My patient with renal insufficiency developed hyponatremia after an IV contrast study.  Is there a connection between hyponatremia and iodinated contrast media?

There are several reports in the literature of hyponatremia (sometimes severe) developing in patients undergoing coronary angiography or routine IV contrast CT studies. 1-3 Although generally asymptomatic, severe hyponatremia with symptoms may also occur, particularly in those at risk of hyponatremia due to other factors.  

In a case series of 5 patients with advanced renal disease who underwent cardiac catheterization and developed post-procedure hyponatremia, the mean plasma sodium concentration decreased from 138.6 mEq/L to 122.6 mEq/L within 2-22 hours post-procedure; no patient had any neurological symptoms associated with hyponatremia. There was a strong correlation between dose of contrast administered and change in sodium level. 2

Severe symptomatic hyponatremia (confusion, stupor) was also reported in an elderly woman with blood creatinine of 0.9 mg/dL following coronary angiography (baseline plasma sodium 142 mmo/L vs. 115 mmol/L >16 hours post-procedure).  The authors suggested that a diagnosis of hyponatremia be considered in any patient who develops behavioral or neurologic manifestations after coronary angiography.3

Aside from coronary angiography, a prospective study among 103 adults (mean serum creatinine 0.79 mg/dl) undergoing contrast-enhanced CT found a drop in serum sodium from a mean concentration of 136 mmol/L to 132 mmol/L 24 hours after the procedure without any associated symptoms.1

Potential mechanisms for the development of hyponatremia after IV contrast studies include hemodilution due to translocation of fluid from intracellular space caused by high osmolality of the contrast media.1  

Bonus Pearl

Did you know that even the newer “low osmolar contrast” agents are more than 3 times the osmolality of blood?4

Liked this post? Download the app on your smart phone and sign up below to catch future pearls right into your inbox, all for free!

Subscribe to Blog via Email

Enter your email address to subscribe to this blog and receive notifications of new posts by email.

References

  1. Sankaran S, Saharia GK, Naik S, et al. Effect of iodinated contrast media on serum electrolyte concentrations in patients undergoing routine contrast computed tomography scan procedure. Int J Appl Basic Med Res 2019;9:217-220. https://www.ijabmr.org/article.asp?issn=2229-516X;year=2019;volume=9;issue=4;spage=217;epage=220;aulast=Sankaran
  2. Sirken G, Raja R, Garces J, et al. Contrast-induced translocational hyponatremia and hyperkalemia in advanced kidney disease. Am J Kidney Dis 2004;43:e9.1-e9.5. https://www.sciencedirect.com/science/article/abs/pii/S0272638603013854?via%3Dihub
  3. Jung ES, Kang WC, Jang YR, et al. Acute severe symptomatic hyponatremia following coronary angiography. Korean Circ J 2011;41:552-554. https://europepmc.org/article/pmc/pmc3193049
  4. Bucher AM, De Cecco CN, Schoefpf UJ, et al. Is contrast medium osmolality a causal factor for contrast-induced nephropathy? BioMed Res International 2014; Volume 2014, article ID 931413. https://www.hindawi.com/journals/bmri/2014/931413/

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

My patient with renal insufficiency developed hyponatremia after an IV contrast study.  Is there a connection between hyponatremia and iodinated contrast media?

What changes should I consider in my diagnostic approach to hospitalized patients with community-acquired pneumonia (CAP) in light of the 2019 guidelines of the American Thoracic Society (ATS) and Infectious Diseases Society of America (IDSA)?

Compared to 2007,1 the 2019 ATS/IDSA guidelines2 have 2 major “Do’s” and 2 major “Dont’s” in the diagnostic approach to CAP in hospitalized patients:

  • DO order sputum and blood cultures in patients empirically treated for methicillin-resistant Staphylococcus aureus (MRSA) or Pseudomonas aeruginosa—in addition to those with severe CAP as in 2007.  
  • DO order rapid influenza molecular assay—in preference to antigen test— when influenza viruses are circulating in community, irrespective of pneumonia severity
  • DON’T routinely order urine antigens for pneumococcal or Legionella antigens, except in severe CAP or in the presence of suggestive epidemiological factors (eg. Legionella outbreak, recent travel)
  • DON’t routinely order serum procalcitonin to determine need for initial antibacterial therapy

Patients at risk of MRSA or P. aeruginosa include those with prior infection with the same pathogens as well as those with hospitalization and treated with parenteral antibiotics—in or out of the hospital— in the last 90 days; HCAP is no longer recognized as an entity.

The definition of severe CAP is unchanged: 1 of 2 major criteria (septic shock or respiratory failure requiring mechanical ventilation) or 3 or more of the following minor criteria or findings listed below:

  • Clinical
    • Respiratory rate ≥30 breath/min
    • Hypotension requiring aggressive fluid resuscitation
    • Hypothermia (core temperature <36 ᵒC, 96.8 ᵒF)
    • Confusion/disorientation
  • Radiographic 
    • Multilobar infiltrates
  • Laboratory 
    • Leukopenia (WBC <4,000/ul)
    • Thrombocytopenia (platelets <100,000/ul)
    • BUN ≥20 mg/dl
    • Pa02/FI02 ratio ≤250

Keep in mind that these guidelines focus on adults who are not immunocompromised or had recent foreign travel and are often based on expert opinion but low or very low quality evidence due to the dearth of properly designed studies.

Bonus Pearl: Did you know that the urine Legionella antigen only tests for L. pneumophila type I, with an overall sensitivity ranging from 45% to 100%!3,4

Liked this post? Download the app on your smart phone and sign up below to catch future pearls right into your inbox, all for free!

Subscribe to Blog via Email

Enter your email address to subscribe to this blog and receive notifications of new posts by email.

 

 

References

  1. Mandell LA, Wunderink RG, Anzueto A. Infectious Disease Society of America/American Thoracic Society Consensus Guidelines on the Management guidelines on the management of community-acquired pneumonia in adults. Clin Infect Dis 2007;44:S27-72. https://www.ncbi.nlm.nih.gov/pubmed/17278083
  2. Metlay JP, Waterer GW, Long AC, et al. Diagnosis and treatment of adults with community-acquired pneumonia. Am J Respir Crit Care Med 2019;200:e45-e67. https://www.ncbi.nlm.nih.gov/pubmed/31573350
  3. Blazquez RM, Espinosa FJ, Martinez-Toldos CM, et al. Sensitivity of urinary antigen test in relation to clinical severity in a large outbreak of Legionella pneumonia in Spain. Eur J Clin Microbiol Infect Dis 2005;24:488-91. https://www.ncbi.nlm.nih.gov/pubmed/15997369
  4. Marlow E, Whelan C. Legionella pneumonia and use of the Legionella urinary antigen test. J Hosp Med 2009;4:E1-E2. https://www.ncbi.nlm.nih.gov/pubmed/19301376

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis or its affiliate healthcare centers, Mass General Hospital, Harvard Medical School or its affiliated institutions. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

 

 

What changes should I consider in my diagnostic approach to hospitalized patients with community-acquired pneumonia (CAP) in light of the 2019 guidelines of the American Thoracic Society (ATS) and Infectious Diseases Society of America (IDSA)?

Can my patient with renal insufficiency safely undergo gadolinium-based contrast MRI?

It may be possible for patients with renal insufficiency, including those with end-stage kidney disease (ESKD), to undergo MRI using potentially safer preparations of gadolinium-based contrast agents (GBCAs) with “very low, if any” risk of the feared nephrogenic systemic sclerosis (NSF). 1

In contrast to the so called “linear” chelates of gadolinium (eg, gadodiamide, gadopentetate), “cyclic” GBCA’s (eg, gadoteridol) have not been clearly associated with NSF. 2 A Veterans Administration study involving gadoteridol identified no cases of NSF among the 141 patients on hemodialysis following 198 exposures. 2 In fact, the 2017 American College of Radiology (ACR) Manual on Contrast Media reports the risk of NSF with cyclic chelates as “very low, if any”. 1 A 2020 systematic review and meta-analysis involving 4931 patients with stage 4 or 5 chronic kidney disease (ie, GFR <30mL/min per 1.73 m2) failed to find any cases of NSF after receiving group II GBCAs (eg, non-linear, including cyclic).2a When a cyclic GBCA is used in patients with ESKD, however, hemodialysis has been recommended as soon as possible after MRI. 3

GBCAs are chelates with 2 major components: gadolinium and either a linear or cyclic ligand. Cyclic ligands bind to gadolinium more avidly, resulting in lower probability of circulating renally-cleared free gadolinium which when deposited in tissue is thought to potentially trigger NSF.2

Although NSF is characterized by progressive fibrosis of skin and soft tissue, it may involve multiple organs with an estimated 30% mortality rate. 4

 Bonus Pearl: Did you know NSF is really a new disease, with no evidence of its existence before 1997?

 

Contributed by Richard Newcomb, MD, Mass General Hospital, Boston, MA.

 

Liked this post? Download the app on your smart phone and sign up below to catch future pearls right into your inbox, all for free!

Subscribe to Blog via Email

Enter your email address to subscribe to this blog and receive notifications of new posts by email.

 

References

  1. “Nephrogenic Systemic Fibrosis”. In ACR Manual on Contrast Media; Version 10.3; May 31, 2017. https://www.acr.org/-/media/ACR/Files/Clinical-Resources/Contrast_Media.pdf
  2. Reilly RF. Risk for nephrogenic systemic fibrosis with gadoteridol (ProHance) in patients who are on long-term hemodialysis. Clin J Am Soc Nephrol 2008;3:747-51. https://www.ncbi.nlm.nih.gov/pubmed/18287249.                                                   2a.  Woolen SA. Shankar PR, Gagnier JJ, et al. Risk of nephrogenic systemic fibrosis in patients with stage 4 or 5 chronic kidney disedse reciving a group II gadolinium-based contrast agent: A systematic review and meta-analysis. JAMA Intern Med 2020;180:223-230. Risk of Nephrogenic Systemic Fibrosis in Patients With Stage 4 or 5 Chronic Kidney Disease Receiving a Group II Gadolinium-Based Contrast Agent: A Systematic Review and Meta-analysis | Chronic Kidney Disease | JAMA Internal Medicine | JAMA Network
  3. Wang Y, Alkasab TK, Nari O, et al. Incidence of nephrogenic systemic fibrosis after adoption of restrictive gadolinium-based contrast agent guidelines. Radiology 2011;260:105-111.  https://www.ncbi.nlm.nih.gov/pubmed/21586680
  4. Schlaudecker JD, Bernheisel CR. Gadolinium-associated nephrogenic systemic fibrosis. Am Fam Physician 2009;80:711-14. https://www.aafp.org/afp/2009/1001/p711.pdf

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

 

Can my patient with renal insufficiency safely undergo gadolinium-based contrast MRI?

200 pearls and counting! Take the Pearls4Peers quiz #2!

Multiple choice (choose 1 answer)
1. Which of the following classes of antibiotics is associated with peripheral neuropathy?
a. Penicillins
b. Cephalosporins
c. Macrolides
d. Quinolones

 

 

2. The best time to test for inherited thrombophilia in a patient with acute deep venous thrombosis is…
a. At least 1 week after stopping anticoagulants and a minimum of 3 months of anticoagulation
b. Just before initiating anticoagulants
c. Once anticoagulation takes full effect
d. Any time, if suspected

 

 

3. All the following is true regarding brain MRI abnormalities following a seizure, except…
a. They are observed following status epilepticus only
b. They are often unilateral
c. They may occasionally be associated with leptomeningeal contrast enhancement
d. Abnormalities may persist for weeks or months

 

 

4. Which of the following is included in the quick SOFA criteria for sepsis?
a. Heart rate
b. Serum lactate
c. Temperature
d. Confusion

 

 

5. All of the following regarding iron replacement and infection is true, except…
a. Many common pathogens such as E.coli and Staphylococcus sp. depend on iron for their growth
b. Association of IV iron replacement and increased risk of infection has not been consistently demonstrated
c. A single randomized-controlled trial of IV iron in patients with active infection failed to show increased infectious complications or mortality with replacement
d. All of the above is true

 

True or false

1. Constipation may precede typical manifestations of Parkinson’s disease by 10 years or more
2. Urine Legionella antigen testing is >90% sensitive in legionnaire’s disease
3. Spontaneous coronary artery dissection should be particularly suspected in males over 50 years of age presenting with acute chest pain
4. Urine dipstick for detection of blood is >90% sensitive in identifying patients with rhabdomyolysis and CK >10,000 U/L
5. Diabetes is an independent risk factor for venous thrombophlebitis

 

 

 

Answer key
Multiple choice questions:1=d; 2=a;3=a;4=d;5=c
True or false questions:1=True; 2,3,4,5=False

 

200 pearls and counting! Take the Pearls4Peers quiz #2!

Can a seizure cause abnormalities on the brain MRI?

Yes it can, and the MRI abnormalities could represent seizure’s effects on the brain, not the seizure’s structural cause. Seizure-related MRI changes are often associated with status epilepticus, but have also been reported in complex partial status epilepticus.1,2

T2-weighted MRI images may show increased signal intensity at the cortical gray matter, subcortical white matter, or hippocampus. The MRI changes are unilateral about one-half of the cases, while in about 8% of patients leptomeningeal contrast-enhancement may be observed. Partial simple and complex seizures are associated with hippocampal involvement.3

The increased signal intensity following seizures is thought to be due to increased metabolism at the epileptogenic area, which in turn results in increased oxygen consumption, hypoxia, hypercarbia, lactic acidosis, and ultimately vasodilation and edema.

Reversibility of MRI changes following seizures has been noted between 15 and 150 days (average, 62 days). A structural abnormality is more likely the cause of a seizure when the MRI changes do not resolve during this period.3 Therefore, seizure-induced brain-MRI abnormalities remain a diagnosis of exclusion.

References

  1. Kim JA, Chung JI, Yoon PH, et al. Transient MR signal changes in patients with generalized tonicoclonic seizure or status epilepticus: periictal diffusion-weighted imaging. Am J Neuroradiol 2001; 22:1149–1160 http://www.ajnr.org/content/22/6/1149.long
  2. Henry TR, Brunberg DI, Pennell PB, et al. Focal cerebral magnetic resonance changes associated with partial status epilepticus. Epilepsia 1994; 35:35–41 http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.916.5237&rep=rep1&type=pdf
  3. Cianfoni A, Caulo M, Cerase A, et al. Seizure-induced brain lesions: a wide spectrum of variably reversible MRI abnormalities. Eur J Radiol. 2013; 82(11):1964-72. http://www.ejradiology.com/article/S0720-048X(13)00271-4/fulltext

 

Contributed by Johan H.L. Boneschansker, MD, Mass General Hospital, Boston, MA.

Can a seizure cause abnormalities on the brain MRI?

How strong is the evidence for IV contrast-induced nephropathy (CIN) following CT scans?

Not as strong as one might expect with an increasing number of investigators questioning the causative role of IV contrast in precipitating CIN.

A 2013 meta-analysis involving observational—mostly retrospective— studies concluded that the risks of AKI, death, and dialysis were similar between IV contrast and non-contrast patients, including those with diabetes or underlying renal insufficiency1.

Two retrospective studies2,3 designed to control for a variety of factors that may affect the risk of AKI by propensity matching found divergent results with the larger and better designed study finding no significant difference in AKI between the 2 groups3. A 2017 retrospective cohort analysis of emergency department patients utilizing a similar propensity-score analysis also failed to find a difference in post-CT AKI between those receiving and not receiving IV contrast4.

Further shedding doubt on the role of IV contrast in causing AKI, a study involving patients with chronic kidney disease found no difference in the rates of excretion of 2 biomarkers of AKI (neutrophil gelatinase-associated lipocalin-NGAL, and kidney injury molecule-1-KIM-1) between patients with and without presumed CIN5.

This is not to say that IV CIN does not exist. Among many findings, in vitro and animal studies have demonstrated that iodinated contrast media exerts cytotoxic effects on renal tubular epithelial cells and promotes hemodynamic changes through renal vasoconstriction to severe renal damage and cellular apoptosis (6). However, some have have criticized experimental animal studies supporting the existence of CIN due to their poor applicability to human renal disease. 1

After all these years, it’s still important to keep an open mind about the pathophysiology and epidemiology of CIN. Stay tuned!

Fun pearl: Did you know that the first case of CIN was described in a patient with multiple myeloma undergoing IV pyelography (before the CT era)?

Liked this post? Download the app on your smart phone and sign up below to catch future pearls right into your inbox, all for free!

Subscribe to Blog via Email

Enter your email address to subscribe to this blog and receive notifications of new posts by email.

References

  1. McDonald JS, McDonald RJ, Comin J, et al. Frequency of acute kidney injury following intravenous contrast medium administration: a systematic review and meta-analysis. Radiology. 2013;267(1):119-128. https://www.ncbi.nlm.nih.gov/pubmed/23319662
  2. Davenport MS, Khalatbari S, Dillman JR, et al. Contrast material-induced nephrotoxicity and intravenous low-osmolality iodinated contrast material. Radiology. 2013;267(1):94-105. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3606541/pdf/121394.pdf
  3. McDonald RJ, McDonald JS, Bida JP, et al. Intravenous contrast material-induced nephropathy: causal or coincident phenomenon? Radiology 2013;267:106-18. https://www.ncbi.nlm.nih.gov/pubmed/23360742
  4. Hinson JS, Ehmann MR, Fine DM, et al. Risk of acute kidney injury after intravenous contrast media administration. Ann Emerg Med 2017; 69:577-586. https://www.ncbi.nlm.nih.gov/pubmed/28131489
  5. Kooiman J, van de Peppel WR, Sijpkens YWJ, et al. No increase in kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin excretion following intravenous contrast enhanced-CT. Eur Radio 2015;25:1926-34. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4457910/pdf/330_2015_Article_3624.pdf
  6. Mamoulakis C, Fragkiadoulaki I, Karkala P, et al. Contrast-induced nephropathy in an animal model: evaluation of novel biomarkers in blood and tissue samples. Toxicol Rep 2019;6:395-400. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6506864/ 

Original contribution by Ginger Jiang, Medical Student, Harvard Medical School

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis or its affiliate healthcare centers, Mass General Hospital, Harvard Medical School or its affiliated institutions. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

How strong is the evidence for IV contrast-induced nephropathy (CIN) following CT scans?

When evaluating for an esophageal perforation, is a water-soluble contrast agent such as Gastrografin a better and safer alternative to barium swallow study?

Water-soluble contrast agents (WCAs) (eg, meglumine diatrizoate or Gastrografin) are often ordered as the initial radiographic test for evaluation of esophageal perforation or leaks, followed by barium swallow if the test is negative because small leaks are better detected with the more radiopaque barium1.  Such practice, however, is based on extrapolation of data on the deleterious effect of barium when extravasated into the peritoneal cavity, not the mediastinum1.   In fact, clinical evidence linking mediastinitis to extravasated barium is lacking, and even in experimental studies, injection of barium into the mediastinum of cats have failed to cause clinically significant mediastinitis2.

When ordering a contrast swallow study, no medium should be considered totally safe or effective in detecting esophageal perforations or leaks and WCAs are no different. Potential disadvantages of WCAs include: 1. Inferior sensitivity (as low as 50%)—due to decreased radio-opacity—when compared to barium3; 2. Risk of pulmonary edema—occasionally lethal— when aspirated into the lung due to high osmolality (analogous to salt water drowning) and intense inflammatory reaction4,5; 3. Contraindication in the setting of tracheoesophageal fistula,6; 4. Risk of serious allergic reaction due to reabsorption of iodinated compounds1; and 5. Added exposure to radiation and cost of testing when the swallow study is repeated with barium.  For these reasons, the standard practice of an initial WCA followed by a barium swallow`study if the former is negative, has been questioned, with some centers foregoing the WCA study altogether in favor of barium swallow in certain patients 1,6.

In short, when evaluating for esophageal perforation, WCAs should not categorically be considered a “better” or “safer” alternative to barium; in certain situations, barium may be the preferred agent. When in doubt, input from a thoracic surgeon is recommended.  

 

References

  1. Gollub MJ, Bains MS. Barium sulfate: a new (old) contrast agent for diagnosis of postoperative esophageal leaks. Radiology 1997;202:360-62. https://www.ncbi.nlm.nih.gov/pubmed/9015057
  2. James AE, Montali RJ, Chaffee V, et al. Barium or gastrografin: which contrast media for diagnosis of esophageal tears? Gastroenterology 1975;68:1103-1113. https://www.ncbi.nlm.nih.gov/pubmed/1126592
  3. Berry BE, Ochsner JL. Perforation of the esophagus: a 30 year review. J Thorac Cardiovasc Surg 1973;65:1-7. http://www.jpedsurg.org/article/0022-3468(73)90248-0/abstract
  4. Trulzsch DV, PenmetsaA, Karim A, et al. Gastrografin-induced aspiration pneumonia: A lethal complication of computed tomography. South Med J 1992;85:1255-56. https://www.ncbi.nlm.nih.gov/pubmed/1470976
  5. Tuladhar R, Patole S, Whitehall J. Gastrografin aspiration in a neonate with tracheoesophageal fistula. J Paediatr Child Health 2000; 36:94-6. https://www.ncbi.nlm.nih.gov/pubmed/10723703
  6. FDA https://www.drugs.com/pro/gastrografin.html.
  7. Roh S, Iannettoni MD, Keech JC, et al. Role of barium swallow in diagnosing clinically significant anastomotic leak following esophagectomy. Korean J Thorac Cardiovasc Surg 2016;49:99-109. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4825910/pdf/kjtcv-49-099.pdf

 

When evaluating for an esophageal perforation, is a water-soluble contrast agent such as Gastrografin a better and safer alternative to barium swallow study?

My patient with a medicated adhesive patch is having an MRI. Should the patch be removed before the procedure?

The nonadhesive backing of some medicated or transdermal patches (TPs) contain aluminum or other metals that can become heated during an MRI1.  FDA is aware of skin burns at the patch site in several patients wearing an aluminized TP during an MRI2.

The following TPs have been reported by the FDA to have aluminized backing: Androderm (testosterone transdermal system); 2. Catapres-TTS (clonidine transdermal system); 3. Nicoderm (nicotine transdermal system); 4. Nicotrol (nicotine transdermal system); 5. Prostep (nicotine transdermal system);6. Habitrol (nicotine transdermal system); 7. Nicotine transdermal system (generic nicotine transdermal system); 8. Transderm Nitro (nitroglycerin transdermal system); 9. Trasnsderm Scop (scopolamine transdermal system).

Other TPs that have metal backing but not necessarily carrying FDA warning include Flector (diclofenac), estradiol, Duragesic (fentanyl), Synera (lidocaine and tetracaine), methyl salicylate and menthol (over the counter), Oxytrol (oxybutynin), Exelon (rivastigmine), Neupro (rotigotine), and Emsam (selegiline)3.  

In short, it is advisable that TPs with metal backing (either listed above or others)  be removed prior to MRI.

 

References

  1. Kuehn B. FDA warning: remove drug patches before MRI to prevent burns to skin. JAMA. 2009;301:1328
  2. https://www.accessdata.fda.gov/scienceforums/forum06/k-26.htm , accessed April 19, 2017.
  3. http://www.pharmacytimes.com/contributor/alexander-kantorovich-pharmd-bcps/2016/08/transdermal-patches-that-must-be-removed-before-mri , accessed April 19,2017.
My patient with a medicated adhesive patch is having an MRI. Should the patch be removed before the procedure?

When should I suspect spinal epidural abscess in my 55 year old patient with severe back pain?

 It cannot be overemphasized that up 50% of patients with spinal epidural abscess (SEA) have no known risk factors,  one-half may have no fever,  and 20-40% lack leukocytosis1. In fact, the “classic triad” of back pain, fever, and neurological deficits is found only in the minority of patients!  No wonder that up to 75% of patients SEA are misdiagnosed on their initial healthcare encounter1!

Potential “red flags” for infectious causes of low back pain include age >50 y, night pain, unremitting pain even when supine, duration > 6 weeks, fever, chills, night sweats, weight loss, conditions associated with Staphylococcus aureus bacteremia (eg intravenous drug use), incontinence, saddle anesthesia, and severe or rapidly progressive neurologic deficits1,2.  

ESR and C-reactive protein (CRP) are almost uniformly elevated in SEA1 and can serve as a good starting point in excluding this condition when in doubt.   In patients ≥50 y of age with low back pain, obtaining ESR routinely has been suggested for detection of systemic disease (eg cancer, infection)3.  Similarly, in a recent algorithm of severe back pain, routine measurements of ESR and CRP, even in the absence of any neurological findings, has been recommended1; elevation of either may necessitate consideration of MRI.

Liked this post? Download the app on your smart phone and sign up below to catch future pearls right into your inbox, all for free!

Subscribe to Blog via Email

Enter your email address to subscribe to this blog and receive notifications of new posts by email.

References:

  1. Bond, A, Manian FA. Spinal epidural abscess: a review with special emphasis on earlier diagnosis. BioMed Res International 2016; https://www.hindawi.com/journals/bmri/2016/1614328/http://dx.doi.org/10.1155/2016/1614328  
  2. Della-Giustina. Acute low back pain: recognizing the “red flags” in the workup. Consultant 2013;53:436-440. http://www.consultant360.com/article/acute-low-back-pain-recognizing-%E2%80%9Cred-flags%E2%80%9D-workup
  3. Jarvik JG, Deyo RA. Diagnostic evaluation of low back pain with emphasis on imaging. Ann Intern Med 2002;137:586-597. http://annals.org/aim/article/715687/diagnostic-evaluation-low-back-pain-emphasis-imaging

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis or its affiliate healthcare centers, Mass General Hospital, Harvard Medical School or its affiliated institutions. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

Additional disclosure: The author of this post (FAM) also coauthored reference 1.

When should I suspect spinal epidural abscess in my 55 year old patient with severe back pain?

My patient with abdominal pain needs a CT scan with IV iodinated contrast, but reports a “shellfish” allergy? Is she at high risk of allergic reaction to IV contrast?

Patients with shellfish allergy appear not to have a significantly higher rate of allergic reactions to iodinated contrast media compared to patients with history of atopy, such as asthma or other food allergies 1,2.  When true shellfish allergy occurs, it is caused by an immunological reaction to the protein, not iodine, content of the food ingested.  “Iodine allergy” cannot exist because iodine is found throughout our bodies and is essential to life. 

The typical IV contrast-related adverse reaction is caused by non-IgE-mediated mast cell and basophil degranulation due to the high osmolality of these agents. Because the resultant “anaphylactoid” reaction is not associated with prior immune system memory, its risk is not increased by previous exposure to IV contrast.  Premedication with corticosteroids and diphenhydramine may be effective in reducing the risk of such reactions, but is not routinely recommended in patients with isolated history of shellfish allergy2.

 

References

  1. Schabelman E, Witting M. The relationship of radioconstrast, iodine, and seafood allergies: a medical myth exposed. J Emerg Med 2010;39: 701-707.
  2. Westermann-Clark E, Pepper AN, Talreja N, Lockey RF. Debunking myths about “allergy” to radioconstrast media in an academic institution. Postgrad Med 2015;127:295-300.
My patient with abdominal pain needs a CT scan with IV iodinated contrast, but reports a “shellfish” allergy? Is she at high risk of allergic reaction to IV contrast?