CT imaging. Although the etiology is not evident, the influence of VZV on the pancreas gained attention, as common contributors, such as cholelithiasis, alcoholism, common infection and immune deficiency, were excluded.
However, the management of viral acute pancreatitis is comparable to acute pancreatitis caused by other etiologies, involving supportive treatment with electrocardiograph monitoring, fluid resuscitation, pain control, and fasting with temporary enteral or total parenteral nutrition.
In conclusion, although rare, this case highlights the need to consider acute pancreatitis as a differential diagnosis for immunocompetent patients with herpes zoster, particularly when the location and quality of the pain changes during the course of the disease.
Early detection and proper treatment is needed when acute pancreatitis is suspected. A year-old woman presented with persistent pain in the upper quadrant and vomiting less than one week after the onset of a rash with stabbing pain, characteristic of varicella, on the abdomen and dorsal right trunk.