MOBILE VIEW  | 

DIPHENOXYLATE

Classification   |    Detailed evidence-based information

Therapeutic Toxic Class

    A) Diphenoxylate hydrochloride is an antidiarrheal agent. It is a weak, long-acting opioid structurally related to meperidine. Marketed products contain atropine in combination with diphenoxylate. Lomotil(R) is an opioid-anticholinergic combination.
    B) The active metabolite of diphenoxylate, difenoxin, is marketed in combination with atropine as Motofen(R).
    C) Refer to "ANTICHOLINERGIC POISONING" management for further information on atropine.

Specific Substances

    1) Isonipecotic acid, 1-(3-cyano-3,3-diphenylpropyl)-4-phenyl-, ethyl ester
    2) 1-(3-Cyano-3,3-diphenylpropyl)-4-phenyl-isonipecotic acid ethyl ester
    3) 4-Piperidinecarboxylic acid, 1-(3-cyano-3,3-diphenylpropyl)-4-phenyl, ethyl ester (9CI)
    4) R-1132
    5) Difenoxin hydrochloride (primary active metabolite)
    6) Difenoxylic acid hydrochloride
    7) Diphenoxylic acid hydrochloride
    8) Diphenoxylate hydrochloride
    9) Diphenatrol
    10) Lofene
    11) Logen
    12) Lomanate
    13) Lonox
    14) Lo-trol
    15) Low-Ouel
    16) Nor-Mil
    17) Molecular Formula: C30-H32-N2-O2 (diphenoxylate)
    18) CAS 915-30-0 (diphenoxylate)
    19) CAS 3810-80-8 (diphenoxylate hydrochloride)
    20) CAS 35607-36-4 (difenoxin hydrochloride)

Available Forms Sources

    A) FORMS
    1) Diphenoxylate/atropine combination contains 2.5 mg of diphenoxylate and 0.025 mg of atropine per tablet. It is also available in a liquid containing 2.5 mg diphenoxylate and 0.025 mg atropine per 5 mL (Prod Info diphenoxylate HCl atropine sulfate oral tablets, 2012; Prod Info diphenoxylate HCl atropine sulfate oral solution, 2012).
    2) Lomotil(R) is classified as a Schedule V controlled substance (Prod Info diphenoxylate HCl atropine sulfate oral tablets, 2012).
    3) The active metabolite of diphenoxylate, difenoxin, is available as a 1 mg tablet combined with atropine 0.025 mg (Prod Info MOTOFEN(R) oral tablets, 2004). It is classified as a Schedule IV controlled substance.
    B) USES
    1) Diphenoxylate, an opioid structurally similar to meperidine, reduces gastrointestinal motility and is used as adjunctive therapy for the management of diarrhea. Atropine is present in the formulation to decrease the potential for abuse (Prod Info diphenoxylate HCl atropine sulfate oral tablets, 2012; S Sweetman , 2001; Liebelt & Shannon, 1993).
    2) Difenoxin, the active metabolite of diphenoxylate, is an opioid structurally similar to meperidine which slows gastrointestinal motility, and is used in the symptomatic treatment of acute and chronic diarrhea. Atropine is present in the formulation to decrease the potential for abuse (Prod Info MOTOFEN(R) oral tablets, 2004).

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Diphenoxylate and atropine combination is used in the symptomatic treatment of diarrhea. Atropine is present in the formulation to decrease the potential for abuse. Information in this management is primarily about the combination product diphenoxylate/atropine (Lomotil(R)). Refer to ANTICHOLINERGIC POISONING for further information on atropine. The active metabolite of diphenoxylate, difenoxin, is marketed in combination with atropine as Motofen(R).
    B) PHARMACOLOGY: Diphenoxylate is an opioid structurally similar to meperidine. It inhibits peristalsis via stimulation of mu and delta opiate receptors in the bowel, which results in a prolonged gastrointestinal transit time. This causes increased water absorption in the large intestine, producing constipation. Atropine has anticholinergic activity. However, in this preparation atropine is included in low doses in an attempt to prevent abuse by deliberate overdosage.
    C) TOXICOLOGY: Although single therapeutic doses of diphenoxylate produce little or no subjective opiate-like effects, high doses (40 to 60 mg) produce effects typical of the opioids, including euphoria, suppression of withdrawal symptoms, and physical dependence with chronic administration.
    D) EPIDEMIOLOGY: Exposure is common. Overdose is rare and may be life-threatening.
    E) WITH THERAPEUTIC USE
    1) Sedation/drowsiness, dizziness, confusion, restlessness, headache, numbness of extremities, euphoria, depression, malaise/lethargy, nausea, vomiting, abdominal discomfort, toxic megacolon, and paralytic ileus may occur following therapeutic doses.
    2) ATROPINE EFFECTS: Hyperthermia, tachycardia, urinary retention, flushing, dryness of the skin and mucous membranes. These effects may occur, especially in children.
    F) WITH POISONING/EXPOSURE
    1) In pharmaceutical products, diphenoxylate is combined with atropine and rarely, if ever, seen in isolation. Competing unpredictable opioid and anticholinergic effects may complicate the clinical presentation and treatment.
    2) LARGE AMOUNTS: Anticholinergic effects generally occur early, opioid effects later.
    3) SMALL AMOUNTS (A few tablets): Anticholinergic effects may not be seen. Delayed onset of opioid effects should be expected.
    4) Drowsiness, lethargy, or excitement combined with dyspnea, hyperactivity, irritability, thirst, ataxia, flaccidity, or rigidity may occur with diphenoxylate/atropine overdose. CNS and respiratory depression may develop. Atropine effects include hyperpyrexia, disorientation, excitement, seizures, mydriasis, generalized red flushed appearance, urinary retention, tachycardia and tachypnea may occur.
    5) ONSET: The onset of symptoms with diphenoxylate/atropine may be delayed up to 6 to 8 hours or longer following ingestion. Because of delayed GI motility, initial effects, especially coma and respiratory depression, may be prolonged up to 30 hours.
    0.2.3) VITAL SIGNS
    A) WITH THERAPEUTIC USE
    1) HYPERTHERMIA, presumably from atropine, may occur (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005) .
    2) TACHYCARDIA, presumably from atropine, may occur (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005).
    B) WITH POISONING/EXPOSURE
    1) HYPERTHERMIA, presumably from atropine, may occur (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005) .
    2) TACHYCARDIA, presumably from atropine, may occur (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005).
    3) BRADYPNEA from opioid effects may recur and may be delayed and prolonged (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005).
    0.2.20) REPRODUCTIVE
    A) Diphenoxylate is classified as FDA pregnancy category C. There are no adequate and well-controlled studies of diphenoxylate use in pregnant women. In animal studies, there was no evidence of embryotoxicity, fetotoxicity, or teratogenicity when pregnant rats, rabbits, and mice were exposed to diphenoxylate at doses up to 10 times the recommended human dose.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, the manufacturer does not report any carcinogenic potential of diphenoxylate in humans.

Laboratory Monitoring

    A) Monitor vital signs frequently, pulse oximetry, and continuous cardiac monitoring.
    B) Monitor for CNS and respiratory depression.
    C) Diphenoxylate/atropine plasma concentrations are not clinically useful or readily available. Urine toxicology screens may confirm exposure, but are not useful in guiding therapy.
    D) Other routine lab work is usually not indicated, unless it is helpful to rule out other causes or if the diagnosis of opioid toxicity is uncertain.
    E) Obtain a chest x-ray for persistent hypoxia.
    F) Consider a head CT and/or lumbar puncture to rule out an intracranial mass, bleeding or infection, if the diagnosis is uncertain.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Patients may only need observation. Although single therapeutic doses of diphenoxylate produce little or no subjective opiate-like effects, high doses (40 to 60 mg) produce effects typical of the opioids.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Administer oxygen and assist ventilation for respiratory depression. Naloxone is the antidote indicated for severe toxicity (respiratory or CNS depression). Orotracheal intubation for airway protection should be performed early in cases of obtundation and/or respiratory depression that do not respond to naloxone, or in patients who develop severe acute lung injury. Seizures are rare, but may be a result of hypoxia. Treatment includes ensuring adequate oxygenation, and administering intravenous benzodiazepines; propofol or barbiturates may be indicated, if seizures persist. Hypotension is often reversed by naloxone. Initially treat with a saline bolus, if patient can tolerate a fluid load; then add adrenergic vasopressors to raise mean arterial pressure if hypotension persists. Urinary retention should be managed with catheterization.
    C) DECONTAMINATION
    1) PREHOSPITAL: GI decontamination not indicated because of the potential for CNS depression and aspiration.
    2) HOSPITAL: Consider activated charcoal if a patient presents soon after an ingestion and is not manifesting signs and symptoms of toxicity. Activated charcoal is generally not recommended in patients with significant signs of toxicity because of the risk of aspiration. Gastric lavage is not recommended as patients usually do well with supportive care.
    D) AIRWAY MANAGEMENT
    1) Administer oxygen and assist ventilation for respiratory depression. Orotracheal intubation for airway protection should be performed early in cases of obtundation and/or respiratory depression that do not respond to naloxone, or in patients who develop severe acute lung injury.
    E) ANTIDOTE
    1) NALOXONE will NOT antagonize the anticholinergic effects from diphenoxylate/atropine combinations. Naloxone, an opioid antagonist, is the specific antidote. Naloxone can be given intravascularly, intramuscularly, subcutaneously, intranasally or endotracheally. The usual dose is 0.4 to 2.0 mg IV. In patients with suspected opioid dependence incremental doses of 0.2 mg IV should be administered, titrated to reversal of respiratory depression and coma, to avoid precipitating acute opioid withdrawal. Doses may be repeated every 2 to 3 minutes up to 20 mg. Very high doses are rarely needed, but may occasionally be necessary. A CONTINUOUS infusion may be necessary in patients that have ingested a large overdose or sustained release formulation. A suggested starting rate is two-thirds of the dose effective for initial reversal that is administered each hour; titrate as needed. DURATION of effect is usually 1 to 2 hours. Because of delayed absorption (from anticholinergic effects) and an active metabolite, it is necessary to observe the patient for 4 to 6 hours after the last dose of naloxone to ensure that the patient does not have recurrent symptoms of toxicity. Naloxone can precipitate withdrawal in an opioid-dependent patients, which is usually not life-threatening; however it can be extremely uncomfortable for the patient.
    F) ENHANCED ELIMINATION
    1) Hemodialysis and hemoperfusion are not of value because of the large volume of distribution.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: Children with inadvertent ingestions of a therapeutic dose for age can be observed at home. Adults with inadvertent ingestion of an extra dose or two can be observed at home.
    2) OBSERVATION CRITERIA: Children who have ingested more than a therapeutic dose for age should be evaluated in the hospital and observed as they are generally opioid-naive and may develop respiratory depression. It is generally advised that children be observed for 12 to 24 hours because of the concern that onset of opioid effects may be delayed by atropine effects. Patients with deliberate ingestions and symptomatic patients should be referred to a healthcare facility.
    3) ADMISSION CRITERIA: Patients who develop central nervous depression should be admitted to the hospital as recurrent or prolonged effects are likely. Patients needing naloxone should be admitted as recurrent CNS depression may develop. Patients with coma, seizures, dysrhythmias, or delirium or those needing a naloxone infusion or intubated patients should be admitted to an intensive care setting.
    4) CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear. Refer patients for substance abuse counseling if indicated.
    H) PITFALLS
    1) Transient recovery of these patients should not produce false confidence for resolution of symptoms. Patients may be discharged prematurely after mental status clears with a dose of naloxone. Naloxone's duration of effect is much shorter than the duration of effect for diphenoxylate/atropine. Other causes of altered mental status must be ruled out, such as hypoxia or hypoglycemia.
    I) PHARMACOKINETICS
    1) Tmax: 2 hours after the administration of 5 mg diphenoxylate. Peak difenoxin concentration occurred 3.3 hours after a 10 mg dose. Both diphenoxylate and atropine are rapidly absorbed from the GI tract after oral ingestion. Vd: 324.2 L. Diphenoxylate is metabolized rapidly to an active metabolite difenoxin plus several inactive metabolites. Difenoxin is more potent and has a longer elimination half-life than diphenoxylate. Less than 1% of a dose is excreted unchanged; 13.6% of a dose may be recovered in the urine as metabolites, within 3 days; 49.2% was excreted in the feces within 4 days, suggesting enterohepatic circulation. Elimination half-life of diphenoxylic acid was approximately 12 to 14 hours. DIFENOXIN: 4.38 hours following 5 mg diphenoxylate administration.
    J) DIFFERENTIAL DIAGNOSIS
    1) Overdose with other sedating agents (eg, ethanol, benzodiazepine/barbiturate, antipsychotics); overdose with anticholinergic agents; CNS infection; intracranial hemorrhage; hypoglycemia or hypoxia.

Range Of Toxicity

    A) TOXICITY: CHILDREN: The lowest toxic doses associated with signs and symptoms of opioid/atropine poisoning were 0.5 to 2 tablets. The lowest published fatal dose is 1.2 mg/kg. As few as 6 tablets have produced coma and respiratory depression in a child.
    B) THERAPEUTIC DOSES: ADULTS: 2 tablets (2.5 mg diphenoxylate and 0.025 mg atropine each) or 10 mL solution orally four times daily; MAX dose 20 mg/day. CHILDREN (2 years and older): 0.3 to 0.4 mg/kg/day oral solution (divided 4 times daily); MAX dose 20 mg/day.

Summary Of Exposure

    A) USES: Diphenoxylate and atropine combination is used in the symptomatic treatment of diarrhea. Atropine is present in the formulation to decrease the potential for abuse. Information in this management is primarily about the combination product diphenoxylate/atropine (Lomotil(R)). Refer to ANTICHOLINERGIC POISONING for further information on atropine. The active metabolite of diphenoxylate, difenoxin, is marketed in combination with atropine as Motofen(R).
    B) PHARMACOLOGY: Diphenoxylate is an opioid structurally similar to meperidine. It inhibits peristalsis via stimulation of mu and delta opiate receptors in the bowel, which results in a prolonged gastrointestinal transit time. This causes increased water absorption in the large intestine, producing constipation. Atropine has anticholinergic activity. However, in this preparation atropine is included in low doses in an attempt to prevent abuse by deliberate overdosage.
    C) TOXICOLOGY: Although single therapeutic doses of diphenoxylate produce little or no subjective opiate-like effects, high doses (40 to 60 mg) produce effects typical of the opioids, including euphoria, suppression of withdrawal symptoms, and physical dependence with chronic administration.
    D) EPIDEMIOLOGY: Exposure is common. Overdose is rare and may be life-threatening.
    E) WITH THERAPEUTIC USE
    1) Sedation/drowsiness, dizziness, confusion, restlessness, headache, numbness of extremities, euphoria, depression, malaise/lethargy, nausea, vomiting, abdominal discomfort, toxic megacolon, and paralytic ileus may occur following therapeutic doses.
    2) ATROPINE EFFECTS: Hyperthermia, tachycardia, urinary retention, flushing, dryness of the skin and mucous membranes. These effects may occur, especially in children.
    F) WITH POISONING/EXPOSURE
    1) In pharmaceutical products, diphenoxylate is combined with atropine and rarely, if ever, seen in isolation. Competing unpredictable opioid and anticholinergic effects may complicate the clinical presentation and treatment.
    2) LARGE AMOUNTS: Anticholinergic effects generally occur early, opioid effects later.
    3) SMALL AMOUNTS (A few tablets): Anticholinergic effects may not be seen. Delayed onset of opioid effects should be expected.
    4) Drowsiness, lethargy, or excitement combined with dyspnea, hyperactivity, irritability, thirst, ataxia, flaccidity, or rigidity may occur with diphenoxylate/atropine overdose. CNS and respiratory depression may develop. Atropine effects include hyperpyrexia, disorientation, excitement, seizures, mydriasis, generalized red flushed appearance, urinary retention, tachycardia and tachypnea may occur.
    5) ONSET: The onset of symptoms with diphenoxylate/atropine may be delayed up to 6 to 8 hours or longer following ingestion. Because of delayed GI motility, initial effects, especially coma and respiratory depression, may be prolonged up to 30 hours.

Vital Signs

    3.3.1) SUMMARY
    A) WITH THERAPEUTIC USE
    1) HYPERTHERMIA, presumably from atropine, may occur (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005) .
    2) TACHYCARDIA, presumably from atropine, may occur (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005).
    B) WITH POISONING/EXPOSURE
    1) HYPERTHERMIA, presumably from atropine, may occur (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005) .
    2) TACHYCARDIA, presumably from atropine, may occur (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005).
    3) BRADYPNEA from opioid effects may recur and may be delayed and prolonged (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005).

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) Both miosis, secondary to opioid effects, and mydriasis, secondary to atropine effects, have been reported in overdose (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005; Liebelt & Shannon, 1993a; Cutler et al, 1980; Ginsburg, 1973).
    2) Cortical blindness believed to be secondary to cerebral hypoxia has occurred following Lomotil(R) overdose ingestion (Wasserman et al, 1975; Bargman & Gardner, 1969).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) TACHYARRHYTHMIA
    1) WITH THERAPEUTIC USE
    a) Tachycardia may occur, presumably due to atropine content (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005).
    2) WITH POISONING/EXPOSURE
    a) Tachycardia may occur, presumably due to atropine content (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005; McCarron et al, 1991).
    B) CARDIAC ARREST
    1) WITH POISONING/EXPOSURE
    a) Cardiopulmonary arrest has been described in a 2-year-old boy 12 hours after the ingestion of an unknown amount of diphenoxylate hydrochloride/atropine sulfate (Cutler et al, 1980).
    b) Cardiopulmonary arrest and death occurred despite naloxone administration in a 2 1/2-year-old who ingested 20 tablets of diphenoxylate/atropine (Lomotil(R)) (Penfold & Volans, 1977).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) DECREASED RESPIRATORY FUNCTION
    1) WITH THERAPEUTIC USE
    a) Respiratory depression characterized by intermittent apnea and respiratory failure are common and may be delayed up to 6 to 8 hours OR LONGER after ingestion (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005; Liebelt & Shannon, 1993a; Cutler et al, 1980; Curtis & Goel, 1979; Ginsburg, 1973).
    b) Respiratory arrest occurred in one case despite induction of emesis within one-half hour of ingestion (Rumack & Temple, 1974a).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) COMA
    1) WITH POISONING/EXPOSURE
    a) Onset of drowsiness and coma may be delayed; 2 cases have been reported in which emesis was induced within 1 hour of ingestion and coma developed 6 to 8 hours later. Coma and respiratory depression may be delayed up to 24 hours after ingestion (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005; Liebelt & Shannon, 1993a; Cutler et al, 1980; Curtis & Goel, 1979).
    b) Overdoses of diphenoxylate may result in severe respiratory depression and coma, possibly leading to permanent brain damage or death. Diphenoxylate should be used with extreme caution in young children, as this patient population may be predisposed to delayed diphenoxylate toxicity and due to greater variability of response in this age group (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005).
    c) CASE REPORT: A 5-month-old infant received a total of 15 mg of diphenoxylate with atropine (approximately 5 times the recommended daily dose) over 12 hours in the treatment of diarrhea and emesis. The infant developed dyspnea with suprasternal tugging with coma and anuria. The cardiac rate was 160 beats/minute with a respiration rate of 30/minute. The pupils were sluggishly reactive to light with a gaze directed upward. The patient was treated with IV fluids and calcium and oxygen and after 7 hours finally responded to stimuli. The infant was discharged on the third hospital day (King & Powell, 1965).
    d) In a series of 10 patients, ages ranging 1 month to 3 years, who received 17.5 to 110 mg (tablets or liquid) of Lomotil(R) for in the treatment of diarrhea, all patients developed significant lethargy and depression of deep tendon reflexes. The infants were subsequently treated with intravenous fluids, gastric lavage, ventilatory support, and 5 to 10 mg/1.73 m2 of nalorphine (Ginsburg, 1973).
    e) In another series of 45 patients age 10 months to 6 3/4 years treated with Lomotil(R), 4 patients had coma and 32 had drowsiness. The average time between ingestion and onset of symptoms was 3 hours (Curtis & Goel, 1979).
    B) HALLUCINATIONS
    1) WITH THERAPEUTIC USE
    a) Hallucinations have been reported.
    C) ATAXIA
    1) WITH POISONING/EXPOSURE
    a) Ataxia has been commonly reported in children (McCarron et al, 1991).
    D) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) Seizure activity occurred in 4/10 patients (40%) with Lomotil(R) overdose in one series (Ginsburg, 1973).
    E) PSYCHOMOTOR AGITATION
    1) WITH POISONING/EXPOSURE
    a) HYPEREXCITABILITY without subsequent mental depression was noted in a 34-month-old woman who ingested 5.2 mg/kg diphenoxylate as Lomotil(R) (McCarron et al, 1991).
    F) NEUROLOGICAL FINDING
    1) WITH THERAPEUTIC USE
    a) During clinical trials, therapeutic administration of Lomotil(R) resulted in the following effects: numbness of extremities, euphoria, depression, malaise/lethargy, confusion, sedation/drowsiness, dizziness, restlessness, and headache (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) DIGESTIVE SYSTEM FINDING
    1) WITH THERAPEUTIC USE
    a) DECREASED BOWEL MOTILITY, which may lead to cyclical or prolonged symptoms, may occur (Liebelt & Shannon, 1993a).
    b) Toxic megacolon has been reported (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005).
    2) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 69-year-old man was treated with 20 mg/day of oral diphenoxylate/atropine for 1 year as a result of drug habituation. He developed small bowel dilatation which presented as abdominal pain, distention and vomiting. Bowel sounds were only occasionally audible and barium enema examination revealed widely patent anastomotic stoma at ileotransverse colostomy site with immediate feeling of grossly dilated small bowel. Many feet of the distal ileum were filled with barium and gas with the luminal diameter averaging 5 to 6 cm. Discontinuation of the drug and conservative treatment resulted in rapid improvement in the patient's condition (Figiel & Figiel, 1973).
    B) PANCREATITIS
    1) WITH THERAPEUTIC USE
    a) CASE REPORT: Acute pancreatitis occurred in a 62-year-old woman following administration of Lomotil(R). The episodes of pancreatitis occurred on 2 occasions within 3 hours following ingestion of 3 tablets (McCormick et al, 1985).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) RETENTION OF URINE
    1) WITH THERAPEUTIC USE
    a) Urinary retention may occur (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005; Liebelt & Shannon, 1993a; Cutler et al, 1980).
    2) WITH POISONING/EXPOSURE
    a) Urinary retention occurred in 7 of 45 patients in one series (Curtis & Goel, 1979).
    b) Urinary retention may require catheterization (Liebelt & Shannon, 1993a).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) FLUSHING
    1) WITH THERAPEUTIC USE
    a) Flushing of the skin, presumably from atropine, may occur (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005).
    2) WITH POISONING/EXPOSURE
    a) Flushing may occur following overdoses (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005).
    b) Flushing occurred in 20 of 45 patients ingesting diphenoxylate/atropine (Lomotil(R)) in one series (Curtis & Goel, 1979).
    B) DRY SKIN
    1) WITH THERAPEUTIC USE
    a) Dryness of the skin, presumably from atropine, may occur (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005).
    2) WITH POISONING/EXPOSURE
    a) Dryness of the skin may occur following overdoses (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005).

Endocrine

    3.16.2) CLINICAL EFFECTS
    A) HYPERGLYCEMIA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Hyperglycemia, to 30.8 mmol/L (555 mg/100 mL) was reported in an 11-month-old boy with severe diphenoxylate/atropine (Lomotil(R)) poisoning at 5 hours after ingestion. At 8 hours after ingestion, blood glucose was normal (Modi, 1981).

Immunologic

    3.19.2) CLINICAL EFFECTS
    A) ACUTE ALLERGIC REACTION
    1) WITH THERAPEUTIC USE
    a) An allergic reaction (anaphylaxis, angioneurotic edema, urticaria, swelling of the gums, pruritus) may occur with Lomotil(R) therapy (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005).

Reproductive

    3.20.1) SUMMARY
    A) Diphenoxylate is classified as FDA pregnancy category C. There are no adequate and well-controlled studies of diphenoxylate use in pregnant women. In animal studies, there was no evidence of embryotoxicity, fetotoxicity, or teratogenicity when pregnant rats, rabbits, and mice were exposed to diphenoxylate at doses up to 10 times the recommended human dose.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) In animal studies, there was no evidence of embryotoxicity, fetotoxicity, or teratogenicity in rats, rabbits, and mice administered diphenoxylate hydrochloride at oral doses of 0.4 mg/kg/day to 20 mg/kg/day (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005).
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) There are no adequate and well-controlled studies of diphenoxylate use in pregnant women (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005).
    2) An infant with multiple defects was born to a mother who had taken diphenoxylate and atropine for diarrhea during the 10th week of gestation. The defects included Ebstein's anomaly, hypertelorism, epicanthal folds, low-set rotated ears, a cleft uvula, deafness, blindness, and medially rotated hands. The definite cause of defects could not be found since the drug exposure was not during the susceptible stages of development (Siebert et al, 1989).
    B) PREGNANCY CATEGORY
    1) The manufacturer has classified diphenoxylate as FDA pregnancy category C (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005).
    2) There are no well controlled studies evaluating the risk of fetal harm during treatment with diphenoxylate. Based on the mechanism of action, it is possible significant fetal harm may occur when administered to a pregnant woman. If a patient becomes pregnant or diphenoxylate is intended to be used during pregnancy, the patient must be advised of the potential harm the medication may have on the fetus (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005).
    C) LACK OF EFFECT
    1) No defects were reported among the children of mothers exposed to diphenoxylate during the first trimester of pregnancy (Heinonen et al, 1977).
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) LACK OF INFORMATION
    1) It is not known whether diphenoxylate is excreted in human milk or absorbed systemically after ingestion. Because atropine (added to diphenoxylate products) is excreted in human milk, caution should be used in administering diphenoxylate to a nursing woman (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005).
    3.20.5) FERTILITY
    A) ANIMAL STUDIES
    1) A reduction in female weight gain and fertility was observed when male and female rats were administered diphenoxylate at doses of 4 mg/kg/day to 20 mg/kg/day (50 times the human dose) during a 3-litter reproduction study.(Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005)

Carcinogenicity

    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, the manufacturer does not report any carcinogenic potential of diphenoxylate in humans.
    3.21.4) ANIMAL STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, the manufacturer does not report any carcinogenic potential of diphenoxylate in animals (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005).

Genotoxicity

    A) At the time of this review, the manufacturer does not report any genotoxic or mutagenic potential of diphenoxylate.

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs frequently, pulse oximetry, and continuous cardiac monitoring.
    B) Monitor for CNS and respiratory depression.
    C) Diphenoxylate/atropine plasma concentrations are not clinically useful or readily available. Urine toxicology screens may confirm exposure, but are not useful in guiding therapy.
    D) Other routine lab work is usually not indicated, unless it is helpful to rule out other causes or if the diagnosis of opioid toxicity is uncertain.
    E) Obtain a chest x-ray for persistent hypoxia.
    F) Consider a head CT and/or lumbar puncture to rule out an intracranial mass, bleeding or infection, if the diagnosis is uncertain.

Methods

    A) OTHER
    1) The diagnosis of Lomotil(R) poisoning is not aided by the laboratory (Curtis & Goel, 1979a).
    2) The availability and sensitivity of methods to detect diphenoxylate in the blood and urine is limited.
    3) Because diphenoxylate is rapidly converted to diphenoxylic acid (diphenoxin), it is frequently undetected in blood or urine.
    B) MULTIPLE ANALYTICAL METHODS
    1) Diphenoxin can be detected in plasma by gas chromatography mass spectrometry and radioimmunoassay (Jackson & Stafford, 1987).

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients who develop central nervous depression should be admitted to the hospital as recurrent or prolonged effects are likely. Patients needing naloxone should be admitted as recurrent CNS depression may develop. Patients with coma, seizures, dysrhythmias, or delirium or those needing a naloxone infusion or intubated patients should be admitted to an intensive care setting.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Children with inadvertent ingestions of a therapeutic dose for age can be observed at home. Adults with inadvertent ingestion of an extra dose or two can be observed at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear. Refer patients for substance abuse counseling if indicated.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) SUMMARY: Children who have ingested more than a therapeutic dose for age should be evaluated in the hospital and observed as they are generally opioid-naive and may develop respiratory depression. It is generally advised that children be observed for 12 to 24 hours because of the concern that onset of opioid effects may be delayed by atropine effects. Patients with deliberate ingestions and symptomatic patients should be referred to a healthcare facility.
    B) In possible overdose, the manufacturer of Lomotil(R) recommends medical observation for at least 48 hours, preferably under continuous hospital care (Prod Info LOMOTIL(R) CV oral tablets, oral liquid, 2005).
    C) CHILDREN 6 YEARS AND YOUNGER
    1) Children (6 years or younger) must be observed for 24 hours in an intensive care facility for delayed symptoms.
    2) In one retrospective study, three of 28 patients had recurrences of opioid symptoms 12 to 24 hours postingestion (McCarron et al, 1991).

Monitoring

    A) Monitor vital signs frequently, pulse oximetry, and continuous cardiac monitoring.
    B) Monitor for CNS and respiratory depression.
    C) Diphenoxylate/atropine plasma concentrations are not clinically useful or readily available. Urine toxicology screens may confirm exposure, but are not useful in guiding therapy.
    D) Other routine lab work is usually not indicated, unless it is helpful to rule out other causes or if the diagnosis of opioid toxicity is uncertain.
    E) Obtain a chest x-ray for persistent hypoxia.
    F) Consider a head CT and/or lumbar puncture to rule out an intracranial mass, bleeding or infection, if the diagnosis is uncertain.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Prehospital GI decontamination is not recommended because of the risk of CNS depression and subsequent aspiration.
    6.5.2) PREVENTION OF ABSORPTION
    A) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Patients may only need observation. Although single therapeutic doses of diphenoxylate produce little or no subjective opiate-like effects, high doses (40 to 60 mg) produce effects typical of the opioids.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Administer oxygen and assist ventilation for respiratory depression. Naloxone is the antidote indicated for severe toxicity (respiratory or CNS depression). Orotracheal intubation for airway protection should be performed early in cases of obtundation and/or respiratory depression that do not respond to naloxone, or in patients who develop severe acute lung injury. Seizures are rare, but may be a result of hypoxia. Treatment includes ensuring adequate oxygenation, and administering intravenous benzodiazepines; propofol or barbiturates may be indicated, if seizures persist. Hypotension is often reversed by naloxone. Initially treat with a saline bolus, if patient can tolerate a fluid load; then add adrenergic vasopressors to raise mean arterial pressure if hypotension persists. Urinary retention should be managed with catheterization.
    B) MONITORING OF PATIENT
    1) Monitor vital signs frequently, pulse oximetry, and continuous cardiac monitoring.
    2) Monitor for CNS and respiratory depression.
    3) Diphenoxylate/atropine plasma concentrations are not clinically useful or readily available.
    4) Urine toxicology screens may confirm exposure, but is not useful in guiding therapy.
    5) Other routine lab work is usually not indicated, unless it is helpful to rule out other causes or if the diagnosis of opioid toxicity is uncertain.
    6) Obtain a chest x-ray for persistent hypoxia.
    7) Consider a head CT and/or lumbar puncture to rule out an intracranial mass, bleeding or infection, if the diagnosis is uncertain.
    C) NALOXONE
    1) Naloxone will NOT antagonize the anticholinergic effects from diphenoxylate/atropine combinations.
    2) NALOXONE/SUMMARY
    a) Naloxone, a pure opioid antagonist, reverses coma and respiratory depression from all opioids. It has no agonist effects and can safely be employed in a mixed or unknown overdose where it can be diagnostic and therapeutic without risk to the patient.
    b) Indicated in patients with mental status and respiratory depression possibly related to opioid overdose (Hoffman et al, 1991).
    c) DOSE: The initial dose of naloxone should be low (0.04 to 0.4 mg) with a repeat dosing as needed or dose escalation to 2 mg as indicated due to the risk of opioid withdrawal in an opioid-tolerant individual; if delay in obtaining venous access, may administer subcutaneously, intramuscularly, intranasally, via nebulizer (in a patient with spontaneous respirations) or via an endotracheal tube (Vanden Hoek,TL,et al).
    d) Recurrence of opioid toxicity has been reported to occur in approximately 1 out of 3 adult ED opioid overdose cases after a response to naloxone. Recurrences are more likely with long-acting opioids (Watson et al, 1998)
    3) NALOXONE DOSE/ADULT
    a) INITIAL BOLUS DOSE: Because naloxone can produce opioid withdrawal in an opioid-dependent individual leading to severe agitation and hypertension, the initial dose of naloxone should be low (0.04 to 0.4 mg) with a repeat dosing as needed or dose escalation to 2 mg as indicated (Vanden Hoek,TL,et al).
    1) This dose can also be given intramuscularly or subcutaneously in the absence of intravenous access (Howland & Nelson, 2011; Prod Info naloxone HCl IV, IM, subcutaneous injection solution, 2008; Maio et al, 1987; Wanger et al, 1998).
    b) Larger doses may be needed to reverse opioid effects. Generally, if no response is observed after 8 to 10 milligrams has been administered, the diagnosis of opioid-induced respiratory depression should be questioned (Howland & Nelson, 2011; Prod Info naloxone HCl IV, IM, subcutaneous injection solution, 2008). Very large doses of naloxone (10 milligrams or more) may be required to reverse the effects of a buprenorphine overdose (Gal, 1989; Jasinski et al, 1978).
    1) Single doses of up to 24 milligrams have been given without adverse effect (Evans et al, 1973).
    c) REPEAT DOSE: The effective naloxone dose may have to be repeated every 20 to 90 minutes due to the much longer duration of action of the opioid agonist used(Howland & Nelson, 2011).
    1) OPIOID DEPENDENT PATIENTS: The goal of naloxone therapy is to reverse respiratory depression without precipitating significant withdrawal. Starting doses of naloxone 0.04 mg IV, or 0.001 mg/kg, have been suggested as appropriate for opioid-dependent patients without severe respiratory depression (Howland & Nelson, 2011). If necessary the dose may be repeated or increased gradually until the desired response is achieved (adequate respirations, ability to protect airway, responds to stimulation but no evidence of withdrawal) (Howland & Nelson, 2011). In the presence of opioid dependence, withdrawal symptoms typically appear within minutes of naloxone administration and subside in about 2 hours. The severity and duration of the withdrawal syndrome are dependant upon the naloxone dose and the degree and type of dependence.(Prod Info naloxone HCl IV, IM, subcutaneous injection solution, 2008)
    2) PRECAUTION should be taken in the presence of a mixed overdose of a sympathomimetic with an opioid. Administration of naloxone may provoke serious sympathomimetic toxicity by removing the protective opioid-mediated CNS depressant effects. Arrhythmogenic effects of naloxone may also be potentiated in the presence of severe hyperkalemia (McCann et al, 2002).
    d) NALOXONE DOSE/CHILDREN
    1) LESS THAN 5 YEARS OF AGE OR LESS THAN 20 KG: 0.1 mg/kg IV/intraosseous/IM/subcutaneously maximum dose 2 mg; may repeat dose every 2 to 5 minutes until symptoms improve (Kleinman et al, 2010; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008)
    2) 5 YEARS OF AGE OR OLDER OR GREATER THAN 20 KG: 2 mg IV/intraosseous/IM/subcutaneouslymay repeat dose every 2 to 5 minutes until symptoms improve (Kleinman et al, 2010; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Krauss & Green, 2006). Although naloxone may be given via the endotracheal tube for pediatric resuscitation, optimal doses are unknown. Some experts have recommended using 2 to 3 times the IV dose (Kleinman et al, 2010)
    3) AVOIDANCE OF OPIOID WITHDRAWAL: In cases of known or suspected chronic opioid therapy, a lower dose of 0.01 mg/kg may be considered and titrated to effect to avoid withdrawal: INITIAL DOSE: 0.01 mg/kg body weight given IV. If this does not result in clinical improvement, an additional dose of 0.1 mg/kg body weight may be given. It may be given by the IM or subQ route if the IV route is not available (Prod Info naloxone HCl IV, IM, subcutaneous injection solution, 2008)
    e) NALOXONE DOSE/NEONATE
    1) The American Academy of Pediatrics recommends a neonatal dose of 0.1 mg/kg IV or intratracheally from birth until age 5 years or 20 kilograms of body weight (AAP, 1989; Kleinman et al, 2010).
    2) Smaller doses (10 to 30 mcg/kg IV) have been successful in the setting of exposure via maternal administration of narcotics or administration to neonates in therapeutic doses for anesthesia (Wiener et al, 1977; Welles et al, 1984; Fischer & Cook, 1974; Brice et al, 1979).
    3) POTENTIAL OF WITHDRAWAL: The risk of precipitating withdrawal in an addicted neonate should be considered. Withdrawal seizures have been provoked in infants from opioid-abusing mothers when the infants were given naloxone at birth to stimulate breathing (Gibbs et al, 1989).
    4) In cases of inadvertent administration of an opioid overdose to a neonate, larger doses may be required. In one case of oral morphine intoxication, 0.16 milligram/kilogram/hour was required for 5 days (Tenenbein, 1984).
    f) NALOXONE/ALTERNATE ROUTES
    1) If intravenous access cannot be rapidly established, naloxone can be administered via subcutaneous or intramuscular injection, intranasally, or via inhaled nebulization in patients with spontaneous respirations.
    2) INTRAMUSCULAR/SUBCUTANEOUS ROUTES: If an intravenous line cannot be secured due to hypoperfusion or lack of adequate veins then naloxone can be administered by other routes.
    3) The intramuscular or subcutaneous routes are effective if hypoperfusion is not present (Prod Info naloxone HCl IV, IM, subcutaneous injection solution, 2008). The delay required to establish an IV, offsets the slower rate of subcutaneous absorption (Wanger et al, 1998).
    4) Naloxone Evzio(TM) is a hand-held autoinjector intended for the emergency treatment of known or suspected opioid overdose. The autoinjector is equipped with an electronic voice instruction system to assist caregivers with administration. It is available as 0.4 mg/0.4 mL solution for injection in a pre-filled auto-injector (Prod Info EVZIO(TM) injection solution, 2014).
    5) INTRANASAL ROUTE: Intranasal naloxone has been shown to be effective in opioid overdose; bioavailability appears similar to the intravenous route (Kelly & Koutsogiannis, 2002). Based on several case series of patients with suspected opiate overdose, the average response time of 3.4 minutes was observed using a formulation of 1 mg/mL/nostril by a mucosal atomization device (Kerr et al, 2009; Kelly & Koutsogiannis, 2002). However, a young adult who intentionally masticated two 25 mcg fentanyl patches and developed agonal respirations (6 breaths per minute), decreased mental status and mitotic pupils did not respond to intranasal naloxone (1 mg in each nostril) administered by paramedics. After 11 minutes, paramedics placed an IV and administered 1 mg of IV naloxone; respirations normalized and mental status improved. Upon admission, 2 additional doses of naloxone 0.4 mg IV were needed. The patient was monitored overnight and discharged the following day without sequelae. Its suggested that intranasal administration can lead to unpredictable absorption (Zuckerman et al, 2014).
    a) Narcan(R) nasal spray is supplied as a single 4 mg dose of naloxone hydrochloride in a 0.1 mL intranasal spray (Prod Info NARCAN(R) nasal spray, 2015).
    b) FDA DOSING: Initial dose: 1 spray (4 mg) intranasally into 1 nostril. Subsequent doses: Use a new Narcan(R) nasal spray and administer into alternating nostrils. May repeat dose every 2 to 3 minutes. Requirement for repeat dosing is dependent on the amount, type, and route of administration of the opioid being antagonized. Higher or repeat doses may be required for partial agonists or mixed agonist/antagonists (Prod Info NARCAN(R) nasal spray, 2015).
    c) AMERICAN HEART ASSOCIATION GUIDELINE DOSING: Usual dose: 2 mg intranasally as soon as possible; may repeat after 4 minutes (Lavonas et al, 2015). Higher doses may be required with atypical opioids (VandenHoek et al, 2010).
    d) ABSORPTION: Based on limited data, the absorption rate of intranasal administration is comparable to intravenous administration. The peak plasma concentration of intranasal administration is estimated to be 3 minutes which is similar to the intravenous route (Kerr et al, 2009). In rare cases, nasal absorption may be inhibited by injury, prior use of intranasal drugs, or excessive secretions (Kerr et al, 2009).
    6) NEBULIZED ROUTE: DOSE: A suggested dose is 2 mg naloxone with 3 mL of normal saline for suspected opioid overdose in patients with some spontaneous respirations (Weber et al, 2012).
    7) ENDOTRACHEAL ROUTE: Endotracheal administration of naloxone can be effective(Tandberg & Abercrombie, 1982), optimum dose unknown but 2 to 3 times the intravenous dose had been recommended by some (Kleinman et al, 2010).
    g) NALOXONE/CONTINUOUS INFUSION METHOD
    1) A continuous infusion of naloxone may be employed in circumstances of opioid overdose with long acting opioids (Howland & Nelson, 2011; Redfern, 1983).
    2) The patient is given an initial dose of IV naloxone to achieve reversal of opioid effects and is then started on a continuous infusion to maintain this state of antagonism.
    3) DOSE: Utilize two-thirds of the initial naloxone bolus on an hourly basis (Howland & Nelson, 2011; Mofenson & Caraccio, 1987). For an adult, prepare the dose by multiplying the effective bolus dose by 6.6, and add that amount to 1000 mL and administer at an IV infusion rate of 100 mL/hour (Howland & Nelson, 2011).
    4) Dose and duration of action of naloxone therapy varies based on several factors; continuous monitoring should be used to prevent withdrawal induction (Howland & Nelson, 2011).
    5) Observe patients for evidence of CNS or respiratory depression for at least 2 hours after discontinuing the infusion (Howland & Nelson, 2011).
    h) NALOXONE/PREGNANCY
    1) In general, the smallest dose of naloxone required to reverse life threatening opioid effects should be used in pregnant women. Naloxone detoxification of opioid addicts during pregnancy may result in fetal distress, meconium staining and fetal death (Zuspan et al, 1975). When naloxone is used during pregnancy, opioid abstinence may be provoked in utero (Umans & Szeto, 1985).
    D) INSERTION OF CATHETER INTO URINARY BLADDER
    1) URINARY RETENTION should be managed with catheterization.

Enhanced Elimination

    A) SUMMARY
    1) Hemodialysis and hemoperfusion are not useful because of the large volume of distribution.

Case Reports

    A) PEDIATRIC
    1) ACUTE EFFECTS
    a) CARDIOPULMONARY ARREST has been described in a 2-year-old male 12 hours after the ingestionof an unknown amount of diphenoxylate hydrochloride/atropine sulfate. Ingestion was initially denied by both the mother and grandmother. The grandmother later admitted that the child had been found with pills in his mouth. Due to the child's respiratory depression and comatose state, a Lomotil(R) ingestion was suspected and naloxone 0.01 mg/kg was given intravenously. Within seconds the child regained consciousness and 24 hours postingestion the patient was alert. Diphenoxylate was found in the gastric contents 18 hours postingestion, although only trace amounts of diphenoxylate were seen in the urine and none was seen in the blood. Forty-eight hours postingestion, the patient's EKG was normal (Cutler et al, 1980).
    b) RESPIRATORY ARREST AND DEATH: A 2-year-old girl, who ingested an unknown amount of Lomotil(R) tablets 12 hours prior to presentation, presented with cyanosis pinpoint pupils, pulse of 128, and temperature of 39.2 degrees C. She received 2 mg nalorphine and 7 repeated doses at 40 to 60 minute intervals. She was placed on a respirator and received several doses of 0.2 mg naloxone. Gastric lavage at 27 hours post-ingestion recovered intact tablets. Thirty-five hours after ingestion, she developed fixed and dilated pupils and died a short time later. At autopsy, she was found to have cerebral edema, atelectasis, bronchial obstruction with hemorrhagic mucous, and encephalomalacia (Rumack & Temple, 1974a).
    c) RESPIRATORY ARREST: An 18-month-old child ingested approximately 8 Lomotil(R) tablets. Syrup of ipecac was given shortly after ingestion with emesis occurring at 30 minutes. The patient was then given lunch and allowed to nap. Four hours later he was found unresponsive. On arrival at the hospital he had pinpoint pupils, temperature 37.8 degree C, heart rate 136, and urinary retention. He had a respiratory arrest, which responded to naloxone 0.1 mg IV. He required 2 additional doses of naloxone over 40 minutes, and two more doses over the next eight hours. He recovered uneventfully (Rumack & Temple, 1974).
    d) RESPIRATORY ARREST: A 2-year-old boy ingested 30 to 40 Lomotil(R) tablets. A rectal temperature of 39.8 degrees C was recorded. He was flushed, tachypneic, and lethargic. Heart rate was 180. By 150 minutes after ingestion, he was admitted to the ward. Five minutes later, respirations ceased and he was intubated. Almost 7 hours after ingestion, he received a total of 24 mg nalorphine in order to sustain respirations. He was extubated the next day and recovered uneventfully (Ament, 1969).
    e) RESPIRATORY ARREST: A 2-year-old girl was brought to the hospital 1.5 to 2 hours after a possible ingestion of 35 to 40 tablets of Lomotil(R). She received gastric lavage approximately 2 hours post-ingestion without recovery of tablets in the gastric aspirate. She was drowsy. Ten hours after ingestion, with a normal heart rate, she suffered respiratory arrest and was managed by positive pressure ventilation and 2 mg nalorphine IM, whereupon she resumed respirations. Sixteen hours post-ingestion, she suffered a second respiratory arrest. She was given another 2 mg of nalorphine. She remained drowsy for a further 24 hours despite 2 mg nalorphine every 4 hours, eventually changed to 1 mg every 4 hours for an additional 24 hours. She recovered and was discharged on hospital day 5 (Wheeldon & Heggarty, 1971).
    f) COMA AND RESPIRATORY DEPRESSION: A 2-year-old boy ingested an unknown amount of Lomotil(R) and presented with acute onset of unexplained lethargy, head rolling, and generalized limpness. There was no initial suspicion of Lomotil(R) ingestion until the parents were sent home to check the bottle. He was tachycardic and flushed with a temperature of 38.6 degrees C. He received 0.4 mg IV naloxone in the emergency department for stupor, flaccidity, and hypoventilation. One hour later, the lethargy and hypotonia returned, necessitating a second 0.4 mg naloxone dose. This cleared sensorium and restored muscle tone. The child was placed on a naloxone infusion 0.4 mg/hour and experienced no further symptoms during 48 hours of subsequent observation (McCarron et al, 1991).
    g) COMA AND ANURIA: King & Powell (1965) report a case of a 5-month-old girl who had received a total of 15 mg of diphenoxylate (approximately 5 times the recommended daily dose) over 12 hours for treatment of diarrhea and emesis. The infant developed dyspnea with suprasternal tugging with coma and anuria. Heart rate was 160 beats/minute with a respiration rate of 30/minute. The pupils were sluggishly reactive to light with a gaze directed upward. The patient was treated with IV fluids and calcium and oxygen and after 7 hours finally responded to stimuli. The infant was discharged on the third hospital day (King & Powell, 1965).

Summary

    A) TOXICITY: CHILDREN: The lowest toxic doses associated with signs and symptoms of opioid/atropine poisoning were 0.5 to 2 tablets. The lowest published fatal dose is 1.2 mg/kg. As few as 6 tablets have produced coma and respiratory depression in a child.
    B) THERAPEUTIC DOSES: ADULTS: 2 tablets (2.5 mg diphenoxylate and 0.025 mg atropine each) or 10 mL solution orally four times daily; MAX dose 20 mg/day. CHILDREN (2 years and older): 0.3 to 0.4 mg/kg/day oral solution (divided 4 times daily); MAX dose 20 mg/day.

Therapeutic Dose

    7.2.1) ADULT
    A) DIPHENOXYLATE HYDROCHLORIDE AND ATROPINE SULFATE
    1) ORAL SOLUTION
    a) The recommended initial dose is 10 mL orally 4 times daily (20 mg/day diphenoxylate). Dose may be reduced once initial control has been achieved; maintenance dose range: 5 to 20 mg diphenoxylate (10 to 40 mL) daily. MAXIMUM DOSE: 20 mg/day. If clinical improvement is not seen within 10 days at the maximum dose, symptom control is unlikely with further administration (Prod Info diphenoxylate HCl atropine sulfate oral solution, 2012).
    2) TABLETS
    a) The recommended initial dose is 2 tablets (5 mg diphenoxylate) orally 4 times daily. Dose may be reduced once initial control has been achieved; maintenance dose range: 5 to 20 mg diphenoxylate daily. MAXIMUM DOSE: 20 mg/day. If clinical improvement is not seen within 10 days at the maximum dose, symptom control is unlikely with further administration (Prod Info diphenoxylate HCl atropine sulfate oral tablets, 2012).
    7.2.2) PEDIATRIC
    A) DIPHENOXYLATE HYDROCHLORIDE AND ATROPINE SULFATE-
    1) ORAL SOLUTION
    a) CHILDREN 13 YEARS OF AGE AND OLDER: The recommended initial dose is 10 mL orally 4 times daily (20 mg/day diphenoxylate). Dose may be reduced once initial control has been achieved; maintenance dose range: 5 to 20 mg diphenoxylate (10 to 40 mL) daily. MAXIMUM DOSE: 20 mg/day. If clinical improvement is not seen within 10 days at the maximum dose, symptom control is unlikely with further administration (Prod Info diphenoxylate HCl atropine sulfate oral solution, 2012).
    b) CHILDREN 2 TO 12 YEARS OF AGE: The recommended initial total daily dose is 0.3 mg/kg/day to 0.4 mg/kg/day in 4 divided doses. Maintenance dose may be as little as one-fourth the initial dose. If no response is seen within 48 hours, this oral solution is unlikely to be effective (Prod Info diphenoxylate HCl atropine sulfate oral solution, 2012).
    c) CHILDREN YOUNGER THAN 2 YEARS OF AGE: Diphenoxylate is not recommended for this age group (Prod Info diphenoxylate HCl atropine sulfate oral solution, 2012).
    2) TABLETS
    a) CHILDREN 13 YEARS OF AGE AND OLDER: The recommended initial dose is 2 tablets (5 mg diphenoxylate) orally 4 times daily. Dose may be reduced once initial control has been achieved; maintenance dose range: 5 to 20 mg diphenoxylate daily. MAXIMUM DOSE: 20 mg/day. If clinical improvement is not seen within 10 days at the maximum dose, symptom control is unlikely with further administration (Prod Info diphenoxylate HCl atropine sulfate oral tablets, 2012).
    b) CHILDREN YOUNGER THAN 13 YEARS OF AGE: Do not administer diphenoxylate tablets to this age group (Prod Info diphenoxylate HCl atropine sulfate oral tablets, 2012).

Minimum Lethal Exposure

    A) PEDIATRIC
    1) UNKNOWN AMOUNT: Fatality resulted from ingestion of a large, but unknown amount in a 3.5-year-old child.
    a) Naloxone was not used, nor was assisted ventilation.
    b) Postmortem analysis showed a diphenoxylate concentration of 340 nanograms/milliliter in the blood, with none detected in the urine (Al Ragheb et al, 1982).
    2) The lowest published fatal dose is 1.2 mg/kg of diphenoxylate as diphenoxylate/atropine (Liebelt & Shannon, 1993).

Maximum Tolerated Exposure

    A) ADULTS
    1) ADULTS would appear to be somewhat less susceptible to intoxication with Lomotil(R) but should be observed for clinical effects.
    B) PEDIATRICS
    1) The lowest toxic doses associated with signs and symptoms of opioid/atropine poisoning were 0.5 to 2 tablets (Liebelt & Shannon, 1993). Serious intoxication with coma has been seen with as few as 6 tablets in a child (Curtis & Goel, 1979; Rumack & Temple, 1974).
    2) RESPIRATORY ARREST: An 18-month-old child ingested approximately 8 Lomotil(R) tablets. Syrup of ipecac was given shortly after ingestion with emesis occurring at 30 minutes. The patient was then given lunch and allowed to nap. Four hours later he was found unresponsive. On arrival at the hospital he had pinpoint pupils, temperature 37.8 degree C, heart rate 136, and urinary retention. He had a respiratory arrest, which responded to naloxone 0.1 mg IV. He required 2 additional doses of naloxone over 40 minutes, and two more doses over the next eight hours. He recovered uneventfully (Rumack & Temple, 1974).
    3) RESPIRATORY ARREST: A 2-year-old boy ingested 30 to 40 Lomotil(R) tablets. A rectal temperature of 39.8 degrees C was recorded. He was flushed, tachypneic, and lethargic. Heart rate was 180. By 150 minutes after ingestion, he was admitted to the ward. Five minutes later, respirations ceased and he was intubated. Almost 7 hours after ingestion, he received a total of 24 mg nalorphine in order to sustain respirations. He was extubated the next day and recovered uneventfully (Ament, 1969).
    4) RESPIRATORY ARREST: A 2-year-old girl was brought to the hospital 1.5 to 2 hours after a possible ingestion of 35 to 40 tablets of Lomotil(R). She received gastric lavage approximately 2 hours post-ingestion without recovery of tablets in the gastric aspirate. She was drowsy. Ten hours after ingestion, with a normal heart rate, she suffered respiratory arrest and was managed by positive pressure ventilation and 2 mg nalorphine IM, whereupon she resumed respirations. Sixteen hours post-ingestion, she suffered a second respiratory arrest. She was given another 2 mg of nalorphine. She remained drowsy for a further 24 hours despite 2 mg nalorphine every 4 hours, eventually changed to 1 mg every 4 hours for an additional 24 hours. She recovered and was discharged on hospital day 5 (Wheeldon & Heggarty, 1971).
    5) COMA AND ANURIA: King & Powell (1965) report a case of a 5-month-old girl who had received a total of 15 mg of diphenoxylate (approximately 5 times the recommended daily dose) over 12 hours for treatment of diarrhea and emesis. The infant developed dyspnea with suprasternal tugging with coma and anuria. Heart rate was 160 beats/minute with a respiration rate of 30/minute. The pupils were sluggishly reactive to light with a gaze directed upward. The patient was treated with IV fluids and calcium and oxygen and after 7 hours finally responded to stimuli. The infant was discharged on the third hospital day (King & Powell, 1965).
    6) PEDIATRIC toxic doses of diphenoxylate:
    a) Pediatric Symptom Summary:
    AGEDOSE (mg)TABLETSSIGNSREF
    18 mo156CRumack, 1974
    5 mo156C, RKing, 1965
    2 yr15-206-8C, RKing, 1965
    18 mo208C, RRumack, 1974
    2 yr208C, RRumack, 1974
    2.5 yr208C, RRumack, 1974
    4.5 yr22.59C, RRumack, 1974
    17 mo25-37.510-15C, RRumack, 1974
    2.5 yr3514RRumack, 1974
    3 yr4518C, RRumack, 1974
    2 yr62.525C, RRumack, 1974
    4 yr82.533C, RRumack, 1974
    2.5 yr10040C, RRumack, 1974
    C = Coma
    R = Respiratory Depression

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) ANIMAL DATA
    1) LD50- (ORAL)MOUSE:
    a) 337 mg/kg (RTECS, 2000)
    2) LD50- (ORAL)RAT:
    a) 221 mg/kg (RTECS, 2000)

Pharmacologic Mechanism

    A) Diphenoxylate structurally resembles meperidine and has a definite constipating effect in man.
    B) Euphoria, suppression of morphine abstinence, and physical dependence do not occur until doses of 40 to 60 mg (in adults) are reached.
    C) Diphenoxylate and all salt forms are virtually insoluble in water, therefore, parenteral abuse is unlikely.

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