PAROXETINE

0.0 OVERVIEW

0.1 LIFE SUPPORT

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

0.2 CLINICAL EFFECTS

0.2.1 SUMMARY OF EXPOSURE

A. Symptoms of toxicity can be delayed because paroxetine is slowly absorbed. Effects have included mild CNS depression, tremors, movement disorders, tachycardia, SIADH, anxiety and vomiting.
B. Side effects reported at therapeutic doses include blurred vision, syncope, increased and decreased blood pressure, PVCs, headache, drowsiness, insomnia, nausea, vomiting, constipation, and difficulty urinating.

0.2.5 CARDIOVASCULAR

A. Tachycardia has been reported in overdose. Orthostatic hypotension, syncope, PVCs and minimal QRS prolongation have developed at therapeutic doses.

0.2.7 NEUROLOGIC

A. Mild CNS depression and tremors have been reported in overdose and as side effects. Sleep disturbance, extrapyramidal effects, movement disorders and EEG changes occur with therapeutic doses.

0.2.8 GASTROINTESTINAL

A. Nausea and vomiting have occurred with overdose and at therapeutic doses. Constipation, diarrhea, dry mouth and anorexia are reported adverse effects.

0.2.12 FLUID-ELECTROLYTE

A. Therapeutic and overdoses of paroxetine have resulted in SIADH and hyponatremia.

0.2.22 OTHER

A. Abrupt discontinuation of paroxetine is associated with a withdrawal syndrome.

0.4 TREATMENT OVERVIEW

0.4.2 ORAL/PARENTERAL EXPOSURE

A. EMESIS: Ipecac-induced emesis is not recommended because of the potential for CNS depression.
B. GASTRIC LAVAGE: Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in Trendelenburg and left lateral decubitus position or by endotracheal intubation. Control any seizures first.

1. CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.

C. ACTIVATED CHARCOAL: Administer charcoal as slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
D. HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid, place in Trendelenburg position. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (0.1 to 0.2 mcg/kg/min), titrate to desired response.

0.5 RANGE OF TOXICITY

A. Overdose of 360 mg in an elderly adult resulted in excessive vomiting and SIADH with decreased serum sodium levels.
B. In a series of 35 patients, minimal or no effects developed after ingestion of 10 to 1000 mg.
C. Overdoses between 10 and 120 mg in 16 children < 5 years of age resulted in no symptoms.
D. Overdoses between 100 and 800 mg in adolescents aged 12 years up to 17 years old resulted in no symptoms in most of these cases.

1.0 SUBSTANCES INCLUDED/SYNONYMS

1.1 THERAPEUTIC/TOXIC CLASS

A. Paroxetine is an antidepressant which is not structurally related to the other selective serotonin reuptake inhibitors, tricyclic or tetracyclic antidepressants.

1.2 SPECIFIC SUBSTANCES

o Paroxetine

o (-)trans-4R-)4'-fluorophenyl)-3S-[(3',4'

o -methylenedioxyphenoxy)methyl]

o piperidine hydrochloride hemihydrate

1.6 AVAILABLE FORMS/SOURCES

A. FORMS

1. Paroxetine is marketed by Smith Kline Beecham with the trade name Paxil(R). Supplied as 20 milligram scored tablets.

B. USES

1. Paroxetine is a selective serotonin reuptake inhibitor (SSRI) widely used and approved for treatment of major depression, obsessive compulsive disorder, panic disorder, and social anxiety disorder.
2. Although not an approved use, paroxetine has been used for the treatment of adult night terrors (Wilson et al, 1997).

3.0 CLINICAL EFFECTS

3.1 SUMMARY OF EXPOSURE

A. Symptoms of toxicity can be delayed because paroxetine is slowly absorbed. Effects have included mild CNS depression, tremors, movement disorders, tachycardia, SIADH, anxiety and vomiting.
B. Side effects reported at therapeutic doses include blurred vision, syncope, increased and decreased blood pressure, PVCs, headache, drowsiness, insomnia, nausea, vomiting, constipation, and difficulty urinating.

3.4 HEENT

3.4.3 EYES

A. BLURRED VISION has been reported at therapeutic doses (Ohrberg et al, 1992).
B. ANISOCORIA has been reported in a patient taking paroxetine 50 milligrams daily (Barrett, 1994).
C. ACUTE ANGLE GLAUCOMA has been associated with therapeutic use of paroxetine. A direct effect on the iris or ciliary body muscle through serotoninergic or anticholinergic mechanisms is suggested (Eke & Bates, 1997).

3.5 CARDIOVASCULAR

3.5.1 SUMMARY

A. Tachycardia has been reported in overdose. Orthostatic hypotension, syncope, PVCs and minimal QRS prolongation have developed at therapeutic doses.

3.5.2 CLINICAL EFFECTS

A. TACHYCARDIA

1. Sinus tachycardia developed in one case of overdose (Boyer & Blumhardt, 1992).

B. HYPOTENSION

1. Syncope associated with a sudden fall in blood pressure and pulse developed in a 71 year-old-woman taking therapeutic doses (Lundmark et al, 1989).
2. An asymptomatic decrease in systolic blood pressure was noted in patients taking therapeutic doses of paroxetine after 4 weeks on therapy (Battegay et al, 1985).
3. Orthostatic dizziness was reported in 6 of 19 patients taking therapeutic doses (Laurson et al, 1985).

C. EXTRASYSTOLES

1. Multiple PVCs without associated symptoms developed on one patient taking therapeutic doses of paroxetine (Battegay et al, 1985).

D. ECG ABNORMAL

1. After 4 weeks at therapeutic doses QRS was prolonged by 0.004 seconds compared to baseline (Edwards et al, 1989).

3.7 NEUROLOGIC

3.7.1 SUMMARY

A. Mild CNS depression and tremors have been reported in overdose and as side effects. Sleep disturbance, extrapyramidal effects, movement disorders and EEG changes occur with therapeutic doses.

3.7.2 CLINICAL EFFECTS

A. CNS DEPRESSION

1. Mild CNS depression has been reported in overdose (Myers et al, 1994).
2. Tiredness, somnolence, lethargy, difficulty concentrating are commonly reported adverse effects (Feighner et al, 1993; Dunbar et al, 1993; Calghorn et al, 1992; Rickels et al, 1989; Laurson et al, 1985).
3. CASE REPORT - Profound psychomotor retardation developed in a mentally retarded 67-year-old woman taking paroxetine 20 milligrams/day (Lewis et al, 1993).

B. TREMOR

1. CASE SERIES - Tremor developed in 2 of 13 patients with paroxetine only overdose in one study (Myers et al, 1994).
2. Tremor is a commonly reported side effect (Dunbar et al, 1993; Feighner et al, 1993; Ohrberg et al, 1992; Claghorn et al, 1992; Dunbar, 1989; Laurson et al, 1985).

C. HEADACHE

1. Headache is reported at therapeutic doses (Ohrberg et al, 1992; Dunbar, 1989; Mertens & Pintens, 1988; Laursen et al, 1985).

D. SLEEP DISORDER

1. Sleep disturbance is common at therapeutic doses (Ohrberg et al, 1992; Claghorn et al, 1992; Laursen et al, 1985).
2. In 12 volunteers paroxetine increased the time required to achieve REM sleep, decreased the proportion of sleep spent as REM sleep, increased the number of awakenings and reduced total sleep (Oswald & Adam, 1986).

E. EXTRAPYRAMIDAL DISORDER

1. Extrapyramidal reactions, particularly dystonic reactions involving the face or mouth, appear to occur more frequently with paroxetine than with other serotonin reuptake inhibitors (Anon, 1993; Gerber & Lynd, 1998).
2. CASE REPORT - A 35-year-old woman with early-onset parkinsonism developed worsening symptoms (tremor, rigidity, postural instability) after taking paroxetine 20 milligrams/day (Jimenez-Jimenez et al, 1994). Symptoms returned to baseline after discontinuing paroxetine.

F. EEG ABNORMAL

1. At therapeutic doses paroxetine induces a decrease in delta and theta activity, and in increase in beta activity (McClelland & Raptopoulos, 1984).

G. HYPERKINESIA

1. CASE REPORT - Akathisia developed in a 63-year-old man treated with paroxetine 20 milligrams/day (Adler & Angrist, 1995). The Adverse Drug Reactions Advisory Committee has received several reports of akathisia (restlessness, constant need to pace), including one case which began 5 months after starting paroxetine and resolved on discontinuation of the drug (Anon, 1996).

H. SOMNOLENCE

1. CASE REPORT - A 38-year-old woman developed narcolepsy 4 weeks after beginning paroxetine 20 milligrams/day (Owley & Flaherty, 1994). Symptoms resolved after paroxetine was discontinued and returned when it was resumed at 10 milligrams/day.

I. DYSKINESIA

1. Orolingual movements (intermittent facial movements, initially involving the tongue and lips) have been described as an adverse effect of SSRIs, including paroxetine (Gerber & Lynd, 1998; Anon, 1996). Bruxism has also been described as an adverse effect of paroxetine (Gerber & Lynd, 1998; Romanelli et al, 1996).

3.8 GASTROINTESTINAL

3.8.1 SUMMARY

A. Nausea and vomiting have occurred with overdose and at therapeutic doses. Constipation, diarrhea, dry mouth and anorexia are reported adverse effects.

3.8.2 CLINICAL EFFECTS

A. NAUSEA VOMITING

1. Spontaneous vomiting developed in one of 13 patients with paroxetine only overdose (Myers et al, 1994). Severe vomiting has rarely been reported (Johnsen & Hoejlyng, 1998). Nausea and vomiting are commonly reported side effects (Dunbar, 1989; Martins & Pintens, 1988; Rickels et al, 1989; Dunbar et al, 1993; De Wilde et al, 1993; Bascara, 1989.)

B. DIARRHEA

1. Diarrhea is reported at therapeutic doses (Claghorn et al, 1992).
2. Paroxetine increases GI motility and reduces orocecal transit time at therapeutic doses (Gorard et al, 1994).

C. CONSTIPATION

1. Constipation is a commonly reported side effect (Dunbar et al, 1993; Claghorn et al, 1992; Rickels et al, 1989).

D. MOUTH DRY

1. Dry mouth occurs at therapeutic doses (Miller et al, 1989; Battegay et al, 1985).

E. ANOREXIA

1. Anorexia and weight loss are reported at therapeutic doses (Feighner et al, 1993; Ohrberg et al, 1992)

3.10 GENITOURINARY

3.10.2 CLINICAL EFFECTS

A. DYSURIA

1. Both urinary frequency and difficulty urinating have been reported as side effects (Feighner et al, 1993; Ohrberg et al, 1992)

B. EJACULATION DISORDER

1. Abnormal ejaculation and impotence occur more frequently than with other serotonin reuptake inhibitors (Feighner et al, 1993; Anon 1993; Claghorn et al, 1992).

C. PRIAPISM

1. CASE REPORT - A 58-year-old man developed priapism following treatment with paroxetine 20 milligrams/day (Ahmad, 1995).

3.12 FLUID-ELECTROLYTE

3.12.1 SUMMARY

A. Therapeutic and overdoses of paroxetine have resulted in SIADH and hyponatremia.

3.12.2 CLINICAL EFFECTS

A. HYPONATREMIA

1. Hyponatremia has been reported in several patients taking therapeutic doses and has been severe in some cases (Odeh et al, 1999; Goddard & Patton, 1992; Chua & Vong, 1994; Chua & Vong, 1993). An unusually rapid onset of hyponatremia, following only 3 doses, was reported in an 82-year-old female (Paul & Sankaran, 1998).

a. Five days after an acute overdose of 360 mg paroxetine, severe hyponatremia (serum sodium 112 mmol/L) occurred in an 83-year-old woman (Johnsen & Hoejlyng, 1998).

B. ANTIDIURETIC HORMONE DISORDER

1. Paroxetine may occasionally induce a syndrome of inappropriate secretion of antidiuretic hormone (SIADH) with resultant hyponatremia. Elderly patients may be more susceptible to SIADH. Cases following therapeutic paroxetine use have been reported (Monmany et al, 1999; Odeh et al, 1999; Paul & Sankaran, 1998; Van Campen & Voets, 1996).

3.13 HEMATOLOGIC

3.13.2 CLINICAL EFFECTS

A. PLATELETS ABNORMAL

1. Spontaneous ecchymosis has been reported in two patients taking therapeutic doses (Ottervanger et al, 1994). Routine coagulation studies were normal in these patients, but in one patient there was no spontaneous platelet aggregation. Spontaneous ecchymoses due to therapeutic paroxetine doses occurred in a 47-year-old patient. Discontinuation of paroxetine resulted in resolution of ecchymoses (Cooper et al, 1998).

3.14 DERMATOLOGIC

3.14.2 CLINICAL EFFECTS

A. SWEATING INCREASED

1. Increased sweating is reported as a side effect (Claghorn et al, 1992; Rickels et al, 1989; Laursen et al, 1985).

B. RASH

1. Rashes have developed during therapeutic use (Dunbar et al, 1993; Claghorn et al, 1992).

3.20 REPRODUCTIVE

3.20.2 TERATOGENICITY

A. ANIMAL STUDIES

1. Following prenatal exposure to a clinically relevant paroxetine dose in mice, NO major behavioral alterations were noted; however, heightened performance on select anxiety testing in infant offspring and on aggressive behavior in adult males were noted (Coleman et al, 1999).

3.20.3 EFFECTS IN PREGNANCY

A. PREGNANCY CATEGORY

1. Pregnancy category C (Prod Info Paxil(R), 1996).

3.20.4 EFFECTS DURING BREAST-FEEDING

A. BREAST MILK

1. Paroxetine is excreted in breast milk at concentrations similar to those found in plasma (Misri et al, 2000; Kaye et al, 1989). In 16 mother and infant serum pairs, no detectable paroxetine was found in the serum of nursing infants (Stowe et al, 2000). Nondetectable breast milk levels were evident over a 24-hour collection from a mother taking chronic paroxetine; the infant's paroxetine serum level was nondetectable (Hendrick et al, 2000).
2. A mean milk/serum concentration ratio of 0.69 was measured with a maternal dose of 20 mg/day and 0.72 with a dose of 40 mg/day. Estimated relative doses to the infant were 1.0% and 2.0%, respectively (Ohman et al, 1999). Similar results were reported in other studies (Misri et al, 2000; Begg et al, 1999).

3.23 OTHER

3.23.1 SUMMARY

A. Abrupt discontinuation of paroxetine is associated with a withdrawal syndrome.

3.23.2 CLINICAL EFFECTS

A. WITHDRAWAL SYNDROME

1. Sweating, dizziness, insomnia, headache, anxiety, fatigue, tremor, confusion and sensory disturbance have been reported after abrupt withdrawal of paroxetine (Anon, 1993; Zajecka et al, 1997). Children may experience withdrawal symptoms within a shorter time after abruptly stopping paroxetine due to their higher rate of drug metabolism (Diler et al, 2000).
2. Vertigo, nausea, vomiting, diarrhea, fatigue and gait instability have been reported in patients whose paroxetine dose was tapered over 7 to 10 days (Barr et al, 1994).
3. Other effects reported after paroxetine withdrawal include anorexia, nausea, vomiting, diarrhea, shaking chills, agitation, abdominal discomfort, and sensations like electric shocks (Frost & Lal, 1995; Phillips, 1995; Pyke, 1995).

B. DRUG INTERACTION

1. MAOI -

a. At least two weeks should elapse between switching from paroxetine to an MAOI or vice versa (Boyer & Feighner, 1992). Patients taking a serotonin reuptake inhibitor within 14 days of discontinuing an MAOI are at risk for developing hyperthermia, rigidity, myoclonus, autonomic instability, and mental status changes. While this serotonin syndrome has not yet been reported with paroxetine, patients ingesting paroxetine within 2 weeks of discontinuing MAOI therapy warrant careful monitoring.

2. CIMETIDINE -

a. Cimetidine increases the bioavailability of paroxetine by about 50%, presumably by decreasing first pass metabolism (Bannister et al, 1989).

3. NEUROLEPTIC/BENZTROPINE -

a. Two patients developed confusion and delirium after starting a combination of paroxetine, a neuroleptic and benztropine (Roth et al, 1994). The timing of the delirium suggests that the combination of fluoxetine and benztropine was responsible.

4. NEUROLEPTICS -

a. Severe dystonia and oculogyric crisis have developed when paroxetine was added to regimens of haloperidol and pimozide respectively (Budman et al, 1995; Horrigan & Barnhill, 1994).

5. TRICYCLIC ANTIDEPRESSANTS -

a. SSRIs, including paroxetine, may be able to increase circulating serum concentrations of tricyclic antidepressants to potentially toxic levels in some patients. This risk is greatest in children and adults who normally clear drugs through hepatic oxidative pathways rapidly (Popli et al, 1994).

C. SEROTONIN SYNDROME

1. Serotonin syndrome is produced most often following the concurrent use of paroxetine (an SSRI) with another drug that enhances central nervous system serotonin activity. This syndrome is characterized by alterations in cognition, behavior, autonomic nervous system function, and neuromuscular activity. The difference between serotonin syndrome and the occurrence of adverse effects due to paroxetine alone is the clustering of the signs and symptoms, their severity, and duration (Lane & Baldwin, 1997).

a. Some drugs that may enhance central nervous system serotonin activity include: moclobemide, selegiline, tramadol, nefazodone, trazodone, dextromethorphan, phentermine, fenfluramine, lithium, tryptophan, and irreversible monoamine oxidase inhibitors. Any of these drugs taken in combination with paroxetine may result in serotonin syndrome (Mitchell, 1997).

2. CASE REPORT - A 29-year-old woman developed agitation, difficulty concentrating, hyperreflexia, tremor, choreiform movements, diaphoresis, shivering, and loose stools 24 hours after paroxetine 20 milligrams/day was added to her regimen of trazodone 50 milligrams at night (Reeves & Bullen, 1995).
3. CASE REPORT - A 51-year-old man taking diltiazem, nitroglycerin, ticlopidine, piroxicam, ranitidine, diazepam and paroxetine developed serotonin syndrome two days after beginning a cold medication containing acetaminophen, doxylamine succinate, pseudoephedrine and dextromethorphan (Skop et al, 1994). Effects included hypertension, headache, confusion, tachycardia, tachypnea, shortness of breath, vomiting, increased muscle tone, rigidity, clonus, and a metabolic acidosis.

a. Clinical presentation was felt to be due to serotonin syndrome which was most likely induced by the combination of paroxetine and dextromethorphan.

4. CASE REPORT - An acute overdose of paroxetine and moclobemide resulted in a severe case of serotonin syndrome in a 28-year-old male. Muscular rigidity, resulting in respiratory distress, and hypotension (BP 80/50 mmHg) necessitated muscular paralysis. The patient improved following symptomatic therapy (FitzSimmons & Metha, 1999).
5. CASE REPORT - Serotonin syndrome was reported in a 51-year-old who started paroxetine 2 days after stopping nefazodone, after a tapering period. A repeat challenge with paroxetine at 7 days post-nefazodone dosing did not result in recurrence of serotonin syndrome (John et al, 1997).

4.0 LABORATORY/MONITORING

4.1 MONITORING PARAMETERS/LEVELS

4.1.2 SERUM/BLOOD

A. Monitor serum electrolytes in symptomatic patients. Paroxetine levels are not widely available or clinically useful.

4.1.4 OTHER

A. Institute continuous cardiac monitoring and obtain ECG.

4.3 METHODS

A. CHROMATOGRAPHY

1. A method for determining the concentrations of paroxetine and metabolites in biologic fluids using column switching HPLC with UV detection has been described (Hartter et al, 1994).
2. An analytical method is available to isolate SSRIs by liquid/liquid extraction at alkaline pH in n-butyl chloride, and analyze by gas chromatography/mass spectrometry (GC/MS). This method is suitable for quantitation of paroxetine and is linear over the range 0.01 to 10.00 mg/L (Goeringer et al, 2000).

5.0 ABSTRACTS

5.1 CASE REPORTS

A. ADULT

1. A 25-year-old man ingested 400 milligrams of paroxetine without serious sequelae. He was treated with activated charcoal and sorbitol and observed for 4 hours (6 hours after ingestion). He experienced no adverse effects other than anxiety (Gorman et al, 1993).

5.2 CASE SERIES

A. ADVERSE EFFECTS

1. In a series of 14 overdose patients ingesting paroxetine alone, 8 patients were asymptomatic, 2 were drowsy, 2 developed tremors and 1 had spontaneous vomiting (Myers et al, 1994). Of 22 patients with coingestants 16 were drowsy and the remainder had symptoms consistent with the coingestants. The amount of paroxetine ingested ranged from 10 to 1000 mg (mean 354 mg).

6.0 TREATMENT

6.1 LIFE SUPPORT

A. Support respiratory and cardiovascular function.

6.3 PATIENT DISPOSITION

6.3.1 DISPOSITION/ORAL EXPOSURE

6.3.1.1 ADMISSION CRITERIA/ORAL

A. Admit patients who have ingested large amounts of paroxetine, those who develop clinical signs (including tachycardia or lethargy), or who have ingested overdoses of paroxetine along with other drugs with significant toxicity (particularly MAOIs).

6.5 ORAL EXPOSURE

6.5.1 PREVENTION OF ABSORPTION/PREHOSPITAL

A. EMESIS/NOT RECOMMENDED -

1. EMESIS: Ipecac-induced emesis is not recommended because of the potential for CNS depression and seizures.

B. ACTIVATED CHARCOAL -

1. PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION

a. Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion.

(1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should be administered by medical or paramedical personnel capable of airway management to prevent aspiration in the event of spontaneous emesis.

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; and 1 gram/kilogram in infants up to 1 year old (USP DI, 2000; Chyka & Seger, 1997).

(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 (Barceloux et al, 1997).

b. ADVERSE EFFECTS/CONTRAINDICATIONS

(1) Complications: emesis, aspiration (Chyka & Seger, 1997). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
(2) Contraindications: unprotected airway, gastrointestinal tract not anatomically intact, therapy may increase the risk or severity of aspiration; ingestion of most hydrocarbons (Chyka & Seger, 1997).

6.5.2 PREVENTION OF ABSORPTION

A. GASTRIC LAVAGE

1. INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).

a. Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.

2. PRECAUTIONS:

a. SEIZURE CONTROL: Is mandatory prior to gastric lavage.
b. AIRWAY PROTECTION: Alert patients - place in Trendelenburg and left lateral decubitus position, with suction available. Obtunded or unconscious patients - cuffed endotracheal intubation.

3. LAVAGE FLUID:

a. Use small aliquots of liquid. Lavage with 150 to 200 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in children over 5 or adults) and 10 milliliters/kilogram body weight of normal saline in young children. Continue until lavage return is clear.
b. The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
c. CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.

4. COMPLICATIONS:

a. Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications.
b. Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).

5. CONTRAINDICATIONS:

a. Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.