June 2017 FAQs

Can olanzapine be administered intravenously for the management of acute agitation?

Introduction

Acute agitation is a prevalent issue in the Emergency Department (ED) setting and requires timely and proper management for the safety of both patients and healthcare workers.¹ Patients may present agitated for a variety of reasons including intoxication, underlying mental illness, head injury, metabolic disturbances, infection, or other social reasons.² To manage patients, both verbal de-escalation approaches and medications are available.¹ The 3 classes of medications that have been studied and used most frequently in the treatment of acute agitation in the ED setting include first-generation antipsychotics, second-generation antipsychotics, and benzodiazepines. Many agents from these drug classes can be administered orally as standard or fast-dissolving tablets, or parenterally via the intramuscular (IM) or intravenous (IV) routes.

In 2012, the American Association for Emergency Psychiatry (AAEP) published recommendations for the management of agitation in the emergency department.¹ According to the AAEP, verbal tactics and environmental adjustments to calm the patient should be exhausted before pharmacological therapy is initiated. A protocol found within these guidelines outlines pharmacological treatment recommendations for acute agitation based on etiology. For patients experiencing agitation that is associated with delirium when alcohol or benzodiazepine overdose is not suspected, second-generation antipsychotics (e.g. olanzapine, risperidone, ziprasidone) are recommended as first-line therapy. Second-generation antipsychotics are also recommended as first-line agents for agitation associated with psychosis in patients with a known psychiatric disorder. For patients who experience agitation due to overdose of recreational drugs or stimulants, and are also considered chronic amphetamine users, second-generation antipsychotics are recommended along with benzodiazepines. To control agitation of unknown etiology, an antipsychotic is recommended only if patients are displaying psychotic features, otherwise, a benzodiazepine is preferred. In general, second-generation antipsychotics are effective and result in fewer side effects (dystonia and akathisia) when compared with older drug choices, such as haloperidol.^3,4 Regardless of the agent used, the goal of pharmacotherapy in the setting of acute agitation is to calm the patient without inducing sleep. Oral agents, if feasible for the patient, are preferred to parenteral therapy.

Olanzapine is a second-generation antipsychotic with multiple mechanisms of action including the blockade of central dopamine (D₂)_, muscarinic (M₁), and serotonin (5-HT_2a) receptors and peripheral alpha (α-1) receptors.⁵ Currently, the United States Food and Drug Administration (FDA) has only approved olanzapine for administration by the IM and oral routes. However, the IV administration of olanzapine has been described in the literature, and the IV administration of other antipsychotic agents that are only approved for IM administration, such as haloperidol, is commonly done in clinical practice.^1,6

Considerations for intravenous administration of olanzapine

Olanzapine solution for intramuscular injection has a neutral pH and contains water, 10 mg of olanzapine, 50 mg of lactose monohydrate, and 3.5 mg of tartaric acid.⁵ Because both lactose and tartaric acid are common ingredients in other intravenous solutions, olanzapine is considered safe for this route of administration.⁷ Although hospitals internationally have been administering the agent via the IV route without any noted differences in efficacy, controversy remains as to whether the IV route is safer or more efficacious when compared to the IM route.⁶

Efficacy and safety data

Few studies have evaluated the efficacy and safety of IV olanzapine administration (see Table 1).^7,8,9 The most recent publication in this arena was a prospective, observational study comparing IM and IV administration of olanzapine for the management of agitation in the ED.⁸ In this study, efficacy between the IV and IM groups was similar, although patients in the IV group did experience more respiratory depression (3.7% vs 2.0%, respectively). Authors postulate that the quicker time to peak onset with IV compared to IM administration may have led to this increase. The use of additional sedatives was similar between both groups. However, patients who received IV olanzapine experienced a decreased median duration of time in the ED compared to those who received IM olanzapine (386 vs. 525 minutes, respectively). Overall, this study concluded that both IV and IM routes are safe and effective, however, respiratory depression is more prevalent with the IV route.

A large retrospective cohort study also evaluated the use and safety of IV olanzapine in the ED patient population.⁹ When compared to the previously mentioned trial, this study reported a higher rate of respiratory complications with the use of IV olanzapine at 14%.^8,9 This may, however, have been due to the 62 patients (35%) that required additional sedatives, of which 47 were reported to experience hypoxia. This study also reported a lower percentage of patients that only required 1 dose of IV olanzapine than that reported in the previously mentioned study (66.8% vs 84%, respectively).^8.9 However, the average times in the ED were similar (6 hours and 18 min vs. 6 hours and 24 min).

Lastly, there was a randomized, double-blind, placebo-controlled trial that compared 5 mg IV droperidol to 5 mg IV olanzapine as an adjunct to midazolam, or midazolam alone, in acutely agitated patients.⁷ Results demonstrated that when compared to monotherapy with midazolam, combination therapy with midazolam and either droperidol or olanzapine resulted in significantly more patients achieving adequate sedation and yield shorter times to sedation. The adverse effect profiles were similar between the groups. However, the olanzapine group experienced less oxygen desaturation and hypotension when compared to both the midazolam monotherapy and droperidol plus midazolam groups.

Suggested dosing

As previously mentioned, the administration of olanzapine via the IV route is an off-label use, therefore, standard dosing has not been established.⁵ The previously mentioned studies all utilized similar olanzapine doses of 5 to 10 mg IV every 5 to 10 minutes when treating agitation.^7,8,9 One of the studies also mentioned that for the control of nausea and vomiting lower doses of 1.25 mg to 2.25 mg IV are sufficient.⁸ Clinicians should be cautious with larger doses due to the risk of adverse events.^7,8,9 Respiratory depression along with QTc prolongation were clinically significant adverse events reported in all of the evaluated studies. 

Conclusion

The studies listed in Table 1 have demonstrated that the IV administration of olanzapine is safe and effective for the treatment of acutely agitated patients at doses ranging from 5 to 10 mg. Patients who have received IV olanzapine achieved adequate sedation, most often without the requirement of additional sedatives. Although the rates of adverse events with IV administration of olanzapine are relatively low, clinicians should remain vigilant of respiratory depression and QTc prolongation with this agent and monitor patients as necessary.  

References

1. Wilson MP, Pepper D, Currier GW, Holloman GH, Feifel D. The psychopharmacology of agitation: Consensus Statement of the American Association for Emergency Psychiatry Project BETA Psychopharmacology Workgroup. Western Journal of Emergency Medicine. 2012;13(1):26-34.
2. Lulla AA, Singh M. The Art of the ED Takedown.  EM Docs website. http://www.emdocs.net/the-art-of-the-ed-takedown/. Updated March 4, 2015. Accessed on May 5^th, 2017.
3. Correll CU, Schenk EM. Tardive dyskinesia and new antipsychotics. Curr Opin Psychiatry. 2008;21:151–156.
4. Dolder CR, Jeste DV. Incidence of tardive dyskinesia with typical versus atypical antipsychotics in very high risk patients. Biol Psychiatry. 2003; 53:1142–1145.
5. Lexicomp [database online]. Hudson, Ohio: Lexi-Comp, Inc.; 2017. http://online.lexi.com/lco/action/home. Accessed April 12^th, 2017.
6. PulmCrit (EMCrit). Intravenous olanzapine: Faster than IM olanzapine, safer than IV haloperidol? EMCrit website. https://emcrit.org/pulmcrit/intravenous-olanzapine-haloperidol. Accessed April 14, 2017.
7. Chan EW, Taylor DM, Knott JC, et al. Intravenous droperidol or olanzapine as an adjunct to midazolam for the acutely agitated patient: a multicenter, randomized, double-blind, placebo-controlled clinical trial. Ann Emerg Med. 2013;61(1):72-81.
8. Cole JB, Moore JC, Dolan BJ, et al. A prospective observational study of patients receiving intravenous and intramuscular olanzapine in the emergency department. Ann Emerg Med. 2017;69(3):327-336.
9. Martel ML, Klein LR, Rivard RL, et al. A large retrospective cohort of patients receiving intravenous olanzapine in the emergency department. Acad Emerg Med. 2016;23(1):29-35.

Prepared by:

Jamie Micheletto, PharmD

PGY1 Pharmacy Practice Resident

College of Pharmacy

The information presented is current as April 14, 2017. This information is intended as an educational piece and should not be used as the sole source for clinical decision-making.

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What evidence supports the use of intravenous sub-dissociative-dose ketamine for pain in the emergency department?

Introduction

In 2013, there were 130.4 million visits to emergency departments (EDs) in the United States.¹ Among ED visits, pain accounts for approximately 45% of chief compliants.² Pharmacological treatment of pain has primarily been managed with opioid analgesics, with use increasing from 2000 to 2010. In 2010, only 22% of visits for non-malignant pain were treated exclusively with non-opioid analgesics. Unfortunately, opioids are associated with many serious potential adverse effects, are linked with the current opioid epidemic, and may have limited effect in chronic or opioid-tolerant pain.^3,4 In the current landscape, alternative non-opioid analgesics or non-pharmacological therapies are needed and encouraged.

Ketamine

Ketamine is an N-methyl-D-aspartate (NMDA) receptor antagonist.⁵ It is approved as a general anesthetic and produces a dissociative state. Additionally, ketamine provides analgesia through its ability to block sensitization to pain. Thus, it has the potential to be useful in opioid-related hyperalgesia. Ketamine is associated with serious adverse effects including emergence phenomenon. However, when used at low doses, ketamine provides an analgesic effect without dissociation and some of the other dose-dependent adverse effects, including hemodynamic changes. Sub-dissociative-dose ketamine (SDDK) is typically defined as < 1 mg/kg.

Literature review – ketamine analgesia in the ED

Recently, there has been a renewed interest in evaluating the use of ketamine for acute pain in the ED. It has been evaluated as both an adjunctive agent in combination with opioids (Table 1) and as a sole analgesic agent (Table 2).^6-14 The current literature is limited to short-term evaluations, ranging from 10 to 120 minutes. Additionally, all studies excluded pediatric and older patients (>55 or 65 years).

Overall, adjunctive use of ketamine with opioids further reduced pain scores compared to use of an opioid alone.^6-10 In addition to the studies reported in Table 1, a retrospective single-center evaluation of adjunctive ketamine (5 to 35 mg) showed significant pain improvement in 54% patients receiving ketamine.¹⁵ The authors hypothesized from the results that patients with a high narcotic tolerance might receive the most benefit from ketamine. For all studies, the most common adverse effects reported were lightheadedness, dizziness, and nausea.^6-10 A few cases of dysphoria and dissociation were reported (ie, “felt like falling”, “felt funny”), but there were no incidences of emergence phenomenon, respiratory distress, or severe hypotension. Most of the dissociation adverse effects were reported in the Ahern study which was unblinded and did not use a weight-based dose.⁹

Comparisons of ketamine versus morphine found no significant differences between the groups in pain scores.^11-14 However, none were designed to establish non-inferiority of ketamine to morphine. Miller and colleagues did note that the lowest pain scores with ketamine occurred within 5 minutes, whereas with morphine, the lowest scores occurred at 2 hours.¹¹ The most common adverse effects reported were nausea, dizziness, dysphoria, and disorientation.^11-14 Additionally, the Majidinejad et al study, which used 0.5 mg/kg of ketamine, reported 1 case of emergence phenomenon. The increase in the number of adverse effects is likely due to the larger doses of ketamine used in these trials, compared to adjunctive use. Lastly, a retrospective safety evaluation of 530 patients receiving SDDK (10 to 15 mg) in a single-center ED reported no cases of significant heart rate or blood pressure changes.¹⁶ Only 3.5% of patients experienced some type of dissociation or dysphoric reaction.

Table 1. Studies evaluating adjunctive use of ketamine for pain in the emergency department.^6-10

Table 2. Studies evaluating ketamine for pain in the emergency department as a replacement for other pain relievers.^11-14

Implementing ketamine in the ED

One of the biggest barriers to using ketamine as an analgesic is its potential for dissociation adverse effects, which can be unpleasant to patients. While there is a dose-relationship with this adverse effect, Motov and colleagues also showed that the administration method can affect it as well.¹⁷ In that study, 48 patients with acute moderate-to-severe pain received 0.3 mg/kg of ketamine, either as an intravenous bolus (over 5 minutes) or a short infusion (over 15 minutes). Patients receiving the intravenous bolus experienced significantly more “feelings of unreality” and sedation, therefore, a 15-minute administration time may be preferred. Additionally in an editorial, Yetim proposes using low-dose midazolam (1 to 2 mg) and anti-emetic prophylaxis to reduce the incidence of adverse effects as well.¹⁸

Additionally, from an operational standpoint, Pourmand and colleagues have noted that a lack of familiarity with ketamine can present a barrier.⁵ Thus, they advocate for use of a protocol to help direct dosing, administration, and monitoring. Additionally, they note that there are several existing advisory nursing opinions on the safe use of SDDK.^19-22

Conclusion

Overall, the current body of evidence highlights the efficacy and safety of ketamine in the ED as an analgesic. Based on this growing body of evidence, the American Academy of Emergency Medicine has recommended SDDK as both a single agent and as an adjunct for the management of acute pain in the ED.⁴ Use as an adjunctive and sole analgesic reduces pain scores and it appears to be well-tolerated. The doses utilized in studies ranged from 0.2 mg/kg to 0.5 mg/kg, with a few studies using a flat 15 mg dose. The studies that used 0.5 mg/kg tended to report more adverse effects, particularly dissociation episodes. Thus, doses between 0.1 and 0.3 mg/kg appear to be the most promising. Additionally, the administration of ketamine as a short infusion is associated with fewer adverse effects, but the optimal use of ketamine as an analgesic in the ED should be further explored and elucidated.

Lastly, while this review focused on intravenous bolus administration, a few other routes have been evaluated as well. These include subcutaneous infusion²³, continuous intravenous infusion^24,25, and intranasal administration.^26-32

References

1.            National Center for Health Statistics: emergency department visits. Centers for Disease Control and Prevention website. https://www.cdc.gov/nchs/fastats/emergency-department.htm. Updated March 17, 2017. Accessed May 17, 2017.

2.         Chang HY, Daubresse M, Kruszewski SP, Alexander GC. Prevalence and treatment of pain in EDs in the United States, 2000 to 2010. Am J Emerg Med. 2014;32(5):421-431.

3.         Cantrill SV, Brown MD, Carlisle RJ, et al. Clinical policy: critical issues in the prescribing of opioids for adult patients in the emergency department. Ann Emerg Med. 2012;60(4):499-525.

4.         Motov S, Rosenbaum S, Vilke GM, Nakajima Y. Is there a role for intravenous subdissociative-dose ketamine administered as an adjunct to opioids or as a single agent for acute pain management in the emergency department? J Emerg Med. 2016;51(6):752-757.

5.         Pourmand A, Mazer-Amirshahi M, Royall C, Alhawas R, Shesser R. Low dose ketamine use in the emergency department, a new direction in pain management [published online ahead of print Mar 02, 2017]. Am J Emerg Med. doi: 10.1016/j.ajem.2017.03.005.

6.         Bowers KJ, McAllister KB, Ray M, Heitz C. Ketamine as an adjunct to opioids for acute pain in the emergency department: a randomized controlled trial [published online ahead of print Feb 08, 2017]. Acad Emerg Med. doi: 10.1111/acem.13172.

7.         Sin B, Tatunchak T, Paryavi M, et al. The use of ketamine for acute treatment of pain: a randomized, double-blind, placebo-controlled trial [published online ahead of print Mar 06, 2017]. J Emerg Med. doi: 10.1016/j.jemermed.2016.12.039.

8.         Beaudoin FL, Lin C, Guan W, Merchant RC. Low-dose ketamine improves pain relief in patients receiving intravenous opioids for acute pain in the emergency department: results of a randomized, double-blind, clinical trial. Acad Emerg Med. 2014;21(11):1193-1202.

9.         Ahern TL, Herring AA, Stone MB, Frazee BW. Effective analgesia with low-dose ketamine and reduced dose hydromorphone in ED patients with severe pain. Am J Emerg Med. 2013;31(5):847-851.

10.       Galinski M, Dolveck F, Combes X, et al. Management of severe acute pain in emergency settings: ketamine reduces morphine consumption. Am J Emerg Med. 2007;25(4):385-390.

11.       Miller JP, Schauer SG, Ganem VJ, Bebarta VS. Low-dose ketamine vs morphine for acute pain in the ED: a randomized controlled trial. Am J Emerg Med. 2015;33(3):402-408.

12.       Motov S, Rockoff B, Cohen V, et al. Intravenous subdissociative-dose ketamine versus morphine for analgesia in the emergency department: a randomized controlled trial. Ann Emerg Med. 2015;66(3):222-229.e221.

13.       Ahmadi O, Isfahani MN, Feizi A. Comparing low-dose intravenous ketamine-midazolam with intravenous morphine with respect to pain control in patients with closed limb fracture. J Res Med Sci. 2014;19(6):502-508.

14.       Majidinejad S, Esmailian M, Emadi M. Comparison of intravenous ketamine with morphine in pain relief of long bones fractures: a double blind randomized clinical trial. Emerg (Tehran). 2014;2(2):77-80.

15.       Lester L, Braude DA, Niles C, Crandall CS. Low-dose ketamine for analgesia in the ED: a retrospective case series. Am J Emerg Med. 2010;28(7):820-827.

16.       Ahern TL, Herring AA, Anderson ES, Madia VA, Fahimi J, Frazee BW. The first 500: initial experience with widespread use of low-dose ketamine for acute pain management in the ED. Am J Emerg Med. 2015;33(2):197-201.

17.       Motov S, Mai M, Pushkar I, et al. A prospective randomized, double-dummy trial comparing intravenous push dose of low dose ketamine to short infusion of low dose ketamine for treatment of moderate to severe pain in the emergency department [published online ahead of print Mar 03, 2017]. Am J Emerg Med. doi: 10.1016/j.ajem.2017.03.004.

18.       Yetim M, Tekindur S, Eyi YE. Low-dose ketamine infusion for managing acute pain. Am J Emerg Med. 2015;33(9):1318.

19.       Off-label administration of ketamine for pain management by a nurse. Texas Board of Nursing Bulletin. 2012;43(4):5-6. https://www.bon.texas.gov/pdfs/newsletter_pdfs/2012/oct2012.pdf.

20.       Advisory opinion: low-dose ketamine. Nebraska Board of Nursing website. http://dhhs.ne.gov/publichealth/Licensure/Documents/LowDoseKetamine.pdf. Published June 2014. Accessed May 30, 2017.

21.       Zittel B. IV drug administration of ketamine for the treatment of intractable pain. New York State Education Department website. http://www.op.nysed.gov/prof/nurse/nurse-iv-ketamine.htm. Published June 2011. Accessed May 30, 2017.

22.       IV administration of ketamine for intractable pain for adults. Wyoming State Board of Nursing website. https://nursing-online.state.wy.us/Resources/ketamine%20advisory%20opinion.pdf. Published October 10, 2013. Accessed May 30, 2017.

23.       Gurnani A, Sharma PK, Rautela RS, Bhattacharya A. Analgesia for acute musculoskeletal trauma: low-dose subcutaneous infusion of ketamine. Anaesth Intensive Care. 1996;24(1):32-36.

24.       Ahern TL, Herring AA, Miller S, Frazee BW. Low-dose ketamine infusion for emergency department patients with severe pain. Pain Med. 2015;16(7):1402-1409.

25.       Goltser A, Soleyman-Zomalan E, Kresch F, Motov S. Short (low-dose) ketamine infusion for managing acute pain in the ED: case-report series. Am J Emerg Med. 2015;33(4):601.e605-607.

26.       Farnia MR, Jalali A, Vahidi E, Momeni M, Seyedhosseini J, Saeedi M. Comparison of intranasal ketamine versus IV morphine in reducing pain in patients with renal colic. Am J Emerg Med. 2017;35(3):434-437.

27.       Shimonovich S, Gigi R, Shapira A, et al. Intranasal ketamine for acute traumatic pain in the Emergency Department: a prospective, randomized clinical trial of efficacy and safety. BMC Emerg Med. 2016;16(1):43.

28.       Graudins A, Meek R, Egerton-Warburton D, Oakley E, Seith R. The PICHFORK (Pain in Children Fentanyl or Ketamine) trial: a randomized controlled trial comparing intranasal ketamine and fentanyl for the relief of moderate to severe pain in children with limb injuries. Ann Emerg Med. 2015;65(3):248-254.e241.

29.       Shrestha R, Pant S, Shrestha A, Batajoo KH, Thapa R, Vaidya S. Intranasal ketamine for the treatment of patients with acute pain in the emergency department. World J Emerg Med. 2016;7(1):19-24.

30.       Yeaman F, Meek R, Egerton-Warburton D, Rosengarten P, Graudins A. Sub-dissociative-dose intranasal ketamine for moderate to severe pain in adult emergency department patients. Emerg Med Australas. 2014;26(3):237-242.

31.       Andolfatto G, Willman E, Joo D, et al. Intranasal ketamine for analgesia in the emergency department: a prospective observational series. Acad Emerg Med. 2013;20(10):1050-1054.

32.       Yeaman F, Oakley E, Meek R, Graudins A. Sub-dissociative dose intranasal ketamine for limb injury pain in children in the emergency department: a pilot study. Emerg Med Australas. 2013;25(2):161-167.

June 2017

The information presented is current as April 28, 2017. This information is intended as an educational piece and should not be used as the sole source for clinical decision-making.

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What is the available evidence for the use of alteplase for occlusion of peritoneal dialysis catheters?

Introduction

The United States Renal Data System estimates there were 678,383 patients with end-stage renal disease (ESRD) in the US at the end of 2014, of whom 6.9% received peritoneal dialysis.¹ One complication of peritoneal dialysis is catheter occlusion and obstructed outflow by formation of a fibrin plug.² If the plug cannot be removed, surgical removal of the catheter may be necessary.³ International Society for Peritoneal Dialysis guidelines on peritoneal dialysis for acute kidney injury recommend sterile saline flushes for fibrin plugs.⁴ Nonoperative management recommended by the Society of American Gastrointestinal and Endoscopic Surgeons includes compression of the dialysis bag, heparinized saline flush, and thrombolytics (ie, alteplase) then irrigation.⁵

Alteplase is a tissue plasminogen activator that exerts its effect as a thrombolytic by binding to fibrin and cleaving plasminogen to form plasmin.⁶ Food and Drug Administration-approved indications for alteplase include acute myocardial infarction, acute ischemic stroke, pulmonary embolism, and central venous catheter occlusion. The purpose of this review is to summarize the evidence available for use of alteplase for the off-label indication of treatment of occlusion of peritoneal dialysis catheters. Table 1 provides a summary of published reports describing use and outcomes with use of alteplase for this off-label indication. Possible reasons for unsuccessful outcomes are also described. Reports of alteplase in patients with active peritonitis were not included.

Summary

Most reports summarized above described use of alteplase in pediatric patients, while 1 case series described use in adults, and 1 report did not discuss patient age.^3,7-12 Data are varied regarding dwell time, concentration, and volume of alteplase used. Most reports used 1 hour dwell time, while 2 case reports used 2 hour dwell time successfully. Hutchinson and Chand described a failed attempt at occluded catheter thrombolysis in a 5 month old infant using a 20 minute dwell time.¹⁰ The authors concluded that the failure may have been due to the short dwell time, so increased to a 1 hour dwell time for subsequent patients based on the half-life of alteplase. The authors calculated that a dwell time of 1 hour would allow alteplase to reach steady state based on its 10 minute elimination half-life. After switching to the longer dwell time, they were successful in thrombolysis in 3 occluded catheter events. Concentrations used in the summarized articles ranged from 2 mg/40 mL to 1 mg/mL, with 1 mg/mL described in most reports.^7-12 While concentration of 8 mg/10 mL was reported in only 1 article, it was used successfully in 24 of 29 occluded catheter events.⁸ Volume instilled also varied by report, and 2 articles used the volume of the catheter.^10,12 In most reports, adverse events were either not reported or not observed; however, 1 article reported adverse events of temporary bloody dialysate after catheter replacement in an unsuccessful case and temporary dialysate leak in another case.¹¹

Overall, use of alteplase has demonstrated success for thrombolysis in occluded peritoneal catheters based on limited reports.

References

1.         2016 USRDS annual report: epidemiology of kidney disease in the United States. United States Renal Data System website. https://www.usrds.org/2016/view/Default.aspx. Accessed May 23, 2017.

2.         Sowinski KM, Churchwell MD, Decker BS. Hemodialysis and peritoneal dialysis. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey L, eds. Pharmacotherapy: A Pathophysiologic Approach. 10th ed. New York, NY: McGraw-Hill;  http://accesspharmacy.mhmedical.com.proxy.cc.uic.edu/content.aspx?bookid=1861&sectionid=146060865. Accessed May 23, 2017.

3.         Pierce DP. Use of alteplase for clearing peritoneal dialysis catheter occlusion. Hosp Pharm. 2016;51(3):252-255.

4.         Cullis B, Abdelraheem M, Abrahams G, et al. Peritoneal dialysis for acute kidney injury. Perit Dial Int. 2014;34(5):494-517.

5.         Haggerty S, Roth S, Walsh D, et al. Guidelines for laparoscopic peritoneal dialysis access surgery. Society of American Gastrointestinal and Endoscopic Surgeons website. https://www.sages.org/publications/guidelines/guidelines-laparoscopic-peritoneal-dialysis-access-surgery/. Published June 2014. Accessed May 24, 2017.

6.         Micromedex [database online]. Greenwood Village, CO: Truven Health Analytics, Inc. 2017. http://micromedex.com/. Accessed May 23, 2017.

7.         Krishnan RG, Moghal NE. Tissue plasminogen activator for blocked peritoneal dialysis catheters. Pediatr Nephrol. 2006;21(2):300.

8.         Zorzanello MM, Fleming WJ, Prowant BF. Use of tissue plasminogen activator in peritoneal dialysis catheters: a literature review and one center’s experience. Nephrol Nurs J. 2004;31(5):534-537.

9.         Sakarcan A, Stallworth JR. Tissue plasminogen activator for occluded peritoneal dialysis catheter. Pediatr Nephrol. 2002;17(3):155-156.

10.       Hutchinson PJ, Chand DH. Use of tissue plasminogen activator in obstructed peritoneal dialysis catheters. Dial Transplant. 2001;30(2):104-108.

11.       Shea M, Hmiel SP, Beck AM. Use of tissue plasminogen activator for thrombolysis in occluded peritoneal dialysis catheters in children. Adv Perit Dial. 2001;17:249-252.

12.       Sahani MM, Mukhtar KN, Boorgu R, Leehey DJ, Popli S, Ing TS. Tissue plasminogen activator can effectively declot peritoneal dialysis catheters. Am J Kidney Dis. 2000;36(3):675.

June 2017

The information presented is current as of May 12, 2017.  This information is intended as an educational piece and should not be used as the sole source for clinical decision making

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