PAIN DRUGS HANDBOOK TABLE
OF CONTENTS
About the
Author
About
the Handbook
Acknowledgments
Forward
to 2rd Edition
Forward
to 1st Edition
DRUGS (Alphabetical Order)
TOPICAL AGENTS
Amitriptyline
Baclofen
Clonidine
Cyclobenzaprine
2-deoxy-d-glucose
Dexamethasone
Dextromethorphan
Diclofenac
Doxepin
DMSO
Gabapentin
Ketamine
Ketoprofen
NEUROLYTIC AGENT
Phenol
APPENDICES
Appendix 1: World Health Organization
Three-step Ladder
Appendix 2: Drug Tables
Appendix 3: Infusion Tables
Appendix 4: Relative Potencies of
Opioids Effects
Appendix 5: Relative Potencies of Steroids
Appendix 6: Intravenous PCA
Standard Orders
Appendix 7: Patient Controlled Analgesia Flow Sheet
Appendix 8: Relative Potencies of Opioids
Appendix 9: Epidural Analgesia Monitoring Orders
Appendix 10: Pain Rating Scales
Appendix 11: Multiplication Factors for Converting the
Daily Dose of a Prior Opioid to the Daily Dose of Oxycontin
Appendix 12: CPR Algorithms
Appendix 13: Pediatric CPR Algorithms
Appendix 14: Trade Name Table
BIBLIOGRAPHY
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Sota
Omoigui's
Pain Drug Handbook
2nd Edition:
Ranitidine
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SECTION
ONE:
Class,
Uses, Dosing,
Elimination
SECTION TWO:
Preparation, Pharmacology, Pharmacokinetics
SECTION THREE:
Interactions, Toxicity
Guidelines/Precautions
Principal Adverse Reactions
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Class
(HISTAMINE H2 ANTAGONIST)
Uses
treatment of duodenal ulcer, gastroesophageal reflux, pathological hypersecretory conditions; prophylaxis against acid pulmonary aspiration, stress ulcers, upper GI bleeding in critically ill patients
Dosing
Treatment: PO: 150 mg twice daily
alternately 150-300 mg at bedtime.
IV/IM: 50 mg q 6-8 hours (dilute IV dose in 20 mls NS and give over 5-15 minutes).
Infusion: 6.25 mg/hr (10.7 mls /hr of 0.6 mg/ml solution)
Elimination
hepatic
HOW SUPPLIED:
Ranitidine (Zantac)
Tablet: 150 mg, 300 mg
Oral Solution: 15 mg/ml
Injection: 25 mg/ml
DILUTION FOR INFUSION: 150 mg (6 mls) in 250 mls D5W or NS (0.6 mg/ml )
Pharmacology
This histamine H2 receptor antagonist blocks histamine, pentagastrin and acetylcholine induced secretion of hydrogen ions by gastric parietal cells. Nocturnal and food-induced gastric secretion are also inhibited. Ranitidine has no significant effect on gastric emptying time, volume, or pancreatic secretions. Single oral dose of 150 mg will provide acid inhibition for a period of 8 to 12 hours. Ranitidine also suppresses histamine induced peripheral vasodilation and inotropic effects. There is minimal entrance into the central nervous system and thus in contrast with cimetidine, ranitidine produces fewer side effects such as CNS dysfunction in elderly patients. Ranitidine produces less inhibition of microsomal drug metabolizing enzymes and less antiandrogenic effects than cimetidine.
Pharmacokinetics
ONSET OF ACTION: IV/IM <15 mins PO<30 mins.
PEAK EFFECT: IV/IM 1-2 hours PO 2-3 hours
DURATION OF ACTION: IV/IM 6-8 hours/PO 8-12 hours
INTERACTIONS: absorption decreased by concurrent antacids; may decrease absorption of diazepam; may increase hypoglycemic effect of glipizide; may interfere with warfarin clearance; may antagonize neuromuscular blockade of nondepolarizing muscle relaxants (by an intrinsic anticholinesterase effect); may potentiate succinylcholine depolarizing blockade
TOXICITY:
Toxic range
Not routinely monitored
Manifestations:
Tachycardia
Respiratory Failure
Headache
Delirium
Psychosis
Antidote:
No specific antidote
Management:
Discontinue or reduce medication
Support ventilation and circulation (Patent Airway, Oxygen, IV Fluids, Vasoactive drugs
Treat tachycardia with a beta blocker e.g. esmolol IV 10-40 mg or propranolol IV 0.5-3 mg
Remove ingested drug by induced emesis
Symptomatic treatment
Guidelines/Precautions
(1) Use with caution in elderly patients.
(2) Full daily dose may be given once a day.
Principal Adverse Reactions
CVS: tachycardia, bradycardia, premature ventricular beats with rapid IV injection
PULM: bronchospasm
CNS: headache, depression, dizziness, confusion
GI/HEPATIC: nausea, vomiting, hepatitis, diarrhea
HEMATOLOGIC: leukopenia, granulocytopenia, thrombocytopenia
DERM: erythema multiforme, alopecia
ROFECOXIB
CLASS: (NONSTEROIDAL ANTI-INFLAMMATORY DRUG)
USE(S): symptomatic treatment of osteoarthritis, mild and moderate pain
DOSING: Osteoarthritis
Initial: PO 12.5 mg once daily
Maintenance: PO 12.5 - 25 mg once daily
Pain
PO 25 - 50 mg once daily. The maximum recommended daily dose for chronic therapy is 25 mg.
Rofecoxib may be administered without regard to meals. Dose adjustment in the elderly is generally not necessary.
Administer medication regularly (not prn). Addition of opioid analgesics, antidepressant agents and use of non-drug therapies e.g. TENS may enhance analgesia (see front matter for drug combinations).
ELIMINATION: hepatic
Preparation
Rofecoxib (Vioxx)
Tablets: 12.5 mg, 25 mg
Oral Suspension: 12.5 mg/5 ml, 25 mg/5 ml
Pharmacology
This histamine H2 receptor antagonist blocks histamine, pentagastrin and acetylcholine induced secretion of hydrogen ions by gastric parietal cells. Nocturnal and food-induced gastric secretion are also inhibited. Ranitidine has no significant effect on gastric emptying time, volume, or pancreatic secretions. Single oral dose of 150 mg will provide acid inhibition for a period of 8 to 12 hours. Ranitidine also suppresses histamine induced peripheral vasodilation and inotropic effects. There is minimal entrance into the central nervous system and thus in contrast with cimetidine, ranitidine produces fewer side effects such as CNS dysfunction in elderly patients. Ranitidine produces less inhibition of microsomal drug metabolizing enzymes and less antiandrogenic effects than cimetidine.
Pharmacokinetics
ONSET OF ACTION: IV/IM <15 mins PO<30 mins.
PEAK EFFECT: IV/IM 1-2 hours PO 2-3 hours
DURATION OF ACTION: IV/IM 6-8 hours/PO 8-12 hours
Interactions
absorption decreased by concurrent antacids; may decrease absorption of diazepam; may increase hypoglycemic effect of glipizide; may interfere with warfarin clearance; may antagonize neuromuscular blockade of nondepolarizing muscle relaxants (by an intrinsic anticholinesterase effect); may potentiate succinylcholine depolarizing blockade
Toxicity
Toxic range
Not routinely monitored
Manifestations:
Tachycardia
Respiratory Failure
Headache
Delirium
Psychosis
Antidote:
No specific antidote
Management:
Discontinue or reduce medication
Support ventilation and circulation (Patent Airway, Oxygen, IV Fluids, Vasoactive drugs
Treat tachycardia with a beta blocker e.g. esmolol IV 10-40 mg or propranolol IV 0.5-3 mg
Remove ingested drug by induced emesis
Symptomatic treatment
Guidelines
(1) Use with caution in elderly patients.
(2) Full daily dose may be given once a day.
Adverse
CVS: tachycardia, bradycardia, premature ventricular beats with rapid IV injection
PULM: bronchospasm
CNS: headache, depression, dizziness, confusion
GI/HEPATIC: nausea, vomiting, hepatitis, diarrhea
HEMATOLOGIC: leukopenia, granulocytopenia, thrombocytopenia
DERM: erythema multiforme, alopecia
ROFECOXIB
CLASS: (NONSTEROIDAL ANTI-INFLAMMATORY DRUG)
USE(S): symptomatic treatment of osteoarthritis, mild and moderate pain
DOSING: Osteoarthritis
Initial: PO 12.5 mg once daily
Maintenance: PO 12.5 - 25 mg once daily
Pain
PO 25 - 50 mg once daily. The maximum recommended daily dose for chronic therapy is 25 mg.
Rofecoxib may be administered without regard to meals. Dose adjustment in the elderly is generally not necessary.
Administer medication regularly (not prn). Addition of opioid analgesics, antidepressant agents and use of non-drug therapies e.g. TENS may enhance analgesia (see front matter for drug combinations).
ELIMINATION: hepatic
PREPARATIONS:
Rofecoxib (Vioxx)
Tablets: 12.5 mg, 25 mg
Oral Suspension: 12.5 mg/5 ml, 25 mg/5 ml
Pharmacology
This nonsteroidal anti-inflammatory drug (NSAID) is a selective inhibitor of cyclooxygenase-2 isoenzyme (COX-2). Compared to celecoxib, rofecoxib lacks a sulfonamide chain and is not primarily dependent on hepatic cytochrome P450 enzymes for metabolism. Rofecoxib is as effective as nonselective NSAIDs such as ibuprofen or diclofenac in treating arthritis pain and inflammation. The analgesic and anti-inflammatory activity of Rofecoxib is partly due to the inhibition of prostaglandin synthesis and/or release secondary to the inhibition of cyclooxygenase-2 isoenzyme (COX-2). Cyclooxygenase enzyme (prostaglandin G/H synthetase) catalyzes the formation of prostaglandin precursors - endoperoxide intermediate prostaglandin G2 (PGG2) - from arachidonic acid. PGG2 is reduced by peroxidase activity to another endoperoxide intermediate prostaglandin H2 (PGH2). These endoperoxide intermediates are the common precursors for the synthesis of prostaglandins, prostacyclins and thromboxanes. The inhibition of cyclooxygenase and thus prostanoid synthesis by classical NSAIDs is associated with side effects such as irritation and ulcer formation in the upper gastrointestinal tract and impairment of kidney function. Mammalian cells express two forms of cyclooxygenase (COX) activity. COX-1 isoenzyme is expressed in many normal tissues and is the major form present in platelets, kidney and gastrointestinal tract. COX-2 isoenzyme is induced in response to pro-inflammatory cytokines, lipopolysaccharide (LPS) and growth factors and subjected to repression by glucocorticosteroids. This second form is generally not detected in healthy tissues but is found in elevated levels in inflammatory exudates. This has led to the hypotheses that COX-1 is mainly associated with homeostasis (including cytoprotection in the stomach and regulation of kidney function) and COX-2 with the edematous, nociceptive and pyretic effects of inflammation. Most classical NSAIDs including diclofenac, naproxen and ibuprofen show little specificity of inhibition towards COX isoforms. Like Celecoxib, Rofecoxib at therapeutic concentration does not inhibit the cyclooxygenase -1 isoenzyme (COX-1). Ulcerogenic-sparing COX-2 inhibition does not inhibit cytoprotective stomach PGE2 production in contrast to non-specific NSAIDs. Rofecoxib is better tolerated than the classical NSAIDs and equipotent doses are associated with less gastric mucosal abnormalities. The antipyretic activity of Rofecoxib may occur secondary to inhibition of pyrogen induced release of prostaglandins in the central nervous system (including the hypothalamus) and possibly to centrally mediated peripheral vasodilation. Rofecoxib (like other NSAIDs) exhibits a ceiling effect for analgesia. Exceeding recommended doses results in increased toxicity without improvement in analgesia. Inhibition of prostaglandin synthesis may result in decreased uterine tone, contractility and prolonged gestation in the parturient and premature closure of the ductus arteriosus in the fetus. Rofecoxib has no effect on platelet aggregation or bleeding time and unlike aspirin cannot be used for cardiovascular prophylaxis.
Pharmacokinetics
ONSET OF ACTION: 15-30 minutes
PEAK EFFECT: variable
DURATION OF ACTION: variable
INTERACTIONS: risks of bleeding increased with concomitant NSAIDs, anticoagulant or heparin therapy, alcohol ingestion; decreases antihypertensive effects of beta adrenergic blocking agents, ACE-inhibitors; decreases the natriuretic effect of furosemide and thiazides in some patients; rate of GI side effects increased with concomitant aspirin; serum levels of Rofecoxib decreased by concomitant rifampin; serum level and toxic effects of lithium increased by concomitant Rofecoxib; GI absorption of Rofecoxib delayed by food, milk and aluminum/magnesium containing antacids.
TOXICITY:
Toxic Range:
Not routinely monitored
Manifestations:
Acute - drowsiness, nausea, vomiting, lethargy, paresthesia, disorientation, epigastric pain, GI bleeding
Antidote:
None
Management:
Discontinue or reduce medication
Correction of fluid, electrolyte and acid-base disturbances
Support ventilation and circulation (Patent Airway, Oxygen, IV Fluids and Vasopressors)
Airway protected - ipecac syrup induced emesis (30 mls or 0.5 mls/kg ipecac syrup followed by 200 mls or 4 mls/kg of water or clear fluid) or gastric lavage (with drug ingestion) followed by administration of activated charcoal (PO 50-100 grams or 1-2 gram/kg)
Symptomatic treatment
Forced diuresis, alkalinization of urine, hemodialysis or hemoperfusion may not be useful due to high protein binding of Rofecoxib.
Guidelines/Precautions
(1) Serious clinically significant upper GI bleeding has been observed in patients receiving Rofecoxib, albeit infrequently
(2) Use with caution in patients with active GI lesions (e.g. erosive gastritis, peptic ulcer), a history of recurrent GI lesions, hepatic/renal dysfunction, preexisting hypoprothrombinemia and vitamin K deficiency. Co-therapies and co-morbid conditions that may increase the risk for GI bleeding include treatment with oral corticosteroids, treatment with anticoagulants, longer duration of NSAID therapy, smoking, alcoholism, older age, and poor general health status.
(3) Rofecoxib may decrease glomerular filtration rate and cause peripheral edema. The drug should be used cautiously in patients with heart failure, hypertension and conditions associated with fluid retention.
(4) Renal prostaglandins may have a supportive role in maintaining renal perfusion in patients with pre-renal conditions. Rofecoxib should be avoided in such patients as it may cause a dose-dependent decrease in prostaglandin formation and thus precipitate renal decompensation
(5) Observe carefully patients with coagulation disorders and those receiving drug therapy that interferes with hemostasis.
(6) Avoid the use of Rofecoxib during pregnancy (especially during the last trimester) or during labor and delivery. Rofecoxib and other NSAIDs inhibit prostaglandin synthesis, which may cause dystocia, interfere with labor, and delay parturition. In the third trimester. Prostaglandin synthesis inhibitors may also have adverse effects on the fetal cardiovascular system (e.g. premature closure of ductus arteriosus), or may produce neonatal primary pulmonary hypertension, and fetal death.
(7) Patient response to NSAIDs is variable. Patients who do not respond to or cannot tolerate Rofecoxib may be successfully treated with another NSAID.
(8) Rofecoxib may be used with low dose aspirin. However concomitant administration of both drugs may result in an increased rate of GI ulcerations or other complications.
(9) Rofecoxib is contraindicated in patients with previously demonstrated hypersensitivity to Rofecoxib or with the complete or partial syndrome of nasal polyps, angioedema or bronchospastic reactivity to aspirin or other nonsteroidal anti-inflammatory drugs (NSAID).
(10) Rofecoxib should not be given to patients who have demonstrated allergic-type reactions to sulfonamides
(11) The antipyretic and anti-inflammatory effects of Rofecoxib may mask signs and symptoms of infection or other diseases.
Principal Adverse Reactions
CVS: congestive heart failure, peripheral edema, fluid retention, hypertension, tachycardia, arrhythmias
PULM: dyspnea, bronchospasm
CNS: drowsiness, dizziness, headache, anxiety, confusion
GI: abdominal pain, diarrhea, dyspepsia, flatulence, nausea, gastritis, hepatic dysfunction, elevated liver enzymes
GU: renal dysfunction, acute renal failure, azotemia, cystitis, hematuria,
DERM: pruritus, urticaria
HEMATOLOGIC: anemia, ecchymosis, epistaxis, thrombocytopenia
OTHER: tinnitus, blurred vision, taste perversion
Reactions
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