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Gastrointestinal (Other)
Alosetron (Lotronex®)
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Drug Category: Selective 5-HT3 Receptor Antagonist.
Indication: Treatment of women with severe
diarrhea-predominant irritable bowel syndrome (IBS) who have failed to
respond to conventional therapy Dosing (Adults) IBS: Female: Oral: Initial: 0.5 mg twice daily for 4 weeks, with or without food; if tolerated, but response is inadequate, may be increased after 4 weeks to 1 mg twice daily. If response is inadequate after 4 weeks of 1 mg twice-daily dosing, discontinue treatment. Note: Discontinue immediately if constipation or signs/symptoms of ischemic colitis occur. Do not reinitiate in patients who develop ischemic colitis. Renal Dosing: The need for dosage adjustment has not been defined (due to limited information on activity of metabolites). Supplied: Tablet: 0.5 mg, 1 mg |
infliximab (Remicade ®):
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CLINICAL PHARMACOLOGY General Infliximab neutralizes the biological activity of TNF  by binding with
high affinity to the soluble and transmembrane forms of TNF and
inhibits binding of TNF with its receptors. Infliximab does not
neutralize TNF (lymphotoxin ), a related cytokine that utilizes the
same receptors as TNF. Biological activities attributed to TNF
include: induction of pro-inflammatory cytokines such as interleukins
(IL) 1 and 6, enhancement of leukocyte migration by increasing
endothelial layer permeability and expression of adhesion molecules by
endothelial cells and leukocytes, activation of neutrophil and
eosinophil functional activity, induction of acute phase reactants and
other liver proteins, as well as tissue degrading enzymes produced by
synoviocytes and/or chondrocytes. Cells expressing transmembrane TNF
bound by infliximab can be lysed in vitro or in vivo. Infliximab
inhibits the functional activity of TNF in a wide variety of in vitro
bioassays utilizing human fibroblasts, endothelial cells, neutrophils, B
and T lymphocytes and epithelial cells. The relationship of these
biological response markers to the mechanism(s) by which REMICADE exerts
its clinical effects is unknown. Anti-TNF antibodies reduce disease
activity in the cotton-top tamarin colitis model, and decrease synovitis
and joint erosions in a murine model of collagen-induced arthritis.
Infliximab prevents disease in transgenic mice that develop
polyarthritis as a result of constitutive expression of human TNF, and
when administered after disease onset, allows eroded joints to heal.INDICATIONS AND USAGE Rheumatoid Arthritis REMICADE, in combination with methotrexate, is indicated for reducing signs and symptoms, inhibiting the progression of structural damage, and improving physical function in patients with moderately to severely active rheumatoid arthritis. Crohn's Disease REMICADE is indicated for reducing signs and symptoms and inducing and maintaining clinical remission in adult and pediatric patients with moderately to severely active Crohn's disease who have had an inadequate response to conventional therapy. REMICADE is indicated for reducing the number of draining enterocutaneous and rectovaginal fistulas and maintaining fistula closure in adult patients with fistulizing Crohn's disease. Ankylosing Spondylitis REMICADE is indicated for reducing signs and symptoms in patients with active ankylosing spondylitis. Psoriatic Arthritis REMICADE is indicated for reducing signs and symptoms of active arthritis, inhibiting the progression of structural damage, and improving physical function in patients with psoriatic arthritis. Plaque Psoriasis REMICADE is indicated for the treatment of adult patients with chronic severe (i.e., extensive and /or disabling) plaque psoriasis who are candidates for systemic therapy and when other systemic therapies are medically less appropriate. REMICADE should only be administered to patients who will be closely monitored and have regular follow-up visits with a physician (See package insert for Boxed WARNINGS, WARNINGS, and PRECAUTIONS). Ulcerative Colitis REMICADE is indicated for reducing signs and symptoms, inducing and maintaining clinical remission and mucosal healing, and eliminating corticosteroid use in patients with moderately to severely active ulcerative colitis who have had an inadequate response to conventional therapy Dosing (Adults): Ankylosing spondylitis: 5 mg/kg IV at 0, 2, and 6 weeks, followed by 5 mg/kg every 6 weeks thereafter. Crohn's disease: Induction regimen: 5 mg/kg IV over 2 hours. Repeat dose at 2 and 6 weeks, followed by 5 mg/kg every 8 weeks. Dose may be increased to 10 mg/kg in patients who respond but then lose their response. If no response by week 14, consider discontinuing therapy. Psoriatic arthritis (with or without methotrexate): 5 mg/kg IV at 0, 2, and 6 weeks, then every 8 weeks. Rheumatoid arthritis: (In combination with methotrexate therapy): 3 mg/kg IV at 0, 2, and 6 weeks then every 8 weeks thereafter. Doses have ranged from 3-10 mg/kg intravenous infusion repeated at 4 to 8 week intervals. Dosage adjustment with CHF: Weigh risk versus benefits for individual patient: NYHA Class III or IV: </=5 mg/kg |
Mesalamine (Asacol ® , Pentasa)
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CLINICAL PHARMACOLOGY Mesalamine is thought to be the major therapeutically active part of the sulfasalazine molecule in the treatment of ulcerative colitis. Sulfasalazine is converted to equimolar amounts of sulfapyridine and mesalamine by bacterial action in the colon. The usual oral dose of sulfasalazine for active ulcerative colitis is 3 to 4 grams daily in divided doses, which provides 1.2 to 1.6 grams of mesalamine to the colon. The mechanism of action of mesalamine (and sulfasalazine) is unknown, but appears to be topical rather than systemic. Mucosal production of arachidonic acid (AA) metabolites, both through the cyclooxygenase pathways, i.e., prostanoids, and through the lipoxygenase pathways, i.e., leukotrienes (LTs) and hydroxyeicosatetraenoic acids (HETEs), is increased in patients with chronic inflammatory bowel disease, and it is possible that mesalamine diminishes inflammation by blocking cyclooxygenase and inhibiting prostaglandin (PG) production in the colon. Adults (usual course of therapy is 3-8 weeks): Oral: Treatment of ulcerative colitis: Capsule: 1 g 4 times/day Tablet: Initial: 800 mg (2 tablets) 3 times/day for 6 weeks Maintenance of remission of ulcerative colitis: Capsule: 1 g 4 times/day Tablet: 1.6 g/day in divided doses Rectal: Retention enema: 60 mL (4 g) at bedtime, retained overnight, approximately 8 hours Rectal suppository (Canasa™): 500 mg: Insert 1 suppository in rectum twice daily; may increase to 3 times/day if inadequate response is seen after 2 weeks. 1000 mg: Insert 1 suppository in rectum daily at bedtime Elderly: See adult dosing; use with caution Administration Oral: Swallow capsules or tablets whole, do not chew or crush. Rectal enema: Shake bottle well. Retain enemas for 8 hours or as long as practical. Suppository: Remove foil wrapper; avoid excessive handling. Should be retained for at least 1-3 hours to achieve maximum benefit. Supplied Capsule, controlled release (Pentasa®): 250 mg Suppository, rectal (Canasa™): 500 mg, 1000 mg [contains saturated vegetable fatty acid esters] Suspension, rectal: 4 g/60 mL (7s) [contains potassium metabisulfite and sodium benzoate] Rowasa®: 4 g/60 mL (7s, 28s) [contains potassium metabisulfite and sodium benzoate] Tablet, delayed release [enteric coated] (Asacol®): 400 mg |
misoprostol (Cytotec ® )
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Pharmacodynamics Misoprostol has both antisecretory (inhibiting gastric acid secretion) and (in animals) mucosal protective properties. NSAIDs inhibit prostaglandin synthesis, and a deficiency of prostaglandins within the gastric mucosa may lead to diminishing bicarbonate and mucus secretion and may contribute to the mucosal damage caused by these agents. Misoprostol can increase bicarbonate and mucus production, but in man this has been shown at doses 200 mcg and above that are also antisecretory. It is therefore not possible to tell whether the ability of misoprostol to reduce the risk of gastric ulcer is the result of its antisecretory effect, its mucosal protective effect, or both. In vitro studies on canine parietal cells using tritiated misoprostol acid as the ligand have led to the identification and characterization of specific prostaglandin receptors. Receptor binding is saturable, reversible, and stereospecific. The sites have a high affinity for misoprostol, for its acid metabolite, and for other E type prostaglandins, but not for F or I prostaglandins and other unrelated compounds, such as histamine or cimetidine. Receptor-site affinity for misoprostol correlates well with an indirect index of antisecretory activity. It is likely that these specific receptors allow misoprostol taken with food to be effective topically, despite the lower serum concentrations attained. Misoprostol produces a moderate decrease in pepsin concentration during basal conditions, but not during histamine stimulation. It has no significant effect on fasting or postprandial gastrin nor on intrinsic factor output. ---------------------- Effects on gastric acid secretion Misoprostol, over the range of 50–200 mcg, inhibits basal and nocturnal gastric acid secretion, and acid secretion in response to a variety of stimuli, including meals, histamine, pentagastrin, and coffee. Activity is apparent 30 minutes after oral administration and persists for at least 3 hours. In general, the effects of 50 mcg were modest and shorter lived, and only the 200-mcg dose had substantial effects on nocturnal secretion or on histamine and meal-stimulated secretion. Uterine effects Misoprostol has been shown to produce uterine contractions that may endanger pregnancy. Other pharmacologic effects Misoprostol does not produce clinically significant effects on serum levels of prolactin, gonadotropins, thyroid-stimulating hormone, growth hormone, thyroxine, cortisol, gastrointestinal hormones (somatostatin, gastrin, vasoactive intestinal polypeptide, and motilin), creatinine, or uric acid. Gastric emptying, immunologic competence, platelet aggregation, pulmonary function, or the cardiovascular system are not modified by recommended doses of misoprostol Dosage - Oral: Adults: Prevention of NSAID-induced gastric ulcers: 200 mcg 4 times/day with food; if not tolerated, may decrease dose to 100 mcg 4 times/day with food or 200 mcg twice daily with food; last dose of the day should be taken at bedtime Medical termination of pregnancy: Refer to Mifepristone monograph. Intravaginal: Adults: Labor induction or cervical ripening (unlabeled use): 25 mcg ( 1 /4 of 100 mcg tablet); may repeat at intervals no more frequent than every 3-6 hours. Do not use in patients with previous cesarean delivery or prior major uterine surgery. Administration Incidence of diarrhea may be lessened by having patient take dose right after meals. Therapy is usually begun on the second or third day of the next normal menstrual period. Supplied Tablet: 100 mcg, 200 mcg |
Neomycin:
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INDICATIONS Orally to prepare GI tract for surgery; topically to treat minor skin infections; treatment of diarrhea caused by E. coli ; adjunct in the treatment of hepatic encephalopathy; bladder irrigation Dosage Children: Oral: Preoperative intestinal antisepsis: 90 mg/kg/day divided every 4 hours for 2 days; or 25 mg/kg at 1 PM, 2 PM, and 11 PM on the day preceding surgery as an adjunct to mechanical cleansing of the intestine and in combination with erythromycin base Hepatic encephalopathy: 50-100 mg/kg/day in divided doses every 6-8 hours or 2.5-7 g/m 2 /day divided every 4-6 hours for 5-6 days not to exceed 12 g/day Children and Adults: Topical: Topical solutions containing 0.1% to 1% neomycin have been used for irrigation =================== Adults: Oral: Preoperative intestinal antisepsis: 1 g each hour for 4 doses then 1 g every 4 hours for 5 doses; or 1 g at 1 PM, 2 PM, and 11 PM on day preceding surgery as an adjunct to mechanical cleansing of the bowel and oral erythromycin; or 6 g/day divided every 4 hours for 2-3 days Hepatic encephalopathy: 500-2000 mg every 6-8 hours or 4-12 g/day divided every 4-6 hours for 5-6 days Chronic hepatic insufficiency: 4 g/day for an indefinite period =================== Supplied Powder, micronized, as sulfate [for prescription compounding] (Neo-Rx): (10 g, 100 g) Solution, oral, as sulfate (Neo-Fradin™): 125 mg/5 mL (60 mL, 480 mL) [contains benzoic acid; cherry flavor] Tablet, as sulfate: 500 mg |
octreotide (Sandostatin ®)
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CLINICAL PHARMACOLOGY Octreotide acetate exerts pharmacologic actions similar to the natural hormone, somatostatin. It is an even more potent inhibitor of growth hormone, glucagon, and insulin than somatostatin. Like somatostatin, it also suppresses LH response to GnRH, decreases splanchnic blood flow, and inhibits release of serotonin, gastrin, vasoactive intestinal peptide, secretin, motilin, and pancreatic polypeptide. By virtue of these pharmacological actions, octreotide acetate has been used to treat the symptoms associated with metastatic carcinoid tumors (flushing and diarrhea), and Vasoactive Intestinal Peptide (VIP) secreting adenomas (watery diarrhea). Octreotide acetate substantially reduces growth hormone and/or IGF-I (somatomedin C) levels in patients with acromegaly. Single doses of octreotide acetate have been shown to inhibit gallbladder contractility and to decrease bile secretion in normal volunteers. In controlled clinical trials the incidence of gallstone or biliary sludge formation was markedly increased. Octreotide acetate suppresses secretion of thyroid stimulating hormone (TSH). Adults: SubQ: Initial: 50 mcg 1-2 times/day and titrate dose based on patient tolerance and response Carcinoid: 100-600 mcg/day in 2-4 divided doses VIPomas: 200-300 mcg/day in 2-4 divided doses Diarrhea: Initial: I.V.: 50-100 mcg every 8 hours; increase by 100 mcg/dose at 48-hour intervals; maximum dose: 500 mcg every 8 hours Esophageal varices bleeding: I.V. bolus: 25-50 mcg followed by continuous I.V. infusion of 25-50 mcg/hour Acromegaly: Initial: SubQ: 50 mcg 3 times/day; titrate to achieve growth hormone levels <5 ng/mL or IGF-I (somatomedin C) levels <1.9 U/mL in males and <2.2 U/mL in females; usual effective dose 100 mcg 3 times/day; range 300-1500 mcg/day Note: Should be withdrawn yearly for a 4-week interval in patients who have received irradiation. Resume if levels increase and signs/symptoms recur. =================== Acromegaly, carcinoid tumors, and VIPomas (depot injection): Patients must be stabilized on subcutaneous octreotide for at least 2 weeks before switching to the long-acting depot: Upon switch: 20 mg I.M. intragluteally every 4 weeks for 2-3 months, then the dose may be modified based upon response =================== Dosage adjustment for acromegaly: After 3 months of depot injections the dosage may be continued or modified as follows: GH </= 2.5 ng/mL, IGF-1 is normal, symptoms controlled: Maintain octreotide LAR® at 20 mg I.M. every 4 weeks GH >2.5 ng/mL, IGF-1 is elevated, and/or symptoms uncontrolled: Increase octreotide LAR® to 30 mg I.M. every 4 weeks GH </= 1 ng/mL, IGF-1 is normal, symptoms controlled: Reduce octreotide LAR® to 10 mg I.M. every 4 weeks Dosages >40 mg are not recommended =================== Dosage adjustment for carcinoid tumors and VIPomas: After 2 months of depot injections the dosage may be continued or modified as follows: Increase to 30 mg I.M. every 4 weeks if symptoms are inadequately controlled. Decrease to 10 mg I.M. every 4 weeks, for a trial period, if initially responsive to 20 mg dose. Dosage >30 mg is not recommended. =================== Supplied Injection, microspheres for suspension, as acetate [depot formulation] (Sandostatin LAR®): 10 mg, 20 mg, 30 mg [with diluent and syringe] Injection, solution, as acetate (Sandostatin®): 0.05 mg/mL (1 mL); 0.1 mg/mL (1 mL); 0.2 mg/mL (5 mL); 0.5 mg/mL (1 mL); 1 mg/mL (5 mL) |
olsalazine (Dipentum ® )
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CLINICAL PHARMACOLOGY After oral administration, olsalazine has limited systemic bioavailability. Based on oral and intravenous dosing studies, approximately 2.4% of a single 1.0 g oral dose is absorbed. Less than 1% of olsalazine is recovered in the urine. The remaining 98 to 99% of an oral dose will reach the colon, where each molecule is rapidly converted into two molecules of 5-aminosalicylic acid (5-ASA) by colonic bacteria and the low prevailing redox potential found in this environment. The liberated 5-ASA is absorbed slowly resulting in very high local concentrations in the colon. The conversion of olsalazine to mesalamine (5-ASA) in the colon is similar to that of sulfasalazine, which is converted into sulfapyridine and mesalamine. It is thought that the mesalamine component is therapeutically active in ulcerative colitis (A.K. Azad-Kahn et al, LANCET, 2: 892-895, 1977). The usual dose of sulfasalazine for maintenance of remission in patients with ulcerative colitis is 2 grams daily, which would provide approximately 0.8 grams of mesalamine to the colon. More than 0.9 grams of mesalamine would usually be made available in the colon from 1 gram of olsalazine. The mechanism of action of mesalamine (and sulfasalazine) is unknown, but appears to be topical rather than systemic. Mucosal production of arachidonic acid (AA) metabolites, both through the cyclooxygenase pathways (i.e., prostanoids) and through the lipoxygenase pathways (i.e., leukotrienes [LTs] and hydroxyeicosatetraenoic acids [HETEs]) is increased in patients with chronic inflammatory bowel disease, and it is possible that mesalamine diminishes inflammation by blocking cyclooxygenase and inhibiting prostaglandin (PG) production in the colon. INDICATIONS AND USAGE Olsalazine is indicated for the maintenance of remission of ulcerative colitis in patients who are intolerant of sulfasalazine. CONTRAINDICATIONS Hypersensitivity to olsalazine, other salicylates, or any of the excipients. Dosing (Adults): Ulcerative colitis: 500mg orally bid. Administration Take with food in evenly divided doses. Supplied Capsule, as sodium: 250 mg |
Orlistat (Xenical ®)
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Mechanism of Action Orlistat is a reversible inhibitor of lipases. It exerts its therapeutic activity in the lumen of the stomach and small intestine by forming a covalent bond with the active serine residue site of gastric and pancreatic lipases. The inactivated enzymes are thus unavailable to hydrolyze dietary fat in the form of triglycerides into absorbable free fatty acids and monoglycerides. As undigested triglycerides are not absorbed, the resulting caloric deficit may have a positive effect on weight control. Systemic absorption of the drug is therefore not needed for activity. At the recommended therapeutic dose of 120 mg three times a day, orlistat inhibits dietary fat absorption by approximately 30%. Dosing (Adults): Weight loss: Oral: Children >/= 12 years and Adults: 120 mg 3 times/day with each main meal containing fat (during or up to 1 hour after the meal); omit dose if meal is occasionally missed or contains no fat. Supplied Capsule: 120 mg |
sucralfate (Carafate ® )
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CLINICAL PHARMACOLOGY Sucralfate is only minimally absorbed from the gastrointestinal tract. The small amounts of the sulfated disaccharide that are absorbed are excreted primarily in the urine. Although the mechanism of sucralfate’s ability to accelerate healing of duodenal ulcers remains to be fully defined, it is known that it exerts its effect through a local, rather than systemic, action. The following observations also appear pertinent: 1]Studies in human subjects and with animal models of ulcer disease have shown that sucralfate forms an ulcer-adherent complex with proteinaceous exudate at the ulcer site. 2]In vitro, a sucralfate-albumin film provides a barrier to diffusion of hydrogen ions. 3]In human subjects, sucralfate given in doses recommended for ulcer therapy inhibits pepsin activity in gastric juice by 32%. 4]In vitro, sucralfate absorbs bile salts. These observations suggest that sucralfate’s antiulcer activity is the result of formation of an ulcer-adherent complex that covers the ulcer site and protects it against further attack by acid, pepsin, and bile salts. There are approximately 14-16 mEq of acid-neutralizing capacity per 1 g dose of sucralfate Dosing Oral: Adults: Stress ulcer prophylaxis: 1 g 4 times/day Stress ulcer treatment: 1 g every 4 hours Duodenal ulcer: Treatment: 1 g 4 times/day on an empty stomach and at bedtime for 4-8 weeks, or alternatively 2 g twice daily; treatment is recommended for 4-8 weeks in adults, the elderly may require 12 weeks Maintenance: Prophylaxis: 1 g twice daily Stomatitis (unlabeled use): 1 g/10 mL suspension, swish and spit or swish and swallow 4 times/day Dosage comment in renal impairment: Aluminum salt is minimally absorbed (<5%), however, may accumulate in renal failure Administration Tablet may be broken or dissolved in water before ingestion. Administer with water on an empty stomach. Supplied Suspension, oral: 1 g/10 mL (10 mL) Carafate®: 1 g/10 mL (420 mL) Tablet (Carafate®): 1 g |
Sulfasalazine (Azulfadine ®)
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CLINICAL PHARMACOLOGY Pharmacodynamics The mode of action of sulfasalazine (SSZ) or its metabolites, 5-aminosalicylic acid (5-ASA) and sulfapyridine (SP), is still under investigation, but may be related to the anti-inflammatory and/or immunomodulatory properties that have been observed in animal and in vitro models, to its affinity for connective tissue, and/or to the relatively high concentration it reaches in serous fluids, the liver and intestinal walls, as demonstrated in autoradiographic studies in animals. In ulcerative colitis, clinical studies utilizing rectal administration of SSZ, SP, and 5-ASA have indicated that the major therapeutic action may reside in the 5-ASA moiety. INDICATIONS AND USAGE Sulfasalazine tablets are indicated: a. in the treatment of mild to moderate ulcerative colitis, and as adjunctive therapy in severe ulcerative colitis; and b. for the prolongation of the remission period between acute attacks of ulcerative colitis. CONTRAINDICATIONS Sulfasalazine tablets are contraindicated in: Patients with intestinal or urinary obstruction, Patients with porphyria, Patients hypersensitive to sulfasalazine, its metabolites, sulfonamides or salicylates Adults: Ulcerative colitis: Initial: 1 g 3-4 times/day, 2 g/day maintenance in divided doses; may initiate therapy with 0.5-1 g/day Rheumatoid arthritis: Enteric coated tablet: Initial: 0.5-1 g/day; increase weekly to maintenance dose of 2 g/day in 2 divided doses; maximum: 3 g/day (if response to 2 g/day is inadequate after 12 weeks of treatment) Dosing interval in renal impairment: Clcr 10-30 mL/minute: Administer twice daily Clcr<10 mL/minute: Administer once daily Dosing adjustment in hepatic impairment: Avoid use Supplied Tablet (Azulfidine®): 500 mg Tablet, delayed release, enteric coated (Azulfidine® EN-tabs®): 500 mg |
Ursodiol (Actigall ®)
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Gallstone dissolution: Oral: 8-10 mg/kg/day in
2-3 divided doses; use beyond 24 months is not established; obtain
ultrasound images at 6-month intervals for the first year of therapy;
30% of patients have stone recurrence after dissolution. Gallstone prevention: Oral: 300 mg twice daily. Primary biliary cirrhosis: Oral: 13-15 mg/kg/day in 2-4 divided doses (with food). Supplied: [Supplied: 300 capsule] |
vasopressin (Pitressin ®)
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CLINICAL PHARMACOLOGY The antidiuretic action of vasopressin is ascribed to increasing reabsorption of water by the renal tubules. Vasopressin can cause contraction of smooth muscle of the gastrointestinal tract and of all parts of the vascular bed, especially the capillaries, small arterioles and venules with less effect on the smooth musculature of the large veins. The direct effect on the contractile elements is neither antagonized by adrenergic blocking agents nor prevented by vascular denervation. Following subcutaneous or intramuscular administration of vasopressin injection, the duration of antidiuretic activity is variable but effects are usually maintained for 2-8 hours. The majority of a dose of vasopressin is metabolized and rapidly destroyed in the liver and kidneys. Vasopressin has a plasma half-life of about 10 to 20 minutes. Approximately 5% of a subcutaneous dose of vasopressin is excreted in urine unchanged after four hours. INDICATIONS Vasopressin is indicated for prevention and treatment of postoperative abdominal distention, in abdominal roentgenography to dispel interfering gas shadows, and in diabetes insipidus. DOSING Diabetes insipidus (highly variable dosage; titrated based on serum and urine sodium and osmolality in addition to fluid balance and urine output): I.M., SubQ: Children: 2.5-10 units 2-4 times/day as needed Adults: 5-10 units 2-4 times/day as needed (dosage range 5-60 units/day) Continuous I.V. infusion: Children and Adults: 0.5 milliunit/kg/hour (0.0005 unit/kg/hour); double dosage as needed every 30 minutes to a maximum of 0.01 unit/kg/hour. Intranasal: Administer on cotton pledget, as nasal spray, or by dropper. ====================== Abdominal distention: Adults: I.M.: 5 units stat, 10 units every 3-4 hours ====================== GI hemorrhage (unlabeled use): I.V. infusion: Dilute in NS or D5W to 0.1-1 unit/mL Children: Initial: 0.002-0.005 units/kg/minute; titrate dose as needed; maximum: 0.01 unit/kg/minute; continue at same dosage (if bleeding stops) for 12 hours, then taper off over 24-48 hours AdAdults: Initial: 0.2-0.4 unit/minute, then titrate dose as needed, if bleeding stops; continue at same dose for 12 hours, taper off over 24-48 hours ====================== Out-of-hospital asystole (unlabeled use): Adults: I.V.: 40 units; if spontaneous circulation is not restored in 3 minutes, then repeat dose Pulseless VT/VF (ACLS protocol): I.V.: 40 units (as a single dose only); if no I.V. access, administer 40 units diluted with NS (to a total volume of 10 mL) endotracheally Vasodilatory shock/septic shock (unlabeled use): Adults: I.V.: Vasopressin has been used in doses of 0.01-0.1 units/minute for the treatment of septic shock. Doses >0.05 units/minute may have more cardiovascular side effects. Most case reports have used 0.04 units/minute continuous infusion as a fixed dose. ====================== Administration I.V.: Use extreme caution to avoid travasation because of risk of necrosis and gangrene. In treatment of varices, infusions are often supplemented with nitroglycerin infusions to minimize cardiac effects. GIGI hemorrhage: Administration requires the use of an infusion pump and should be administered in a peripheral line. Vasodilatory shock: Administration through a central catheter is recommended. ====================== Supplied Injection, solution: 20 units/mL (0.5 mL, 1 mL, 10 mL) Pitressin®: 20 units/mL (1 mL) |
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