Chloramphenicol + Lidocaine Hydrochloride interactions

Checked as Chloramphenicol + Lidocaine in this data source.

Full monograph for Chloramphenicol + Lidocaine Hydrochloride Check it against another medicine

Medicines

710 documented

Severity

Mechanism

Medicines documented to interact with Chloramphenicol + Lidocaine Hydrochloride, worst severity first.
Medicine	Severity	Mechanism	Effect	Sources
Brigatinibvia Chloramphenicol	Major	Metabolism	Coadministration with moderate inhibitors of CYP450 3A4 may significantly increase the plasma concentrations of brigatinib, which is partially metabolized by…	4 sources — open the full entry
Bromocriptine Mesylatevia Chloramphenicol	Major	Metabolism	Coadministration with moderate inhibitors of CYP450 3A4 may significantly increase the plasma concentrations of bromocriptine. Orally administered…	7 sources — open the full entry
Bupivacaine Hydrochloridevia Lidocaine, Chloramphenicol	Major	Synergy · Unknown	Additive toxicities may occur when bupivacaine is coadministered with other local anesthetics. The potential for increased risk of systemic toxicities such as…2 documented mechanisms	3 sources — open the full entry
Bupivacaine Hydrochloride + Dextrosevia Lidocaine, Chloramphenicol	Major	Synergy · Unknown	Additive toxicities may occur when bupivacaine is coadministered with other local anesthetics. The potential for increased risk of systemic toxicities such as…2 documented mechanisms	3 sources — open the full entry
Bupropion Hydrochloridevia Lidocaine	Major	Synergy	The use of bupropion is associated with a dose-related risk of seizures. The risk may be further increased when coadministered with selective serotonin…	19 sources — open the full entry
Chloroquine Phosphatevia Lidocaine, Chloramphenicol	Major	Metabolism · Synergy	Coadministration of local anesthetics with other oxidizing agents that can also induce methemoglobinemia such as antimalarials (e.g., chloroquine, primaquine…2 documented mechanisms	8 sources — open the full entry
Clozapinevia Chloramphenicol	Major	Synergy	Coadministration of clozapine with other agents that can cause neutropenia or agranulocytosis may increase the risk and/or severity of hematologic toxicity.	9 sources — open the full entry
Dapsonevia Lidocaine, Chloramphenicol	Major	Synergy	Coadministration of local anesthetics with other oxidizing agents that can also induce methemoglobinemia such as antimalarials (e.g., chloroquine, primaquine…2 documented mechanisms	9 sources — open the full entry
Deferipronevia Chloramphenicol	Major	Synergy	Coadministration of deferiprone and other drugs that can cause neutropenia or agranulocytosis may increase the risk and/or severity of hematologic toxicity…	5 sources — open the full entry
Dextromethorphan + Bupropionvia Lidocaine	Major	Synergy	The use of bupropion is associated with a dose-related risk of seizures. The risk may be further increased when coadministered with selective serotonin…	19 sources — open the full entry
Elacestrantvia Chloramphenicol	Major	Metabolism	Coadministration with potent or moderate inhibitors of CYP450 3A4 may significantly increase the plasma concentrations of elacestrant, which is primarily…	1 sources — open the full entry
Everolimusvia Chloramphenicol	Major	Absorption · Metabolism	Coadministration with moderate inhibitors of CYP450 3A4 and P-glycoprotein may significantly increase the plasma concentrations of everolimus following oral…	2 sources — open the full entry
Finerenonevia Chloramphenicol	Major	Metabolism	Coadministration with moderate inhibitors of CYP450 3A4 may significantly increase the plasma concentrations of finerenone, which is primarily metabolized by…	3 sources — open the full entry
Flibanserinvia Chloramphenicol	Major	Metabolism	Coadministration with moderate and potent inhibitors of CYP450 3A4 may significantly increase the plasma concentrations of flibanserin, which is primarily…	2 sources — open the full entry
Flutamidevia Lidocaine	Major	Synergy	Coadministration of local anesthetics with other oxidizing agents that can also induce methemoglobinemia such as antimalarials (e.g., chloroquine, primaquine…	5 sources — open the full entry
Hydroxyureavia Lidocaine, Chloramphenicol	Major	Synergy	Coadministration of local anesthetics with other oxidizing agents that can also induce methemoglobinemia such as antimalarials (e.g., chloroquine, primaquine…2 documented mechanisms	13 sources — open the full entry
Ifosfamidevia Lidocaine, Chloramphenicol	Major	Synergy	Coadministration of local anesthetics with other oxidizing agents that can also induce methemoglobinemia such as antimalarials (e.g., chloroquine, primaquine…2 documented mechanisms	13 sources — open the full entry
Iohexolvia Lidocaine	Major	Synergy	Intrathecal administration of iodinated contrast media may induce seizures. Although clinical data are generally lacking, there may be a theoretical risk of…	5 sources — open the full entry
Iopamidolvia Lidocaine	Major	Synergy	Intrathecal administration of iodinated contrast media may induce seizures. Although clinical data are generally lacking, there may be a theoretical risk of…	5 sources — open the full entry
Isosorbide Dinitrate + Hydralazine Hydrochloridevia Lidocaine, Chloramphenicol	Major	Synergy	Coadministration of local anesthetics with other oxidizing agents that can also induce methemoglobinemia such as antimalarials (e.g., chloroquine, primaquine…2 documented mechanisms	9 sources — open the full entry
Isosorbide Mononitratevia Lidocaine	Major	Synergy	Coadministration of local anesthetics with other oxidizing agents that can also induce methemoglobinemia such as antimalarials (e.g., chloroquine, primaquine…	5 sources — open the full entry
Lidocaine + Prilocainevia Lidocaine	Major	Synergy	Prilocaine can cause dose-related methemoglobin formation via its ortho-toluidine metabolite. Coadministration with other oxidizing agents that can also induce…2 documented mechanisms	13 sources — open the full entry
Lurbinectedinvia Chloramphenicol	Major	Metabolism	Coadministration with a moderate CYP450 3A4 inhibitor is predicted to increase lurbinectedin systemic exposure, which may increase the incidence and severity…	2 sources — open the full entry
Mavacamtenvia Lidocaine, Chloramphenicol	Major	Metabolism	Coadministration with inhibitors of CYP450 2C19 or CYP450 3A4 may increase the plasma concentrations of mavacamten.2 documented mechanisms	5 sources — open the full entry
Metoclopramide Hydrochloridevia Lidocaine, Chloramphenicol	Major	Synergy · Unknown	Coadministration of local anesthetics with other oxidizing agents that can also induce methemoglobinemia such as antimalarials (e.g., chloroquine, primaquine…2 documented mechanisms	5 sources — open the full entry
Neratinib Maleatevia Chloramphenicol	Major	Metabolism	Coadministration with potent or moderate inhibitors of CYP450 3A4 may significantly increase the plasma concentrations of neratinib, which is primarily…	7 sources — open the full entry
Nitrofurantoinvia Lidocaine, Chloramphenicol	Major	Synergy	Coadministration of local anesthetics with other oxidizing agents that can also induce methemoglobinemia such as antimalarials (e.g., chloroquine, primaquine…2 documented mechanisms	9 sources — open the full entry
Nitrofurantoin + Nitrofurantoin Microcrystalsvia Lidocaine, Chloramphenicol	Major	Synergy	Coadministration of local anesthetics with other oxidizing agents that can also induce methemoglobinemia such as antimalarials (e.g., chloroquine, primaquine…2 documented mechanisms	9 sources — open the full entry
Nitroglycerinbase IV Infusion Ointmentvia Lidocaine	Major	Synergy	Coadministration of local anesthetics with other oxidizing agents that can also induce methemoglobinemia such as antimalarials (e.g., chloroquine, primaquine…	5 sources — open the full entry
Paracetamol + Tramadol Hydrochloridevia Lidocaine, Chloramphenicol	Major	Metabolism · Synergy · Unknown	The risk of seizures may be increased during coadministration of tramadol with any substance that can reduce the seizure threshold, such as selective serotonin…3 documented mechanisms	12 sources — open the full entry
Primaquine Phosphatevia Lidocaine	Major	Synergy	Coadministration of local anesthetics with other oxidizing agents that can also induce methemoglobinemia such as antimalarials (e.g., chloroquine, primaquine…	5 sources — open the full entry
Quinine Sulfatevia Lidocaine	Major	Synergy	Coadministration of local anesthetics with other oxidizing agents that can also induce methemoglobinemia such as antimalarials (e.g., chloroquine, primaquine…	5 sources — open the full entry
Selpercatinibvia Lidocaine, Chloramphenicol	Major	Metabolism	Coadministration with moderate inhibitors of CYP450 3A4 may significantly increase the plasma concentrations of selpercatinib, which is primarily metabolized…2 documented mechanisms	40 sources — open the full entry
Sulphamethoxazole + Trimethoprimvia Chloramphenicol, Lidocaine	Major	Synergy · Unknown	Coadministration of local anesthetics with other oxidizing agents that can also induce methemoglobinemia such as antimalarials (e.g., chloroquine, primaquine…3 documented mechanisms	5 sources — open the full entry
Tramadol Hydrochloridevia Lidocaine, Chloramphenicol	Major	Metabolism · Synergy	The risk of seizures may be increased during coadministration of tramadol with any substance that can reduce the seizure threshold, such as selective serotonin…2 documented mechanisms	12 sources — open the full entry
Abametapirvia Lidocaine	Moderate	Metabolism	Based on in vitro inhibition data, a single topical application of abametapir lotion may increase plasma concentrations of drugs that are substrates of CYP450…	1 sources — open the full entry
Abemaciclibvia Chloramphenicol	Moderate	Metabolism	Coadministration with inhibitors of CYP450 3A4 may increase the plasma concentrations of abemaciclib and its pharmacologically active metabolites, all of which…	2 sources — open the full entry
Acalabrutinibvia Chloramphenicol	Moderate	Metabolism	Coadministration with inhibitors of CYP450 3A4 may increase the plasma concentrations of acalabrutinib, which is primarily metabolized by the isoenzyme.	3 sources — open the full entry
Adalimumabvia Lidocaine, Chloramphenicol	Moderate	Metabolism · Synergy	Plasma concentrations of drugs that are CYP450 substrates may decrease following the initiation of interleukin (IL) inhibitors, tumor necrosis factor (TNF)…2 documented mechanisms	23 sources — open the full entry
Afliberceptvia Chloramphenicol	Moderate	Synergy	Coadministration of chloramphenicol with other agents that can cause bone marrow depression or aplastic anemia may increase the risk and/or severity of…	8 sources — open the full entry
Alfuzosin Hydrochloridevia Chloramphenicol	Moderate	Metabolism	Coadministration with moderate inhibitors of CYP450 3A4 may increase the plasma concentrations of alfuzosin, which is primarily metabolized by the isoenzyme…	2 sources — open the full entry
Alprazolamvia Lidocaine	Moderate	Synergy	The concomitant use of local anesthetics and benzodiazepines may have additive CNS-depressant effects. Both types of drugs are CNS depressants.	7 sources — open the full entry
Amiodarone Hydrochloridevia Lidocaine, Chloramphenicol	Moderate	Metabolism · Synergy	Limited data suggest additive depressive effects of amiodarone and lidocaine on the sinoatrial node. The proposed mechanism is amiodarone inhibition of…2 documented mechanisms	11 sources — open the full entry
Amitriptyline Hydrochloride + Chlordiazepoxidevia Lidocaine	Moderate	Synergy · Unknown	The concomitant use of local anesthetics and benzodiazepines may have additive CNS-depressant effects. Both types of drugs are CNS depressants.2 documented mechanisms	7 sources — open the full entry
Amlodipine Besilatevia Chloramphenicol, Lidocaine	Moderate	Metabolism · Unknown	Coadministration with CYP450 3A4 inhibitors may increase the plasma concentrations of amlodipine, which is a substrate of the isoenzyme.2 documented mechanisms	5 sources — open the full entry
Amlodipine Besilate + Atenololvia Chloramphenicol, Lidocaine	Moderate	Metabolism · Synergy · Unknown	Coadministration with CYP450 3A4 inhibitors may increase the plasma concentrations of amlodipine, which is a substrate of the isoenzyme.4 documented mechanisms	15 sources — open the full entry
Amlodipine Besilate + Atorvastatinvia Chloramphenicol, Lidocaine	Moderate	Metabolism · Synergy · Unknown	Coadministration with CYP450 3A4 inhibitors may increase the plasma concentrations of amlodipine, which is a substrate of the isoenzyme.4 documented mechanisms	9 sources — open the full entry
Amlodipine Besilate + Benazepril Hydrochloridevia Chloramphenicol, Lidocaine	Moderate	Metabolism · Unknown	Coadministration with CYP450 3A4 inhibitors may increase the plasma concentrations of amlodipine, which is a substrate of the isoenzyme.2 documented mechanisms	5 sources — open the full entry
Amlodipine Besilate + Olmesartan Medoxomilvia Chloramphenicol, Lidocaine	Moderate	Metabolism · Unknown	Coadministration with CYP450 3A4 inhibitors may increase the plasma concentrations of amlodipine, which is a substrate of the isoenzyme.2 documented mechanisms	5 sources — open the full entry
Amlodipine Besilate + Telmisartanvia Chloramphenicol, Lidocaine	Moderate	Metabolism · Unknown	Coadministration with CYP450 3A4 inhibitors may increase the plasma concentrations of amlodipine, which is a substrate of the isoenzyme.3 documented mechanisms	5 sources — open the full entry

Conditions

Conditions in which Chloramphenicol + Lidocaine Hydrochloride needs care, as documented in this source.

Arrhythmias, Cardiac
Major
Antiarrhythmic agents can induce or worsen ventricular arrhythmias. Ventricular tachycardia, ventricular fibrillation, and torsades de pointes have occurred in some patients. Patients with underlying cardiac dysfunction, bradycardia, hypokalemia, hypomagnesemia, or high antiarrhythmic serum concentrations are at increased risk for drug-induced arrhythmias. Therapy with antiarrhythmics should be used with extreme caution in patients with or predisposed to arrhythmias. Evidence of improved survival is lacking for use of antiarrhythmic therapy in asymptomatic, non-life-threatening arrhythmias. Therapy with antiarrhythmic agents should be reserved for patients with life-threatening arrhythmias.
62 sources
1. Anderson JL, Popat KD "Paradoxical ventricular tachycardia and fibrillation after intravenous bretylium therapy." Arch Intern Med 141 (1981): 801-2
2. Sclarovsky S, Lewin RF, Kracoff O, Strasberg B, Arditti A, Agmon J "Amiodarone-induced polymorphous ventricular tachycardia." Am Heart J 105 (1983): 6-12
3. Strasberg B, Sclarovsky S, Erdberg A, et al. "Procainamide-induced polymorphous ventricular tachycardia." Am J Cardiol 47 (1981): 1309-14
4. Stratmann H, Walter K, Kennedy H "Torsade de pointes associated with elevated N-acetylprocainamide levels." Am Heart J 109 (1985): 375-6
5. Lo KS, Gantz KB, Stetson PL, et al. "Disopyramide-induced ventricular tachycardia." Arch Intern Med 140 (1980): 413-4
6. Kinney EL, Field EH, Salmon MP, Zelis R "Cardiac arrhythmias associated with disopyramide." N Engl J Med May (1990): 1146
7. Chia BL "Disopyramide induced atypical ventricular tachycardia." Aust N Z J Med 10 (1980): 665-8
8. Tzivoni D, Keren A, Stern S, Gottlieb S "Disopyramide-induced Torsade de pointes." Arch Intern Med 141 (1981): 946-7
Show all 62 sourcesShow fewer sources
1. Schweitzer P, Mark H "Torsade de pointes caused by disopyramide and hypokalemia." Mt Sinai J Med 49 (1982): 110-4
2. Riccioni N, Castiglioni M, Bartolomei C "Disopyramide-induced QT prolongation and ventricular tachyarrhythmias." Am Heart J 105 (1983): 870-1
3. Andrivet P, Beaslay V, Canh VD "Torsades de pointe with flecainide-amiodarone therapy." Intensive Care Med 16 (1990): 342-3
4. Cocco G, Strozzi C, Chu D, Pansini R "Torsades de pointes as a manifestation of mexiletine toxicity." Am Heart J 100 (1980): 878-80
5. Nora MO, Chandrasekaran K, Hammill SC, Reeder GS "Prolongation of ventricular depolarization: ECG manifestation of mexiletine toxicity." Chest 95 (1989): 925-8
6. Morganroth J, Pratt CM "Prevalence and characteristics of proarrhythmia from moricizine (themozine)." Am J Cardiol 63 (1989): 172-6
7. Damle R, Levine J, Matos J, et al. "Efficacy and risks of moricizine in inducible sustained ventricular tachycardia." Ann Intern Med 116 (1992): 375-81
8. Nathan AW, Hellestrand KJ, Bexton RS, Camm AJ "Fatal ventricular tachycardia in association with propafenone, a new class IC antiarrhythmic agent." Postgrad Med J 60 (1984): 155-6
9. Stavens CS, McGovern B, Garan H, Ruskin JN "Aggravation of electrically provoked ventricular tachycardia during treatment with propafenone." Am Heart J 110 (1985): 24-9
10. Hii JT, Wyse DG, Gillis AM, et al. "Propafenone-induced torsade de pointes: cross-reactivity with quinidine." Pacing Clin Electrophysiol 14 (1991): 1568-70
11. Cheesman M, Ward DE "Exacerbation of ventricular tachycardia by tocainide." Clin Cardiol 8 (1985): 47-50
12. Bauman JL, Bauernfeind RA, Hoff JV, et al. "Torsade de pointes due to quinidine: observations in 31 patients." Am Heart J 107 (1984): 425-30
13. Koenig W, Schinz AM "Spontaneous ventricular flutter and fibrillation during quinidine medication." Am Heart J 105 (1983): 863-5
14. Morganroth J, Horowitz LN "Incidence of proarrhythmic effects from quinidine in the outpatient treatment of benign or potentially lethal ventricular arrhythmias." Am J Cardiol 56 (1985): 585-7
15. Au PK, Bhandari AK, Bream R, et al. "Proarrhythmic effects of antiarrhythmic drugs during programmed ventricular stimulation in patients without ventricular tachycardia." J Am Coll Cardiol 9 (1987): 389-97
16. Engler RL, LeWinter M "Tocainide-induced ventricular fibrillation." Am Heart J 101 (1981): 494-6
17. Wesley RC Jr, Turnquest P "Torsades de pointe after intravenous adenosine in the presence of prolonged QT syndrome." Am Heart J 123 (1992): 794-6
18. Orebaugh SL, Handy M "Intravenous adenosine therapy accelerating rate of paroxysmal supraventricular tachycardia." Am J Emerg Med 10 (1992): 326-30
19. Reed R, Falk JL, O'Brien J "Untoward reaction to adenosine therapy for supraventricular tachycardia." Am J Emerg Med 9 (1991): 566-70
20. Meurer MK "A 21-year-old woman with rapid atrial fibrillation after adenosine administration." J Emerg Nurs 17 (1991): 135-6
21. Dougherty AH, Gilman JK, Wiggins S, Jalal S, Naccarelli GV "Provocation of atrioventricular reentry tachycardia: a paradoxical effect of adenosine." Pacing Clin Electrophysiol 16 (1993): 8-12
22. "Product Information. Tonocard (tocainide)." Merck & Co., Inc (2002):
23. "Product Information. Ethmozine (moricizine)." DuPont Pharmaceuticals (2002):
24. "Product Information. Cordarone (amiodarone)." Wyeth-Ayerst Laboratories (2002):
25. "Product Information. Bretylol (bretylium)." DuPont Pharmaceuticals (2002):
26. "Product Information. Xylocaine (lidocaine)." Astra-Zeneca Pharmaceuticals (2002):
27. "Product Information. Procan SR (procainamide)." Parke-Davis (2001):
28. "Product Information. Pronestyl (procainamide)." Apothecon Inc (2001):
29. Raehl CL, Patel AK, LeRoy M "Drug-induced torsade de pointes." Clin Pharm 4 (1985): 675-90
30. Buss J, Neuss H, Bilgin Y, Schlepper M "Malignant ventricular tachyarrhythmias in association with propafenone treatment." Eur Heart J 6 (1985): 424-8
31. Sulke AN, Holt P, Sowton GE "Acceleration of conduction within an accessory pathway with propafenone." Int J Cardiol 28 (1990): 105-7
32. "Product Information. Adenocard (adenosine)." Fujisawa (2001):
33. "Product Information. Tambocor (flecainide)." 3M Pharmaceuticals (2001):
34. "Product Information. Mexitil (mexiletine)." Boehringer-Ingelheim (2001):
35. "Product Information. Rythmol (propafenone)." Knoll Pharmaceutical Company
36. Ben-Sorek ES, Wiesel J "Ventricular fibrillation following adenosine administration. A case report." Arch Intern Med 153 (1993): 2701-2
37. Said SAM, Somer ST, Luttikhuis HAO "Flecainide-induced JT prolongation, t wave inversion and ventricular tachycardia during treatment for symptomatic atrial fibrillation." Int J Cardiol 44 (1994): 285-7
38. Makkar RR, Fromm BS, Steinman RT, Meissner MD, Lehmann MH "Female gender as a risk factor for torsades de pointes associated with cardiovascular drugs." JAMA 270 (1993): 2590-7
39. "Product Information. Norpace (disopyramide)." Searle (2001):
40. Oberg KC, Otoole MF, Gallastegui JL, Bauman JL "''late'' proarrhythmia due to quinidine." Am J Cardiol 74 (1994): 192-4
41. Romer M, Candinas R "Adenosine-induced non-sustained polymorphic ventricular tachycardia." Eur Heart J 15 (1994): 281-2
42. Hohnloser SH, Klingenheben T, Singh BN "Amiodarone-associated proarrhythmic effects - a review with special reference to torsade de pointes tachycardia." Ann Intern Med 121 (1994): 529-35
43. Celiker A, Tokel K, Cil E, Ozkutlu S, Ozme S "Adenosine induced torsades de pointes in a child with congenital long QT syndrome." Pacing Clin Electrophysiol 17 (1994): 1814-7
44. Exner DV, Muzyka T, Gillis AM "Proarrhythmia in patients with the Wolff-Parkinson-White Syndrome after standard doses of intravenous adenosine." Ann Intern Med 122 (1995): 351-2
45. Williamson BD, Hummel J, Niebauer M, Man C, Strickberger SA, Daoud E, Morady F "Bradycardia-facilitated polymorphic ventricular tachycardia caused by amiodarone after radiofrequency modification of atrioventricular conduction." Am Heart J 130 (1995): 399-401
46. Dhein S, Schott M, Gottwald E, Klaus W "Electrocardiological profile and proarrhythmic effects of quinidine, verapamil and their combination: a mapping study." Naunyn Schmiedebergs Arch Pharmacol 352 (1995): 94-101
47. "Product Information. Cordarone (amiodarone)." Apothecon Inc (2022):
48. Hohnloser SH, Vandeloo A, Baedeker F "Efficacy and proarrhythmic hazards of pharmacologic cardioversion of atrial fibrillation: prospective comparison of sotalol versus quinidine." J Am Coll Cardiol 26 (1995): 852-8
49. "Product Information. Corvert (ibutilide)." Pharmacia and Upjohn (2001):
50. Silverman AJ, Machado C, Baga JJ, Meissner MD, Lehmann MH, Steinman RT "Adenosine-induced atrial fibrillation." Am J Emerg Med 14 (1996): 300-1
51. Boriani G, Biffi M, Frabetti L, Azzolini U, Sabbatani P, Bronzetti G, Capucci A, Magnani B "Ventricular fibrillation after intravenous amiodarone in wolff-parkinson-white syndrome with atrial fibrillation." Am Heart J 131 (1996): 1214-6
52. Faggiano P, Gardini A, Daloia A, Benedini G, Giordano A "Torsade de pointes occurring early during oral amiodarone treatment." Int J Cardiol 55 (1996): 205-8
53. Heisler BE, Ferrier GR "Proarrhythmic actions of flecainide in an isolated tissue model of ischemia and reperfusion." J Pharmacol Exp Ther 279 (1996): 317-24
54. Strickberger SA, Man KC, Daoud EG, et al. "Adenosine-induced atrial arrhythmia: a prospective analysis." Ann Intern Med 127 (1997): 417-22
Bone Marrow Failure Disorders
Major
Chloramphenicol may cause bone marrow depression and other hematologic toxicities, which can be irreversible or reversible. The former type is independent of dose and results in aplastic anemia with a high rate of mortality, generally from hemorrhage or infection. It has been reported following both systemic and topical administration of chloramphenicol and has an estimated incidence of 1 in 25,000 to 1 in 40,000 courses of therapy. Bone marrow aplasia or hypoplasia may occur after a single dose but more often develops weeks or months after the drug has been discontinued. A reversible myelosuppression occurs much more frequently and is characterized by anemia, vacuolation of red blood cells, decreased reticulocyte count, leukopenia, thrombocytopenia, increased serum iron concentrations, and increased serum iron-binding capacity. It is dose-dependent, occurring regularly at chloramphenicol dosages exceeding 4 g/day (in adults) or at plasma drug concentrations >= 25 mcg/mL, and usually responds to withdrawal of the drug. Therapy with chloramphenicol should be administered cautiously, if at all, in patients with preexisting blood dyscrasias and/or bone marrow depression. Complete blood counts and differential reticulocyte counts should be performed in all patients prior to initiating therapy and approximately every 2 days during therapy. Marked depression of blood counts and/or development of other hematologic abnormalities may be indication for withdrawal of chloramphenicol therapy.
10 sources
1. Abrams SM, Degnan TJ, Vinciguerra V "Marrow aplasia following topical application of chloramphenicol eye ointment." Arch Intern Med 140 (1980): 576-7
2. Calderwood SB, Moellering RC "Common adverse effects of antibacterial agents on major organ systems." Surg Clin North Am 60 (1980): 65-81
3. Del Giacco GS, Petrini MT, Jannelli S, Carcassi U "Fatal bone marrow hypoplasia in a shepherd using chloramphenicol spray." Lancet 1 (1981): 945
4. Farber BF, Brody JP "Rapid development of aplastic anemia after intravenous chloramphenicol and cimetidine therapy." South Med J 74 (1981): 1257-8
5. Fraunfelder FT, Bagby GC, Kelly DJ "Fatal aplastic anemia following topical administration of ophthalmic chloramphenicol." Am J Ophthalmol 93 (1982): 356-60
6. Alavi JB "Aplastic anemia associated with intravenous chloramphenicol." Am J Hematol 15 (1983): 375-9
7. West BC, DeVault GA Jr, Clement JC, Williams DM "Aplastic anemia associated with parenteral chloramphenicol: review of 10 cases, including the second case of possible increased risk with cimetidine." Rev Infect Dis 10 (1988): 1048-51
8. "Product Information. Chloromycetin (chloramphenicol)." Parke-Davis (2002):
Show all 10 sourcesShow fewer sources
1. American Medical Association, Division of Drugs and Toxicology "Drug evaluations annual 1994." Chicago, IL: American Medical Association; (1994):
2. Doona M, Walsh JB "Use of chloramphenicol as topical eye medication: time to cry halt? bone marrow aplasia also occurs with ocular use." BMJ 310 (1995): 1217-8
Cardiomyopathies
Major
Antiarrhythmic agents can induce severe hypotension (particularly with IV administration) or induce or worsen congestive heart failure (CHF). Patients with primary cardiomyopathy or inadequately compensated CHF are at increased risk. Antiarrhythmic agents should be administered cautiously and dosage and/or frequency of administration modified in patients with hypotension or adequately compensated CHF. Alternative therapy should be considered unless these conditions are secondary to cardiac arrhythmia.
17 sources
1. Halkin H, Meffin P, Melmon KL, Rowland M "Influence of congestive heart failure on blood levels of lidocaine and its active monodeethylated metabolite." Clin Pharmacol Ther 17 (1975): 669-76
2. Crouthamel WG "The effect of congestive heart failure on quinidine pharmacokinetics." Am Heart J 90 (1975): 335-9
3. Ravid S, Podrid PJ, Lampert S, Lown B "Congestive heart failure induced by six of the newer antiarrhythmic drugs." J Am Coll Cardiol 14 (1989): 1326-30
4. Swiryn S, Kim SS "Quinidine-induced syncope." Arch Intern Med 143 (1983): 314-6
5. Gottlieb SS, Packer M "Deleterious hemodynamic effects of lidocaine in severe congestive heart failure." Am Heart J 118 (1989): 611-2
6. Ochs HR, Grube E, Greenblatt DJ, Arendt R "Intravenous quinidine in congestive cardiomyopathy." Eur J Clin Pharmacol 19 (1981): 173-6
7. Prescott LF, Adjepon-Yamoah KK, Talbot RG "Impaired lignocaine metabolism in patients with myocardial infarction and cardiac failure." Br Med J 1 (1976): 939-41
8. "Product Information. Cordarone (amiodarone)." Wyeth-Ayerst Laboratories (2002):
Show all 17 sourcesShow fewer sources
1. "Product Information. Xylocaine (lidocaine)." Astra-Zeneca Pharmaceuticals (2002):
2. "Product Information. Quinidex Extentabs (quiNIDine)." Wyeth-Ayerst Laboratories
3. "Product Information. Quiniglute (quinidine)." Berlex, Richmond, CA.
4. "Product Information. Adenocard (adenosine)." Fujisawa (2001):
5. "Product Information. Mexitil (mexiletine)." Boehringer-Ingelheim (2001):
6. Thomson P, Melmon K, Richardson J, Cohn K Steinbrunn W, Cudihee R, Rowland M "Lidocaine pharmacokinetics in advanced heart failure, liver disease, and renal failure in humans." Ann Intern Med 78 (1973): 499-508
7. Singh SN, Fletcher RD, Fisher SG, et al. "Amiodarone in patients with congestive heart failure and asymptomatic ventricular arrhythmia." N Engl J Med 333 (1995): 77-82
8. "Product Information. Cordarone (amiodarone)." Apothecon Inc (2022):
9. "Product Information. Corvert (ibutilide)." Pharmacia and Upjohn (2001):
Colitis
Major
Clostridioides difficile-associated diarrhea (CDAD), formerly pseudomembranous colitis, has been reported with almost all antibacterial drugs and may range from mild diarrhea to fatal colitis. The most common culprits include clindamycin and lincomycin. Antibacterial therapy alters the normal flora of the colon, leading to overgrowth of C difficile, whose toxins A and B contribute to CDAD development. Morbidity and mortality are increased with hypertoxin-producing strains of C difficile; these infections can be resistant to antimicrobial therapy and may require colectomy. CDAD must be considered in all patients who present with diarrhea after antibacterial use. Since CDAD has been reported to occur more than 2 months after antibacterial use, careful medical history is necessary. Therapy with broad-spectrum antibacterials and other agents with significant antibacterial activity should be administered cautiously in patients with history of gastrointestinal disease, particularly colitis; pseudomembranous colitis (generally characterized by severe, persistent diarrhea and severe abdominal cramps, and sometimes associated with the passage of blood and mucus), if it occurs, may be more severe in these patients and may be associated with flares in underlying disease activity. Antibacterial drugs not directed against C difficile may need to be stopped if CDAD is suspected or confirmed. Appropriate fluid and electrolyte management, protein supplementation, antibacterial treatment of C difficile, and surgical evaluation should be started as clinically indicated.
31 sources
1. "Product Information. Omnipen (ampicillin)." Wyeth-Ayerst Laboratories (2002):
2. "Product Information. Ceftin (cefuroxime)." Glaxo Wellcome (2002):
3. "Product Information. Zinacef (cefuroxime)." Glaxo Wellcome (2002):
4. "Product Information. Cleocin (clindamycin)." Pharmacia and Upjohn (2002):
5. "Product Information. Macrobid (nitrofurantoin)." Procter and Gamble Pharmaceuticals (2002):
6. "Product Information. Macrodantin (nitrofurantoin)." Procter and Gamble Pharmaceuticals (2002):
7. "Product Information. Amoxil (amoxicillin)." SmithKline Beecham (2001):
8. "Product Information. Merrem (meropenem)." Astra-Zeneca Pharmaceuticals (2001):
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1. "Product Information. Coly-Mycin M Parenteral (colistimethate)." Parke-Davis (2001):
2. "Product Information. Lincocin (lincomycin)." Pharmacia and Upjohn (2001):
3. "Product Information. Cubicin (daptomycin)." Cubist Pharmaceuticals Inc (2003):
4. "Product Information. Xifaxan (rifaximin)." Salix Pharmaceuticals (2004):
5. "Product Information. Doribax (doripenem)." Ortho McNeil Pharmaceutical (2007):
6. "Product Information. Penicillin G Procaine (procaine penicillin)." Monarch Pharmaceuticals Inc (2009):
7. "Product Information. Vibativ (telavancin)." Theravance Inc (2009):
8. "Product Information. Teflaro (ceftaroline)." Forest Pharmaceuticals (2010):
9. "Product Information. Penicillin G Sodium (penicillin G sodium)." Sandoz Inc (2022):
10. "Product Information. Dalvance (dalbavancin)." Durata Therapeutics, Inc. (2014):
11. "Product Information. Orbactiv (oritavancin)." The Medicines Company (2014):
12. "Product Information. Bicillin C-R (benzathine penicillin-procaine penicillin)." A-S Medication Solutions (2017):
13. "Product Information. Baxdela (delafloxacin)." Melinta Therapeutics, Inc. (2017):
14. "Product Information. Polymyxin B Sulfate (polymyxin B sulfate)." AuroMedics Pharma LLC (2022):
15. "Product Information. Zemdri (plazomicin)." Achaogen (2018):
16. "Product Information. Seysara (sarecycline)." Allergan Inc (2018):
17. "Product Information. Nuzyra (omadacycline)." Paratek Pharmaceuticals, Inc. (2018):
18. "Product Information. Aemcolo (rifamycin)." Aries Pharmaceuticals, Inc. (2018):
19. "Product Information. Fetroja (cefiderocol)." Shionogi USA Inc (2019):
20. "Product Information. Biaxin (clarithromycin)." AbbVie US LLC (2019):
21. "Product Information. Zithromax (azithromycin)." Pfizer U.S. Pharmaceuticals Group (2021):
22. "Product Information. E.E.S.-400 Filmtab (erythromycin)." Arbor Pharmaceuticals (2018):
23. "Product Information. Priftin (rifapentine)." sanofi-aventis (2020):
Kidney Diseases
Major
Lidocaine is primarily eliminated by the kidney. Less than 10% is eliminated unchanged in the urine. Two active metabolites (MEGX and GX) have been identified that exhibit antiarrhythmic and convulsant properties. GX accumulates during prolonged intravenous lidocaine infusion. Serum concentrations of lidocaine and the active metabolites are increased and the half-life prolonged in patients with renal impairment. Therapy with lidocaine should be administered cautiously and dosing modified for repeated or maintenance doses in patients with compromised renal function. Clinical monitoring of cardiac function (continual ECG) is required and serum metabolite concentrations and monitoring renal function are recommended.
8 sources
1. Eriksson E, Granberg P-O, Ortengren B "Study of renal excretion of prilocaine and lidocaine." Acta Chem Scand 358 (1966): 55-69
2. Thomson PD, Rowland M, Melmon KL "The influence of heart failure, liver disease, and renal failure on the disposition of lidocaine in man." Am Heart J 82 (1971): 417-21
3. Collinsworth KA, Strong JM, Atkinson AJ Jr, et al. "Pharmacokinetics and metabolism of lidocaine in patients with renal failure." Clin Pharmacol Ther 18 (1975): 59-64
4. Jacobi J, McGory RW, McCoy H, Matzke GR "Hemodialysis clearance of total and unbound lidocaine." Clin Pharm 2 (1983): 54-7
5. Vaziri ND, Saiki JK, Hughes W "Clearance of lidocaine by hemodialysis." South Med J 72 (1979): 1567-8
6. "Product Information. Xylocaine (lidocaine)." Astra-Zeneca Pharmaceuticals (2002):
7. Grossman S, Davis D, Kitchell B, Shand D, Routledge P "Diazepam and lidocaine plasma protein binding in renal disease." Clin Pharmacol Ther 31 (1982): 350-7
8. Thomson P, Melmon K, Richardson J, Cohn K Steinbrunn W, Cudihee R, Rowland M "Lidocaine pharmacokinetics in advanced heart failure, liver disease, and renal failure in humans." Ann Intern Med 78 (1973): 499-508
Liver Diseases
Major
Lidocaine is rapidly and extensively metabolized by the liver. Less than 10% is eliminated unchanged in the urine. Several inactive and two active forms (MEGX and GX) have been identified. MEGX and GX exhibit antiarrhythmic and convulsant properties. GX accumulates during prolonged intravenous lidocaine infusion. The pharmacokinetic disposition of lidocaine is altered by changes in hepatic function, including hepatic blood flow. Therapy with lidocaine should be administered cautiously and dosing modifications for repeated or loading and maintenance doses may be necessary. Clinical monitoring of cardiac (continuous ECG) is required and serum metabolite concentrations and monitoring hepatic function are recommended.
13 sources
1. Williams RL, Blaschke TF, Meffin PJ, et al. "Influence of viral hepatitis on the disposition of two compounds with high hepatic clearance: lidocaine and indocyanine green." Clin Pharmacol Ther 20 (1976): 290-9
2. Huet P-M, LeLorier J "Effects of smoking and chronic hepatitis B on lidocaine and indocyanine green kinetics." Clin Pharmacol Ther 28 (1980): 208-15
3. Bauer LA, Brown T, Gibaldi M, et al. "Influence of long-term infusions on lidocaine kinetics." Clin Pharmacol Ther 31 (1982): 433-7
4. Barry M, Keeling PW, Weir D, Feely J "Severity of cirrhosis and the relationship of a1-acid glycoprotein concentration to plasma protein binding of lidocaine." Clin Pharmacol Ther 47 (1990): 366-70
5. Thomson AH, Elliott HL, Kelman AW, et al. "The pharmacokinetics and pharmacodynamics of lignocaine and MEGX in healthy subjects." J Pharmacokinet Biopharm 15 (1987): 101-15
6. Forrest JA, Finlayson ND, Adjepon-Yamoah KK, Prescott LF "Antipyrine, paracetamol, and lignocaine elimination in chronic liver disease." Br Med J 1 (1977): 1384-7
7. Colli A, Buccino G, Cocciolo M, et al. "Disposition of a flow-limited drug (lidocaine) and a metabolic capacity-limited drug (theophylline) in liver cirrhosis." Clin Pharmacol Ther 44 (1988): 642-9
8. Villeneuve JP, Thibeault MJ, Ampelas M, et al. "Drug disposition in patients with HBsAg-positive chronic liver disease." Dig Dis Sci 32 (1987): 710-4
Show all 13 sourcesShow fewer sources
1. Huet PM, Villeneuve JP "Determinants of drug disposition in patients with cirrhosis." Hepatology 3 (1983): 913-8
2. "Product Information. Xylocaine (lidocaine)." Astra-Zeneca Pharmaceuticals (2002):
3. Huang YS, Lee SD, Deng JF, Wu JC, Lu RH, Lin YF, Wang YJ, Lo KJ "Measuring lidocaine metabolite - monoethylglycinexylidide as a quantitative index of hepatic function in adults with chronic hepatitis and cirrhosis." J Hepatol 19 (1993): 140-7
4. Thomson P, Melmon K, Richardson J, Cohn K Steinbrunn W, Cudihee R, Rowland M "Lidocaine pharmacokinetics in advanced heart failure, liver disease, and renal failure in humans." Ann Intern Med 78 (1973): 499-508
5. Shiffman ML, Luketic VA, Sanyal AJ, Duckworth PF, Purdum PP, Contos MJ, Mills AS, Edinboro LE, Poklis A "Hepatic lidocaine metabolism and liver histology in patients with chronic hepatitis and cirrhosis." Hepatology 19 (1994): 933-40
Liver Diseases
Major
Chloramphenicol is primarily inactivated by glucuronyl transferase in the liver and eliminated in the urine as both parent drug and metabolites. In adults with normal renal and hepatic function, only 5% to 15% of a dose of chloramphenicol is excreted unchanged by the kidney, but approximately 30% is excreted when chloramphenicol is administered intravenously as the sodium succinate ester. However, the fraction of drug excreted unchanged may be highly variable, especially in neonates and children. Therapy with chloramphenicol should be administered cautiously in patients with significantly impaired renal and/or hepatic function, since drug accumulation may occur in such patients. The dosage should be reduced based on the degree of impairment as well as plasma drug concentrations.
7 sources
1. Azzollini F, Gazzaniga A, Lodola E, Natangelo R "Elimination of chloramphenicol and thiamphenicol in subjects with cirrhosis of the liver." Int J Clin Pharmacol Ther Toxicol 6 (1972): 130-4
2. Koup JR, Lau AH, Brodsky B, Slaughter RL "Chloramphenicol pharmacokinetics in hospitalized patients." Antimicrob Agents Chemother 15 (1979): 651-7
3. Slaughter RL, Pieper JA, Cerra FB, et al. "Chloramphenicol sodium succinate kinetics in critically ill patients." Clin Pharmacol Ther 28 (1979): 69-77
4. Nahata MC, Powell DA "Bioavailability and clearance of chloramphenicol after intravenous chloramphenicol succinate." Clin Pharmacol Ther 30 (1981): 368-72
5. Narang AP, Dattta DV, Nath N, Mathur VS "Pharmacokinetic study of chloramphenicol in patients with liver disease." Eur J Clin Pharmacol 20 (1981): 479-83
6. Burke JT, Wargin WA, Sheretz RJ, et al. "Pharmacokinetics of intravenous chloramphenicol sodium succinate in adult patients with normal renal and hepatic function." J Pharmacokinet Biopharm 10 (1982): 601-14
7. "Product Information. Chloromycetin (chloramphenicol)." Parke-Davis (2002):
Seizures
Major
Seizures have occurred during lidocaine therapy and have been associated with the rapid administration of a large intravenous doses or accumulation of active metabolites with maintenance therapy. Therapy with lidocaine should be administered cautiously to patients with or predisposed to seizure disorders. Clinical monitoring of cardiac (continuous ECG) is required, and serum metabolite concentrations are recommended.
7 sources
1. Crampton RS, Oriscello RG "Petit and grand mal convulsions during lidocaine hydrochloride treatment of ventricular tachycardia." JAMA 204 (1968): 109-12
2. Sundaram MB "Seizures after intraurethral instillation of lidocaine." Can Med Assoc J 137 (1987): 219-20
3. Pelter MA, Vollmer TA, Blum RL "Seizure-like reaction associated with subcutaneous lidocaine injection ." Clin Pharm 8 (1989): 767-8
4. "Product Information. Xylocaine (lidocaine)." Astra-Zeneca Pharmaceuticals (2002):
5. Fortuna A, Fortuna AO "Convulsion during lignocaine infiltration." Anaesth Intensive Care 21 (1993): 483
6. Ryan CA, Robertson M, Coe JY "Seizures due to lidocaine toxicity in a child during cardiac catheterization." Pediatr Cardiol 14 (1993): 116-8
7. Wu FL, Razzaghi A, Souney PF "Seizure after lidocaine for bronchoscopy: case report and review of the use of lidocaine in airway anesthesia." Pharmacotherapy 13 (1993): 72-8
Sick Sinus Syndrome
Major
The use of lidocaine is contraindicated in patients with Stokes-Adam syndrome, Wolff-Parkinson White syndrome, or second- or third-degree AV block in the absence of a functional artificial pacemaker, or congenital QT prolongation.
4 sources
1. Tagliente TM, Jayagopal S "Transient left bundle branch block following lidocaine." Anesth Analg 69 (1989): 545-7
2. Hilleman DE, Mohiuddin SM, Destache CJ "Lidocaine-induced second-degree mobitz type II heart block." Drug Intell Clin Pharm 19 (1985): 669-73
3. Keidar S, Grenadier E, Palant A "Sinoatrial arrest due to lidocaine injection in sick sinus syndrome during amiodarone administration." Am Heart J 104 (1982): 1384-5
4. "Product Information. Xylocaine (lidocaine)." Astra-Zeneca Pharmaceuticals (2002):
Water-Electrolyte Imbalance
Moderate
Electrolyte imbalance can alter the therapeutic effectiveness of antiarrhythmic agents. Hypokalemia and hypomagnesemia can reduce the effectiveness of antiarrhythmic agents. In some cases, these disorders can exaggerate the degree of QTc prolongation and increase the potential for torsade de pointes. Hyperkalemia can potentiate the toxic effects of antiarrhythmic agents. Electrolyte imbalance should be corrected prior to initiating antiarrhythmic therapy. Clinical monitoring of cardiac function and electrolyte concentrations is recommended.
13 sources
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2. "Product Information. Ethmozine (moricizine)." DuPont Pharmaceuticals (2002):
3. "Product Information. Cordarone (amiodarone)." Wyeth-Ayerst Laboratories (2002):
4. "Product Information. Xylocaine (lidocaine)." Astra-Zeneca Pharmaceuticals (2002):
5. "Product Information. Procan SR (procainamide)." Parke-Davis (2001):
6. "Product Information. Pronestyl (procainamide)." Apothecon Inc (2001):
7. "Product Information. Quinidex Extentabs (quiNIDine)." Wyeth-Ayerst Laboratories
8. "Product Information. Tambocor (flecainide)." 3M Pharmaceuticals (2001):
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1. "Product Information. Mexitil (mexiletine)." Boehringer-Ingelheim (2001):
2. "Product Information. Rythmol (propafenone)." Knoll Pharmaceutical Company
3. "Product Information. Norpace (disopyramide)." Searle (2001):
4. "Product Information. Cordarone (amiodarone)." Apothecon Inc (2022):
5. "Product Information. Corvert (ibutilide)." Pharmacia and Upjohn (2001):

Therapeutic duplication

Drug classes that overlap with Chloramphenicol + Lidocaine Hydrochloride, so taking both doubles up the same effect. This source publishes no per-row citations for duplication.

local injectable anesthetics
The recommended maximum number of medicines in the 'local injectable anesthetics' category to be taken concurrently is usually one.Your list includes two medicines belonging to the 'local injectable anesthetics' category.
Example product in the source data (US market): Epinephrine/prilocaine
local injectable anesthetics
The recommended maximum number of medicines in the 'local injectable anesthetics' category to be taken concurrently is usually one.Your list includes two medicines belonging to the 'local injectable anesthetics' category.
Example product in the source data (US market): Vivacaine
local injectable anesthetics
The recommended maximum number of medicines in the 'local injectable anesthetics' category to be taken concurrently is usually one.Your list includes two medicines belonging to the 'local injectable anesthetics' category.
Example product in the source data (US market): Zynrelef

Medicines

Conditions

Arrhythmias, Cardiac

Bone Marrow Failure Disorders

Cardiomyopathies

Colitis

Kidney Diseases

Liver Diseases

Liver Diseases

Seizures

Sick Sinus Syndrome

Water-Electrolyte Imbalance

Therapeutic duplication

local injectable anesthetics

local injectable anesthetics

local injectable anesthetics