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About Bryan D. Hayes, PharmD, DABAT, FAACT, FASHP

Leadership Team, ALiEM
Creator and Lead Editor, Capsules and EM Pharm Pearls Series
Attending Pharmacist, EM and Toxicology, MGH
Associate Professor of EM, Division of Medical Toxicology, Harvard Medical School

EM Pharm Pearls: Estimated rise in blood glucose concentration with dextrose administration

A common question is how much should we expect the blood glucose concentration to increase after dextrose 50% (D50) administration. Fortunately, there is an answer from 3 studies.

  1. Balentine JR, Gaeta TJ, Kessler D, Bagiella E, Lee T. Effect of 50 milliliters of 50% dextrose in water administration on the blood sugar of euglycemic volunteers. Acad Emerg Med. 1998;5(7):691-694. doi:10.1111/j.1553-2712.1998.tb02487.x PMID 9678393
    • Population: Healthy volunteers in the ED
    • Intervention: 25 gm (1 ampule of D50)
    • Result: Mean increase of 162 mg/dL at 5 min. Glucose concentrations returned to baseline by 30 minutes.
  1. Murthy MS, Duby JJ, Parker PL, Durbin-Johnson BP, Roach DM, Louie EL. Blood glucose response to rescue dextrose in hypoglycemic, critically ill patients receiving an insulin infusion. Ann Pharmacother. 2015;49(8):892-896. doi:10.1177/1060028015585574. PMID 25986006
    • Population: Critically ill patients experiencing hypoglycemia while on insulin infusions
    • Intervention: D50
    • Result: Median increase of 4 mg/dL per gm of D50 administered
  1. Adler PM. Serum glucose changes after administration of 50% dextrose solution: pre- and in-hospital calculations. Am J Emerg Med. 1986;4(6):504-506. doi:10.1016/S0735-6757(86)80004-3. PMID 3778594
    • Population: ED patients with altered mental status (23 with diabetes, 28 without diabetes)
    • Intervention: 25 gm (50 mL of D50)
    • Result: Mean increase of 166 mg/dL

Take Home Points

  • Glucose concentrations increase 4-6 mg/dL per gm of dextrose administered
    • 50 mL of D50 = 25 gm = expected 100-150 mg/dL glucose rise
  • D50 rescue glucose is short-lived (30 minutes)
  • If the blood glucose does not respond as anticipated, investigate further (e.g., IV decannulation)

 

Want to learn more about EM Pharmacology?

Read other articles in the EM Pharm Pearls Series and find previous pearls on the PharmERToxguy site.

By |2022-07-14T18:25:07-07:00Jul 18, 2022|EM Pharmacy Pearls, Endocrine-Metabolic|
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Interpretation and Limitations of Opiate Urine Drug Tests

Background

Urine drug tests are commonly sent for patients in the emergency department, however care should be taken when interpreting the results of these tests given their limitations. The American College of Medical Toxicology published a position statement on the interpretation of urine opiate and opioid tests [1]. In this publication, they outline many of the limitations of opioid urine drug tests and explain why they exist.

Evidence

  • Though often used interchangeably, the terms opiate and opioid are not the same. ‘Opioid’ is the broad category name while ‘opiate’ simply refers to the naturally occurring opioids. The term ‘opioid’ encompasses opiates (e.g., morphine, codeine, opium), semi-synthetic agents (eg, heroin, hydrocodone, hydromorphone, oxycodone), and synthetic agents (eg, methadone, fentanyl, tramadol). Notice the name of the urine drug test next time you order one, it is likely specific for opiates (not opioids). This is because many tests are designed to identify morphine, though they will also detect codeine and heroin as they are both ultimately metabolized to morphine.
  • The standard urine drug tests do not specifically look for oxycodone, hydrocodone, etc. However, they can trigger a positive result due to their structural similarities, but not in every case. Therefore, a negative result doesn’t rule out use of these common drugs.
  • Similarly, synthetic opioids will not reliably cross-react with the opiate urine drug test as they are quite structurally dissimilar. In order to detect some of these agents, a test specific for the compound in question should be used.
  • As there are numerous different manufacturers of urine drug tests, hospitals may not utilize the same tests. In order to further understand the methods and cross-reactivity of a hospital’s specific urine drug test, the hospital’s laboratory should be contacted to request the package insert. Below is an example of the cross reactivity between various opioids with a opiate urine drug test [2].
Cross-reactivity of Various Opioids with Morphine Urine Drug Test [2]
CompoundEquivalent to 300 ng/mL Morphine (ng/mL)Cross-reactivity (%)
Codeine224134
Heroin36682
Hydrocodone1,08628
Hydromorphone1,42521
Oxycodone>75,000<0.4
Meperidine>100,000<0.3

 

Previous ALiEM posts discuss further limitations of urine drug tests, specifically for benzodiazepines and opiates.

Bottom Line

  • The term ‘opioid’ is the broad class of substances, while ‘opiate’ refers to the naturally occurring opioids (e.g., morphine, codeine)
  • Many urine drug tests are designed to identify morphine and will also detect codeine and heroin, as they are ultimately metabolized to morphine
  • Due to structural similarity, some semi-synthetic opioids may cross-react but fully synthetic opioids are unlikely to cross-react

Want to learn more about EM Pharmacology?

Read other articles in the EM Pharm Pearls Series and find previous pearls on the PharmERToxguy site.

References

  1. Stolbach A, Connors N, Nelson L, Kulig K. Acmt position statement: interpretation of urine opiate and opioid tests. J Med Toxicol. 2022;18(2):176-179. doi: 10.1007/s13181-021-00864-1. PMID: 34780053.
  2. Opiates II [package insert]. Indianapolis, IN: Roche Diagnostics; 2006.
By |2022-07-11T19:51:16-07:00Apr 23, 2022|EM Pharmacy Pearls, Tox & Medications|
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Should Diphenhydramine be included in an Acute Agitation Regimen?

Background

Acute agitation in the emergency department is a common issue that frequently requires the use of chemical sedation to preserve safety for patients and healthcare workers. A commonly employed treatment regimen is the combination of haloperidol 5 mg + lorazepam 2 mg + diphenhydramine 50 mg (B-52). Diphenhydramine is included in this treatment regimen primarily to prevent extrapyramidal symptoms [1,2]. However, the incidence of extrapyramidal symptoms (EPS) with haloperidol is quite low when treating agitation in the emergency department (ED) [3,4]. Therefore, the excessive and prolonged sedation from adding prophylactic diphenhydramine may outweigh the intended benefit and should be reserved for treatment of EPS if symptoms occur.

Evidence

Jeffers et al. conducted a multicenter, retrospective, cohort study which compared the efficacy and safety of haloperidol, lorazepam, and diphenhydramine (B-52) (n=200) vs. haloperidol and lorazepam (52) (n=200) in treating patients >18 years old with acute agitation in the ED [5]. Their primary outcome was the administration of additional agitation medication(s) within 2 hours.

Outcomes52 (n=200)B52 (n=200)p-Value
Administration of additional sedative within 2 h, n (%)40 (20)28 (14)0.11
Median ED LOS (hours)13.8170.03
Use of restraints, n (%)53 (26.5)86 (43)0.001
Hypotension, n (%)7 (3.5)32 (16)<0.001
Administration of anticholinergic within 2 days, n (%)15 (7.5%)6 (3%)0.04
    Itching/allergies, n (%)1 (0.5)1 (0.5)1.00
    Home benztropine, n (%)2 (1)4 (2)0.41
    Insomnia, n (%)4 (2)0 (0)0.06
    Unknown, n (%)8 (4)1 (0.5)0.02

 

Overall, the B-52 combination resulted in more oxygen desaturation, hypotension, physical restraint use, and longer length of stay. However, the conclusions from this study may be limited as it was a relatively small study and  it used surrogate markers to assess clinical endpoints.

Further discussion regarding the onset and duration of IM medications for acute agitation may be found in this blog post.

Bottom Line

  • The risk of extrapyramidal symptoms following haloperidol for agitation in the ED is relatively low
  • Diphenhydramine may not be necessary when using haloperidol + lorazepam to treat agitation in the ED
  • ED length of stay is increased with the addition of diphenhydramine to haloperidol + lorazepam

Want to learn more about EM Pharmacology?

Read other articles in the EM Pharm Pearls Series and find previous pearls on the PharmERToxguy site.

References

  1. Mokhtari A, Yip O, Alain J, Berthelot S. Prophylactic administration of diphenhydramine to reduce neuroleptic side effects in the acute care setting: a systematic review and meta-analysis. J Emerg Med. 2021 Feb;60(2):165–74. doi: 10.1016/j.jemermed.2020.09.031. PMID: 33131965.
  2. Vinson DR, Drotts DL. Diphenhydramine for the prevention of akathisia induced by prochlorperazine: a randomized, controlled trial. Ann Emerg Med. 2001 Feb;37(2):125–31. doi: 10.1067/mem.2001.113032. PMID: 11174228. 
  3. Klein LR, Driver BE, Miner JR, Martel ML, Hessel M, Collins JD, et al. Intramuscular midazolam, olanzapine, ziprasidone, or haloperidol for treating acute agitation in the emergency department. Ann Emerg Med. 2018 Oct;72(4):374–85. doi: 10.1016/j.annemergmed.2018.04.027. PMID: 29885904.
  4. Schneider A, Mullinax S, Hall N, Acheson A, Oliveto AH, Wilson MP. Intramuscular medication for treatment of agitation in the emergency department: A systematic review of controlled trials. Am J Emerg Med. 2021 Aug;46:193–9. doi: 10.1016/j.ajem.2020.07.013. PMID: 33071100.
  5. Jeffers T, Darling B, Edwards C, Vadiei N. Efficacy of combination haloperidol, lorazepam, and diphenhydramine vs. Combination haloperidol and lorazepam in the treatment of acute agitation: a multicenter retrospective cohort study. J Emerg Med. 2022 Mar 11;S0736-4679(22)00057-9. doi: 10.1016/j.jemermed.2022.01.009. PMID: 35287982.
By |2022-04-09T10:15:43-07:00Apr 16, 2022|EM Pharmacy Pearls, Psychiatry, Tox & Medications|
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Are Thrombolytics Safe for Acute Ischemic Strokes in Patients on DOACs?

Background

Direct-acting oral anticoagulants (DOACs), including apixaban, rivaroxaban, edoxaban, and dabigatran, are widely used for various indications and considered first-line therapy for prevention of acute ischemic stroke in patients with nonvalvular atrial fibrillation [1]. The management of acute ischemic stroke in patients on DOACs presents a difficult clinical scenario in the emergency department due to concern for increased risk of hemorrhage. IV thrombolytics (e.g., alteplase, tenecteplase), a mainstay in acute ischemic stroke management, are not recommended in current guidelines for patients whose last DOAC dose was within the last 48 hours [2, 3]. Therefore, patients with an acute ischemic stroke who are compliant with their DOACs are often excluded from guideline recommended therapy. Additionally, as covered in a previous ALiEM post, it is not recommended to reverse anticoagulation status in order to administer a thrombolytic.

Evidence

The use of IV thrombolytics in patients on DOACs was evaluated by Kam et al in a 2022 study published in JAMA [4]. This retrospective analysis included 163,038 patients from the AHA/ASA Get With The Guidelines-Stroke registry with acute ischemic stroke who received IV alteplase within 4.5 hours of symptom onset. Of the total number of patients, only 2207 had documented use of a DOAC within the last 7 days, with 25 of these patients reporting DOAC use within 48 hours. Patients on warfarin or other anticoagulants were excluded. The primary outcome was symptomatic intracranial hemorrhage (ICH) within 36 hours of IV alteplase administration. After adjusting for clinical factors, the rate of symptomatic ICH was not significantly different between patients taking DOACs and those not on anticoagulation (3.7% vs. 3.2%, adjusted OR 0.88, 95% CI 0.70 to 1.10). However, when stratified based on time from last DOAC dose, patients who took their DOAC 0-48 hours prior had an 8% rate of symptomatic ICH compared to 3.2% among those not on DOACs. Furthermore, the rate of any alteplase complication was 12% vs. 6% in those taking DOACs within 48 hours vs. no DOAC.

Limitations

  • The population at highest risk for bleeding is patients who took a DOAC within the last 48 hours, and this study only included 25 such patients.
    • A similar study tried to answer the same question for warfarin patients with an INR between 1.5-1.7. They also failed to include enough patients to make any definitive conclusions. [5]
  • Timing from the last DOAC dose was given as a range, with the majority of patients reporting use sometime within the last 7 days. It has been established in current AHA/ASA guidelines that receipt of DOACs past 48 hours prior is considered safe for thrombolytic administration, and if the included institutions were following current recommendations, thrombolytics were likely administered mostly to patients outside the 48-hour window.
  • Large potential for selection bias, since it was reported that almost 23,000 patients on DOACs from the original registry (who were otherwise eligible) did not receive thrombolytics.
  • Not clear how patients were determined to be on DOACs or if the authors were able to confirm this in unresponsive/intubated/deceased patients retrospectively. This could have resulted in DOAC patients being included in the non-DOAC group, which could have falsely evened-out the bleeding rates.

Bottom Line

  • The management of acute ischemic stroke in patients receiving prior anticoagulation presents a challenging clinical scenario.
  • Studies to date fail to include enough patients to evaluate the true risk of bleeding.
  • This study supports the current guideline recommendation to avoid alteplase in patients receiving a DOAC within 0-48 hours due to the increased risk of intracranial hemorrhage.

Want to learn more about EM Pharmacology?

Read other articles in the EM Pharm Pearls Series and find previous pearls on the PharmERToxguy site.

References

  1. January CT, Wann LS, Calkins H, et al. 2019 AHA/ACC/HRS focused update of the 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation. Published correction appears in Circulation. 2019;140(6):e285. Circulation. 2019;140(2):e125-e151. doi: 10.1161/CIR.0000000000000665. PMID: 30686041.
  2. Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the early management of patients with acute ischemic stroke: 2019 update to the 2018 guidelines for the early management of acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2019;50(12):e344-e418. doi: 10.1161/STR.0000000000000211. PMID: 31662037.
  3. Berge E, Whiteley W, Audebert H, et al. European Stroke Organisation (ESO) guidelines on intravenous thrombolysis for acute ischaemic stroke. Eur Stroke J. 2021;6(1):I-LXII. doi: 10.1177/2396987321989865. PMID: 33817340.
  4. Kam W, Holmes DN, Hernandez AF, et al. Association of Recent Use of Non-Vitamin K Antagonist Oral Anticoagulants With Intracranial Hemorrhage Among Patients With Acute Ischemic Stroke Treated With Alteplase. JAMA. 2022;327(8):760-771. doi:10.1001/jama.2022.0948. doi: 10.1001/jama.2022.0948. PMID: 35143601.
  5. Xian Y, Liang L, Smith EE, et al. Risks of intracranial hemorrhage among patients with acute ischemic stroke receiving warfarin and treated with intravenous tissue plasminogen activator. JAMA. 2012;307(24):2600-2608. doi:10.1001/jama.2012.6756. doi: 10.1001/jama.2012.6756. PMID: 22735429.

 

Primary author:

Jessica Mason, PharmD

PGY-2 Emergency Medicine Pharmacy Resident

Massachusetts General Hospital

By |2022-03-18T08:03:52-07:00Apr 2, 2022|EM Pharmacy Pearls, Heme-Oncology, Neurology, Tox & Medications, Uncategorized|
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Blood Pressure Differences in Patients with Acute Aortic Dissections

Background

An acute aortic dissection (AAD) can be a life-threatening emergency which frequently requires rapid and precise control of the patient’s heart rate and blood pressure. The 2010 guidelines for management of patients with thoracic aortic disease suggest a heart rate goal of <60 bpm and a systolic blood pressure between 100-120 mmHg. In order to achieve this, a rapid-acting beta-blocker (i.e., esmolol) may be used in combination with an IV calcium channel blocker (i.e., nicardipine or clevidipine). These medications need to be monitored closely to avoid overshooting these goals and causing hemodynamic compromise. Ideally, an arterial line would be used to monitor the patient’s blood pressure, however this may not always be feasible so a traditional, noninvasive blood pressure cuff can be used. This may be complicated if the patient has the classic, but not universal, finding of unequal systolic blood pressure values between their left and right extremities. This raises the question, in a patient with an AAD and disparate blood pressures in each arm, which arm reading should be used for monitoring?

Evidence

A 2018 study from Um et al. evaluated 111 patients with an AAD and compared them with 111 control patients. This study found that while a systolic blood pressure difference of >20 mmHg between sides was a positive predictor for an AAD, the presence of a pulse deficit had a higher diagnostic accuracy. For the purpose of this study, a pulse deficit was defined as “any recorded difference in volume/force or difference in obvious signs of malperfusion”. The cause of an unequal blood pressure or pulse deficit in the upper extremities in this population is typically due to dissection of the brachiocephalic or subclavian arteries. In order to properly achieve the desired blood pressure reduction in patients with divergent blood pressure values, the higher value should be used for titration of antihypertensives. This is due to the occurrence of pseudohypotension occurring in the limb with the dissected artery.

Bottom-line

  • Aggressive and precise heart rate and blood pressure control are critical for patients with an acute aortic dissection
  • The presence of a pulse deficit may provide better diagnostic accuracy than a difference in systolic blood pressure
  • When titrating blood pressure medications in patients with unequal blood pressure readings between extremities, the higher value should be utilized

Want to learn more about EM Pharmacology?

Read other articles in the EM Pharm Pearls Series and find previous pearls on the PharmERToxguy site.

References:

  1. Hiratzka LF, Bakris GL, Beckman JA, et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease Circulation. 2010;121(13):e266-369. doi: 10.1161/CIR.0b013e3181d4739e. PMID: 20233780.
  2. Um SW, Ohle R, Perry JJ. Bilateral blood pressure differential as a clinical marker for acute aortic dissection in the emergency department. Emerg Med J. 2018;35(9):556-558. doi: 10.1136/emermed-2018-207499. PMID: 30021832.
By |2022-03-18T07:53:35-07:00Mar 19, 2022|Cardiovascular, EM Pharmacy Pearls|
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Extracorporeal Treatment Options in Poisoned Patients

Background

Caring for a patient that is critically-ill secondary to a toxic ingestion is complicated and, in severe cases, extracorporeal treatments (ECTRs) may be considered. The most commonly used ECTRs are intermittent hemodialysis (iHD) and continuous renal replacement therapy (CRRT), but ECTRs also include exchange transfusion, hemoperfusion, liver dialysis, and therapeutic plasma exchange. Finding and evaluating the supporting literature for these treatment modalities in a timely manner is not feasible in most situations. In order to assist in this effort, the EXtracorporeal Treatments In Poisoning (EXTRIP) workgroup has reviewed and provided free, evidence-based recommendations regarding the use of ECTRs for many common toxins and toxicants [1]. These recommendations can be found in a summarized format on the EXTRIP website and the links to their comprehensive reviews are published on PubMed with direct links on their website. This international workgroup is made up of experts in toxicology, nephrology, emergency medicine, pediatrics, pharmacology, critical care, and more. An excellent example of this resource is their review and recommendations on ECTRs for poisoning secondary to beta-adrenergic antagonists (BAAs).

Evidence

The EXTRIP workgroup included 76 publications in this comprehensive review on the use of ECTRs in BAA poisoning [2]. They evaluated pharmacokinetic/toxicokinetic data for a total of 334 patients poisoned with various BAAs, of which ~90% of the data was published prior to 1990 and does not necessarily represent the improved clearance of these medications with modern ECTR modalities. Based on this evidence, they deemed atenolol, nadolol, and sotalol as dialyzable BAAs. They also reviewed case reports/series of 37 patients with BAA toxicity and made recommendations for those agents with sufficient evidence. Based on the above data, the EXTRIP group recommends iHD over CRRT in patients severely poisoned with atenolol or sotalol and kidney impairment. They make no recommendation for or against ECTR in patients severely poisoned with atenolol or sotalol with normal kidney function and they recommend against ECTR in patients severely poisoned with propranolol.

 Bottom Line

  • Some toxic ingestions may require invasive treatment strategies (e.g., ECTRs) but a comprehensive review of the literature may not be possible
  • The EXTRIP website is an excellent resource to assess if patients should receive emergent ECTRs due to specific toxins
  • Hemodialysis is recommended in severely symptomatic patients poisoned with atenolol or sotalol and with impaired kidney function

Want to learn more about EM Pharmacology?

Read other articles in the EM Pharm Pearls Series and find previous pearls on the PharmERToxguy site.

References:

  1. Ghannoum M, Nolin TD, Lavergne V, Hoffman RS, EXTRIP workgroup. Blood purification in toxicology: nephrology’s ugly duckling. Adv Chronic Kidney Dis. 2011;18(3):160-166. doi: 10.1053/j.ackd.2011.01.008. PMID: 21531321.
  2. Bouchard J, Shepherd G, Hoffman RS, et al. Extracorporeal treatment for poisoning to beta-adrenergic antagonists: systematic review and recommendations from the EXTRIP workgroup. Crit Care. 2021;25(1):201. doi: 10.1186/s13054-021-03585-7. PMID: 34112223.
By |2022-02-02T13:49:01-08:00Feb 5, 2022|EM Pharmacy Pearls, Tox & Medications|
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Balanced Fluids in Diabetic Ketoacidosis

Background

Many guidelines and treatment algorithms for diabetic ketoacidosis (DKA) recommend sodium chloride 0.9% as the replacement fluid of choice, though alternative fluids may be a better option [1-4]. Randomized trials, in adult and pediatric patients, demonstrate faster resolution of DKA when using balanced solutions (e.g., PlasmaLyte-A, lactated Ringer’s) compared to sodium chloride [5-7]. Dr. Josh Farkas provides further review of this topic in 3 excellent and detailed EMCrit posts [8-10].

Evidence

A phase-2 study published in 2021, SCOPE-DKA, randomized 93 patients with severe DKA (median venous pH 7.0) to receive PlasmaLyte-148 (PlasmaLyte-A) or sodium chloride 0.9% [11]. During the first 48 hours of treatment, patients received a average of ~6.5 L of fluid. At 24-hours, more patients in the PlasmaLyte group had resolution of DKA (defined as base excess ≥ -3 mEq/L) as compared to the sodium chloride group (69% vs 36%, p=0.002). However, by 48-hours, both groups had similar rates of DKA resolution (96% vs 86%, p=0.111). The study authors concluded that PlasmaLyte-148 may lead to faster resolution of metabolic acidosis in patients with DKA without an increase in ketosis, in line with findings from previous studies, but these results need to be confirmed in a larger, Phase 3 trial.

To further explore the nuances, strengths, and weaknesses of this study, please read the REBEL EM review by Dr. Mark Ramzy [13].

Bottom Line

  • The available data suggests that balanced fluids are beneficial in mild, moderate, and severe DKA.
  • PlasmaLyte-148 (PlasemaLyte A) may lead to faster resolution of metabolic acidosis than sodium chloride 0.9%. Though these findings need confirmation in a large, Phase 3 trial.
  • Generally, the composition of the initial liter is less important than prompt administration. However, for subsequent liters, a balance crystalloid (e.g., PlasmaLyte-148, or lactated Ringer’s) should be used instead of sodium chloride 0.9%.

Want to learn more about EM Pharmacology?

Read other articles in the EM Pharm Pearls Series and find previous pearls on the PharmERToxguy site.

References:

  1. Wolfsdorf J, Glaser N, Sperling MA, American Diabetes Association. Diabetic ketoacidosis in infants, children, and adolescents: A consensus statement from the American Diabetes Association. Diabetes Care. 2006;29(5):1150-1159. PMID: 16644656. doi: 10.2337/diacare.2951150.
  2. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. Diabetes Care. 2009;32(7):1335-1343. PMID: 19564476. doi: 10.2337/dc09-9032.
  3. Canadian Diabetes Association Clinical Practice Guidelines Expert Committee, Goguen J, Gilbert J. Hyperglycemic emergencies in adults. Can J Diabetes. 2013;37 Suppl 1:S72-76. PMID: 24070967. doi: 10.1016/j.jcjd.2013.01.023.
  4. Joint British Diabetes Societies Inpatient Care Group. The Management of Diabetic Ketoacidosis in Adults. 2021; online publication. Accessed January 3, 2022. https://abcd.care/sites/abcd.care/files/site_uploads/JBDS_02%20_DKA_Guideline_amended_v2_June_2021.pdf.
  5. Mahler SA, Conrad SA, Wang H, Arnold TC. Resuscitation with balanced electrolyte solution prevents hyperchloremic metabolic acidosis in patients with diabetic ketoacidosis. Am J Emerg Med. 2011;29(6):670-674. PMID: 20825879. doi: 10.1016/j.ajem.2010.02.004.
  6. Williams V, Jayashree M, Nallasamy K, Dayal D, Rawat A. 0.9% saline versus Plasma-Lyte as initial fluid in children with diabetic ketoacidosis (SPinK trial): a double-blind randomized controlled trial. Crit Care. 2020;24(1):1. PMID: 31898531. doi: 10.1186/s13054-019-2683-3.
  7. Self WH, Evans CS, Jenkins CA, et al. Clinical effects of balanced crystalloids vs saline in adults with diabetic ketoacidosis: a subgroup analysis of cluster randomized clinical trials. JAMA Netw Open. 2020;3(11):e2024596. PMID: 33196806. doi: 10.1001/jamanetworkopen.2020.24596.
  8. Farkas J. Four DKA Pearls. 2014. Accessed January 3, 2022. https://emcrit.org/pulmcrit/four-dka-pearls.
  9. Farkas J. Dominating the acidosis in DKA. 2016. Accessed January 3, 2022. https://emcrit.org/pulmcrit/bicarbonate-dka.
  10. Farkas J. IBCC – Diabetic Ketoacidosis (DKA). 2021. Accessed January 3, 2022. https://emcrit.org/ibcc/dka.
  11. Ramanan M, Attokaran A, Murray L, et al. Sodium chloride or Plasmalyte-148 evaluation in severe diabetic ketoacidosis (Scope-dka): a cluster, crossover, randomized, controlled trial. Intensive Care Med. 2021;47(11):1248-1257. PMID: 34609547. doi: 10.1007/s00134-021-06480-5.
  12. Ramzy M. SCOPE-DKA: Normal Saline vs Plasmalyte in Severe DKA. 2021. Accessed January 3, 2022. https://rebelem.com/scope-dka-normal-saline-vs-plasmalyte-in-severe-dka.
By |2022-01-03T10:16:35-08:00Jan 8, 2022|EM Pharmacy Pearls, Endocrine-Metabolic, Tox & Medications|
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