Paraquat treatment - MICROMEDEX®

6/27/2016 Toxicology details MICROMEDEX®

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PARAQUATPOISINDEX® Managements

TREATMENT

ORAL EXPOSURE

6.5.1) PREVENTION OF ABSORPTION/PREHOSPITALA) EMESIS/NOT RECOMMENDED1) Inducing emesis is NOT recommended.

B) ACTIVATED CHARCOAL1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATIONa) Consider prehospital administration of activated charcoal as an aqueous slurry in patientswith a potentially toxic ingestion who are awake and able to protect their airway. Activatedcharcoal is most effective when administered within one hour of ingestion. Administration inthe prehospital setting has the potential to significantly decrease the time from toxiningestion to activated charcoal administration, although it has not been shown to affectoutcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002). 1) In patients who are at risk for the abrupt onset of seizures or mental status depression,activated charcoal should not be administered in the prehospital setting, due to the risk ofaspiration in the event of spontaneous emesis.

2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activatedcharcoal improves the palatability for children and may facilitate successful administration(Guenther Skokan et al, 2001; Dagnone et al, 2002).

2) CHARCOAL DOSEa) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimumdose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1gram/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 noevidence that cathartics reduce drug absorption and cathartics are known to cause adverseeffects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionallyhypotension (None Listed, 2004).

b) ADVERSE EFFECTS/CONTRAINDICATIONS1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated byacute 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 ACTIVATEDCHARCOAL/TREATMENT management for further information.

2) Contraindications: unprotected airway (increases risk/severity of aspiration) ,nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of mosthydrocarbons (Chyka et al, 2005).

C) DERMAL EXPOSURE1) Remove contaminated clothing and wash the exposure area thoroughly with soap andwater.

6.5.2) PREVENTION OF ABSORPTIONA) GASTRIC EMPTYING



1) Inducing emesis is NOT recommended. Gastric lavage may be useful when performedwithin one hour of ingestion, although some authors advocate its use up to 24 hours afteringestion (Huang et al, 2005). Because paraquat is a liquid a small nasogastric tube may beused. Risk of bleeding or perforation must be weighed against potential benefit of paraquatremoval. Administer activated charcoal or clays (Fuller's Earth; Bentonite).

B) ACTIVATED CHARCOAL1) Paraquat irreversibly binds to clays and activated charcoal. Activated charcoal should beadministered if the ingestion is within the last 24 hours and the patient is alert or the airwayis protected. 2) CHARCOAL ADMINISTRATIONa) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka etal, 2005). Administer charcoal as an aqueous slurry; most effective when administered withinone hour of ingestion.

3) CHARCOAL DOSEa) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimumdose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1gram/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 noevidence that cathartics reduce drug absorption and cathartics are known to cause adverseeffects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionallyhypotension (None Listed, 2004).

b) ADVERSE EFFECTS/CONTRAINDICATIONS1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated byacute 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 ACTIVATEDCHARCOAL/TREATMENT management for further information.

2) Contraindications: unprotected airway (increases risk/severity of aspiration) ,nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of mosthydrocarbons (Chyka et al, 2005).

4) One animal study (Gaudreault et al, 1985) demonstrated increased efficacy of activatedcharcoal combined with magnesium citrate. C) CLAYS 1) BENTONITE CLAY: DOSE: ADULT: 100 to 150 g; CHILD less than 12 years of age: 2 g/kg(7% suspension) (Bronstein, 2004)2) FULLER'S EARTH: DOSE: ADULT: 100 to 150 g; CHILD less than 12 years of age: 2 g/kg(30% suspension) (Bronstein, 2004).3) EXPERIMENTAL THERAPY: SODIUM POLYSTYRENE SULFONATEa) CONCLUSION: Additional studies are needed before the use of SPS can be recommended.b) The dose of SPS used in these studies was excessive compared to the dose used to treathyperkalemia. c) The survival data in the only trial in humans is not impressive. No details were providedon the actual cause of death in the 16 patients who died despite aggressive treatment withSPS and cathartics. d) Sodium polystyrene sulfonate (SPS) (Kayexalate(R)) has been reported to have anadsorption capacity for paraquat 15 times greater than activated charcoal and 6 timesgreater than adsorption in vitro. The LD50 in rats increased from 144 mg/kg to 296 mg/kgwhen sodium polystyrene sulfonate (1,000 milligrams/kilogram) was instilled into thestomach a few minutes after the paraquat (Takagi et al, 1983). There were only 8 rats ineach study group. e) The effect of time between paraquat and sodium polystyrene sulfonate administration wasexamined in another study in rats. These animals were given 2 grams/kilogram of SPS at 0,0.5, 1, 2, 3, and 4 hours after 200 mg/kg of paraquat. When survival was used as a measure



0.5, 1, 2, 3, and 4 hours after 200 mg/kg of paraquat. When survival was used as a measureof efficacy, 7 of 8 rats survived for 7 days when SPS was administered immediately after theparaquat, however, only 3 of 8 rats survived for 7 days when SPS administration was delayeduntil 4 hours after paraquat administration (Yamashita et al, 1987).

f) Yamashita et al (1987) used SPS in 22 patients with paraquat poisoning and reportedsurvival in only 6 of 22 patients. There were no details on the severity of poisoning in anypatients and the time elapsed between ingestion and treatment. The following protocol wasused:

1) Gastric lavage was performed using 5 to 10 liters of normal saline containing 100grams/Liter of SPS.

2) Intestinal lavage was performed by placing a duodenal tube under xray examination andadministering 600 to 800 milliliter/hour of normal saline solution containing 100 grams/Literof SPS.

3) Magnesium sulfate, magnesium citrate, or sorbitol was administered every 4 hours toinduce catharsis.

D) WHOLE BOWEL IRRIGATION (WBI)1) Whole bowel irrigation has NOT been shown to be of any benefit in paraquat poisoning(Meredith & Vale, 1995).

6.5.3) TREATMENTA) AIRWAY MANAGEMENT1) Airway management should be considered for patients with severe CNS depression orthose at risk of aspiration.

2) OXYGEN THERAPY: Do NOT administer supplemental oxygen(Rhodes et al, 1976). Someclinicians advocate hypoxic (10% to 12%) atmospheres. Allow additional oxygen only invictims considered beyond rescue to relieve air hunger and terminal disease.

B) MONITORING OF PATIENT1) A full laboratory analysis, including liver function tests, basic metabolic panel, completeblood count, chest xray and urinalysis, should be performed on anyone ingesting paraquat.Arterial blood gas analysis should be performed on those with a late presentation or thosewith hypoxia. Those with chronic dermal exposures and systemic symptoms or those withhypoxia. Those with chronic dermal exposures and systemic symptoms should have the sametesting as those acute ingestions. No testing is indicated in patients with acute dermalexposures without systemic symptoms.

2) Bedside testing can be performed using a 1% aqueous sodium dithionite in 0.1 normalsodium hydroxide to form a stable blue radical in the urine. If paraquat is present, the urinewill appear blue compared with the control (another urine sample).

3) Serum paraquat concentrations (information available 24 hours a day 7 days a weekthrough Zeneca Emergency Information Network, 18003278633,[email protected]) can be useful for prognosis.

C) FLUID/ELECTROLYTE BALANCE REGULATION1) Replace fluid and electrolytes lost from vomiting or catharsis.

D) ACUTE TUBULAR NECROSIS1) Acute tubular necrosis is almost always reversible. Adequate fluid resuscitation is primarytherapy to limit secondary renal injury. Hemodialysis for oliguric renal failure is occasionallyneeded as a temporizing measure until renal function improves.

E) IMMUNOSUPPRESSIVE THERAPY1) SUMMARYa) The combination of corticosteroids and cyclophosphamide have been shown in 2, small,randomized controlled studies to reduce mortality in severe paraquat poisoning (Lin et al,2006; Afzali & Gholyaf, 2008).

b) COCHRANE REVIEW: In a systematic review, patients with paraquatinduced lung fibrosisgiven standard therapy (eg, decontamination, hemoperfusion) and steroids andcyclophosphamide had a reduced risk of death of 28% (range: 11% to 41% reduction in



cyclophosphamide had a reduced risk of death of 28% (range: 11% to 41% reduction indeaths; RR 0.72; 95% Confidence Interval (CI) 0.59 to 0.89) compared to patients treatedwith standard therapy alone. The review was based on 3 small randomized control trials(RCTs) and included 164 patients with moderate to severe paraquat poisoning. The findingsshould be interpreted with caution because the studies were small and one was of poormethodological quality. Further randomized controlled trials were suggested by the authors(Li et al, 2012).

c) The use of immunosuppressive therapy is limited and large, adequately controlledrandomized trials have not been conducted. In one uncontrolled study, no survival benefitwas observed with the use of cyclophosphamide and dexamethasone (Gunawardena et al,2007).

2) PULSE THERAPYa) PULSE THERAPY PROTOCOL: The protocol used in one study was as follows (Lin et al,2006):

b) Gastric lavage followed by administration of 1 gram/kilogram of activated charcoal in 250milliliters of magnesium citrate in patients presenting within 24 hours of ingestion.

c) Two 8 hours courses of activated charcoal hemoperfusion within 24 hours of paraquatingestion.

d) After hemoperfusion, administer intravenous cyclophosphamide 15milligrams/kilogram/day in 200 ml D5NS infused over 2 hours for two consecutive days. Alsoadminister 1 gram methylprednisolone in 200 milliliters D5NS infused over 2 hours daily for 3consecutive days.

e) After the initial pulse therapy, administer dexamethasone 5 milligrams intravenously every6 hours until PaO2 is 80 mmHg (11.5 kPa) or greater.

f) If PaO2 < 60 mmHg (8.64 kPa), repeat intravenous methylprednisolone 1 gram in 200milliliters D5NS infused over 2 hours daily for 3 consecutive days. If WBC > 3000/m(3) and ithas been 2 weeks since the initial pulse of cyclophosphamide, repeat intravenous infusion ofcyclophosphamide 15 milligrams/kilogram in 200 milliliters D5NS infused over 2 hours as asingle dose.

g) Then continue intravenous dexamethasone 5 milligrams every 6 hours until PaO2 is 80mmHg (kPa 11.5) or greater. Then reduce dexamethasone dose gradually.

3) ALTERNATIVE THERAPIESa) Other treatment methods have included the following: 1) Highdose therapy includes the same initial treatment (activated charcoal andhemoperfusion) as pulse therapy along with highdose cyclophosphamide (5 mg/kg/d) anddexamethasone 24 mg/d for 14 days. However, this treatment remains controversial due toa lack of proven efficacy (Lin et al, 1999). Another study used a slightly different high dosetherapy using cyclophosphamide 100 mg/day orally and 15 mg/day of IV dexamethasone for14 days (Hsu et al, 2003).

2) Another method includes early decontamination and 15 mg/kg of cyclophosphamide inD5NS in 200 mL infused over 2 hrs for 2 days and methylprednisolone 1 g in 200 mL D5NSIV infused over 4 hrs and repeated for 3 consecutive days. Mesna (15 mg/kg) was alsoadministered over 4 days to avoid side effects to cyclophosphamide (Li et al, 2012).

4) EVIDENCEa) POSITIVE STUDY: A prospective randomized controlled trial evaluated 23 paraquatpoisoned patients with greater than 50% and less than 90% predictive mortality. The controlgroup (n=7) received conventional therapy and the study group (n=16) received the novelrepeated pulse treatment with longterm steroid therapy [methylprednisolone 1 g/day for 3days, cyclophosphamide 15 mg/kg/day for 2 days, and then dexamethasone 20 mg/day untilPaO2 was greater than 11.5 kPa (80 mm Hg) and repeated pulse therapy withmethylprednisolone 1 g/day for 3 days and cyclophosphamide 15 mg/kg/day for 1 day,repeated if PaO2 was less than 8.64 kPa (60 mm Hg)]. The mortality rate of the study groupwas lower than that of the control group (5 of 16, 31.3% of study group vs 6 of 7, 85.7% ofcontrol group; p=0.0272) (Lin et al, 2006).

b) POSITIVE STUDY: A dramatic fall (68%: 41/61 cases compared to 28%: 20/72 cases) inmortality of paraquat poisoning was indicated by the combination therapy or treatment for 2



mortality of paraquat poisoning was indicated by the combination therapy or treatment for 2weeks with high doses of two immunosuppressants, dexamethasone and cyclophosphamide,and standard therapy to inactivate and eliminate the poison from gut and blood. Not all caseswere confirmed by serum paraquat levels (Addo & PoonKing, 1986).

c) POSITIVE STUDY: In a retrospective study of 29 cases of paraquat poisoning, therapywith cyclophosphamide, dexamethasone, furosemide and vitamins B and C was associatedwith survival of 1 out of 11 patients ingesting <45 milliliters of 20% paraquat whileconventional therapy (gastric decontamination and supportive care) was associated withsurvival in 0 of 6 patients (Botella de Magila & Tarin, 2000).

d) POSITIVE STUDY: In a prospective study of paraquat poisoning, use of cyclophosphamideand corticosteroids was associated with survival in 18 of 22 patients with moderate poisoningcompared with 12 of 28 controls with moderate poisoning (Lin et al, 1999). No patientspresenting with fulminant poisoning survived in either treatment group. When these data arereanalyzed on an intention to treat basis, this effect loses statistical significance (18 survivorsof 56 patients in the treatment group vs 12 survivors of 65 control patients) (Buckley, 2001).

e) NEGATIVE STUDY: A prospective, nonrandomized study of paraquat poisoning treatedwith standard therapy (lavage, bentonite, magnesium sulfate, metoclopramide; 14 cases) orstandard therapy plus dexamethasone/cyclophosphamide (33 cases) found no difference insurvival between groups. Complications of immunosuppressant therapy included septicemia(2 cases), alopecia (9 cases), and acne (8 cases) (Perriens et al, 1992).

f) METAANALYSIS: A metaanalysis of 10 clinical studies (1 randomized clinical trial and 9nonrandomized studies) was conducted to determine the effectiveness of immunosuppressivetherapy for treatment of paraquatinduced lung fibrosis. The results of the metaanalysiswere inconclusive due to various confounding factors of each study (Eddleston et al, 2003).

F) ACETYLCYSTEINE1) Cotgreave et al (1987) demonstrated that the combination of Ebselen (PZ51:2phenyl1,2benzoisoselenazol3(H)one) and Nacetylcysteine may provide an effective antidote in casesof overexposure to paraquat through an in vitro study using isolated hepatocytes, but this hasNOT been established clinically.

2) Drault et al (1999) reported a patient who survived the ingestion of 60 g of paraquat aftertreatment with IV Nacetylcysteine and early hemodialysis (within 4 hours of ingestion). G) TRANSPLANT1) LUNG TRANSPLANTATION: Lung transplants, both single and bilateral, have beenperformed in several patients who ingested toxic amounts of paraquat. Many patients dieddespite transplant (Toronto Lung Transplant Group, 1985; Kamholz et al, 1984; Cooke et al,1973). Occasional survival has since been reported (Licker et al, 1998; Walder et al, 1997).

H) EXTRACORPOREAL MEMBRANE OXYGENATION1) CASE REPORT: A 23yearold man presented to a local ED after inadvertently ingesting amouthful of paraquat 20% (about 6 to 10 g). He immediately induced vomiting afteringestion. On admission, his paraquat concentrations in serum and urine were 2.12 mg/L and350 mg/L, respectively, indicating a lethal dose. Despite decontamination with a gastriclavage and activated charcoal, he developed acute nonoliguric kidney injury within 48 hoursand was transferred to a tertiary care center. His physical examination showed mild jaundiceand swelling and redness of the throat while his laryngoscopy revealed redness and necrosesof the hypopharynx, epiglottis, and vocal cords. Laboratory results revealed elevated liverenzymes, mildly elevated inflammatory markers and acute kidney injury. He underwenthemodialysis and received IV methylprednisolone and cyclophosphamide to delay thedevelopment of pulmonary fibrosis. In addition, he received tamoxifen (3 x 20 mg orally) dueto its antiproliferative and antiinflammatory effects in retroperitoneal fibrosis. About 72 hourspostingestion, his condition deteriorated and he developed respiratory failure, necessitatingoxygen supplementation. On day 9, invasive ventilation was required due to the progressionof pulmonary fibrosis. He was placed on a high urgency lung transplantation list; however, hiscondition continued to deteriorate with the onset of systemic inflammatory responsesyndrome. On day 12, an extracorporeal membrane oxygenation (ECMO) was implemented,but despite further supportive care, he developed hemodynamic instability and septicmultiorgan dysfunction with kidney, liver, and hemodynamic failure. The patient died 32 days



multiorgan dysfunction with kidney, liver, and hemodynamic failure. The patient died 32 dayspostingestion from cardiac failure with pulseless electrical activity (Bertram et al, 2013).

2) CASE REPORT: A 24yearold woman with a history of chronic hepatitis B and depressionpresented to a local ED about 2 hour after ingesting about 50 mL of 20% of paraquat (about188 mg/kg). Despite supportive care, including gastric lavage, activated charcoal,cyclophosphamide, methylprednisolone, and hemoperfusion (3 sessions), her symptoms didnot improve significantly. On day 2, she developed elevated liver enzymes, renal insufficiency,pulmonary fibrosis, and severe respiratory failure. Her condition gradually deteriorated and onday 44, she underwent venovenous extracorporeal membrane oxygenation (ECMO) as abridge to lung transplantation. She received a bilateral sequential lung transplantation on day56. Following further supportive care, including respiratory and physical rehabilitation, hercondition gradually improved and she was discharged on day 80 (Tang et al, 2015).

I) PROLONGED QT INTERVAL1) In a retrospective study, the prognostic value of QTc prolongation in severely paraquatpoisoned patients was evaluated. Overall, 53 nonsurvivors and 7 survivors were included inthe study. QTc intervals ranged from 0.35 to 0.48 seconds and 0.32 to 0.63 seconds in thesurvivor and nonsurvivor groups, respectively. One (14.3%) survivor and 32 (60.4%) nonsurvivors had a QTc of 0.45 seconds or higher, with a median survival time of 26 hours; 50%of these patients died within 1 day. QTc of less than 0.45 seconds was observed in 6 (85.7%)survivors and 21 (39.6%) nonsurvivors, with a median survival time of 95 hours. It wasconcluded that QTc prolongation can be a useful prognostic factor for predicting the severityof poisoning and mortality risk in acute paraquatpoisoned patients. In addition, QTcprolongation of greater than 45 msec predicted mortality regardless of potassiumconcentration (Lin et al, 2014).

J) EXPERIMENTAL THERAPY1) Nonsteroidal antiinflammatory agents, colchicine, collagen synthesis inhibitors,deferoxamine, or total exclusion from external respiration may prevent lung fibrosis. However,the efficacy of these treatments has yet to be established in the treatment of human paraquatpoisonings (Bismuth et al, 1990; Shahar et al, 1989; Akahori & Oehme, 1983; Vincken et al,1981; Pasi, 1978; Fogt & Zilker, 1989; Jaeger et al, 1995; Pond, 1990). 2) GLUCOCORTICOID WITH CYCLOPHOSPHAMIDE: In 3 small randomized controlled trials ofpatients (n=164) with moderate or severe paraquat poisoning, the use of glucocorticoid andcyclophosphamide with standard care was beneficial in treating patients with paraquatinduced lung fibrosis. Overall, the risk of death in patients receiving this combination wasreduced by 28% (statistically estimated likely range of reduced deaths from 41% to 11%) ascompared with patients receiving just standard care (Li et al, 2012). 3) L'Heureux et al (1995) reported the survival of a man who ingested 50 to 60 mL of aparaquatcontaining solution and benzodiazepine tablets. Treatment included earlydecontamination, hemodialysis, 100 mg deferoxamine/kg in 24 hours, and 300 mgacetylcysteine/kg/day for a 3 week period. Reversible, acute renal failure and mild hepaticenzyme elevation occurred. Pulmonary effects were limited. Fibrosis did not occur (L'Heureuxet al, 1995). 4) Paraquatspecific IgG and Fab fragments have reduced cellular uptake of paraquat byisolate rat alveolar type II cells (Chen et al, 1994). 5) High molecularweight polyvinyl sulfate (PVP) or polyvinyl sulfonate (PVS), as well as lowmolecular weight alkylsulfonates, resulted in 100% survival of mice given paraquat dichlorideat 200 mg/kg (Tsuchiya et al, 1995). a) The mechanism of their protection appears to be prevention of paraquat absorption fromthe intestine. The low molecular weight alkyldisulfonates also inhibited the formation ofpulmonary lipid peroxides.

6) NITRIC OXIDE INHALATION: Nitric Oxide (NO) is a vasodilating gas that has been usedsuccessfully to increase the pO2 in patients with adult respiratory distress syndrome (ARDS)(Bismuth, 1995). a) NO inhalation did improve the pO2 and stabilized the pulmonary status for three days inone patient with acute paraquat poisoning (Koppel et al, 1994).

b) While still experimental, in serious paraquat poisoning cases, NO inhalation to maintain



b) While still experimental, in serious paraquat poisoning cases, NO inhalation to maintaintissue oxygenation in anticipation of lung transplantation once all absorbed paraquat hasbeen eliminated deserves further study.

7) SIROLIMUS: A man ingested approximately 120 mL of Gramoxone Inteon(R) anddeveloped diffuse pulmonary fibrosis and pneumomediastinum about 12 days after exposureand was started on sirolimus to limit further pulmonary fibrosis. Therapy was continued for 15days. Sirolimus, a triene macrolide immunosuppressant, has antiproliferative effects onfibroblasts and on lymphoid and nonlymphoid tumor cells. Other agents includedcyclophosphamide, methylprednisolone and dexamethasone. The patient gradually improvedand his oxygen saturation increased to 90% on 2 liters of oxygen by hospital day 39(Barrueto et al, 2008). The authors suggested that sirolimus along with the other concomitanttherapies were responsible for halting the progression of paraquatinduced pulmonaryfibrosis. 8) SURFACTANT THERAPY: Exogenous surfactant did improve lung function for several hoursin paraquat poisoned rats (So et al, 1998). No human data was located at the time of thisrevision. 9) HIGHDOSE VITAMIN C: In one study, the administration of highdose vitamin C, incombination with antiinflammatory and immunosuppressant agents, was effective inpreventing acute renal injury in patients with paraquat poisoning (an average ingestion of134.1 +/ 126.3 mL of 24.5% liquid paraquat; serum paraquat concentration of 30.8 +/ 45.5mcg/mL). Fiftyseven patients received pulse therapy (cyclophosphamide andmethylprednisolone, then dexamethasone) for 2 weeks and 77 patients received the samepulse therapy with highdose vitamin C for 2 weeks. A significant decrease in the incidence ofparaquatinduced acute renal injury was observed in the highdose vitamin C group. Inaddition, the use of vitamin C with pulse therapy was significantly associated with anincreased survival of the patients (Moon & Chun, 2010).

Last Modified: April 12, 2016

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Paraquat treatment - MICROMEDEX®