a) Abnormal ocular movements, nystagmus, miosis, and diplopia have been reported after ingestions (Park et al, 2013; Ohtake et al, 2001; Koyama, 1995; Oyanagi et al, 1993; Ishizawa et al, 1992).

a) CASE REPORT: A 34-year-old man presented to the ED after intentionally ingesting 150 mL of glufosinate ammonium. Gastric lavage was performed 1 hour after ingestion and about 5 hours after ingestion hemodialysis was performed for 2 hours. Despite these interventions, 11 hours after exposure the patient became stuporous and was transferred to a higher level of care. Initial vital signs and diagnostic and laboratory studies were normal. Twelve hours after ingestion, the patient developed a sudden increase in bronchial secretions, hypoxia and CO2 retention requiring immediate intubation and mechanical ventilation. Lipid emulsion therapy (a loading dose followed by an infusion) was initiated. By day 2, the patient remained drowsy. Hemoperfusion was added for ongoing management. During the same day, the patient developed tonic-type seizure activity and was treated with lorazepam. By day 5, the patient was successfully extubated and had a new complaint of double vision; ophthalmologic examination revealed evidence of bilateral sixth cranial nerve palsy. Diplopia and nystagmus gradually improved over several days. The patient was discharged on day 11 without any ophthalmologic abnormalities and no permanent sequelae (Park et al, 2013).

a) Glufosinate ammonium induced no eye sensitization when tested in rabbits (Ebert et al, 1990).

a) Circulatory failure may occur. In fatal cases, death occurs from circulatory failure 1 to 3 days after ingestion (Bergmann et al, 2000; Watanabe & Sano, 1998; Hashimoto et al, 1994). Decreased total vascular resistance with an increase or a decrease in cardiac output is reported in human oral poisonings (Koyama et al, 1997). Anionic surfactants, which are contained in varying quantities in some glufosinate-based herbicides, are suspected to be contributory to the cardiovascular effects (Koyama, 1999).
b) CASE REPORT: A 64-year-old man was reported with a blood pressure of 70/0 mmHg, no detectable pulse, and no audible heart tones following an intentional ingestion of approximately 33.3 grams glufosinate ammonium. His central venous pressure, while on a respirator, was 9 cmH2O (normal range, 4 to 8 cmH2O). Blood pressure returned to normal 5 hours after receiving IV fluids and dopamine (Watanabe & Sano, 1998).
c) CASE REPORT: At 27 hours after ingestion of glufosinate, a 66-year-old woman experienced sudden decrease in blood pressure and apnea, which quickly resolved. At 44 hours she experienced restlessness and high blood pressure followed suddenly by hypotension. She died 50 hours postingestion (Hashimoto et al, 1994).
d) CASE REPORT: A 58-year-old woman intentionally ingested 250 mL of Basta(R) (18.5% GLA, 30% sodium polyoxyethylene alkylether sulfate (as a surfactant)) and developed irritability and vomiting. Upon admission (5 hours after ingestion), the patient was alert with normal vital signs. Arterial blood gas analysis revealed mild respiratory alkalosis. Despite supportive care, she developed confusion 4 hours later and her spontaneous respiration deteriorated. She also developed hypotension (BP 60/40 mm Hg). Seizure activity (tonic-clonic) developed on day 2. By day 3, her vital signs and mental status had started to clinically improve. However, she developed a new onset of ventricular tachycardia on day 7 and died (Lee et al, 2009).

a) Tachycardia has been reported as a delayed effect following ingestions (Ishizawa et al, 1992).
b) CASE REPORT: A 58-year-old woman intentionally ingested 250 mL of Basta(R) (18.5% GLA, 30% sodium polyoxyethylene alkylether sulfate (as a surfactant)) and developed irritability and vomiting. Upon admission (5 hours after ingestion), the patient was alert with normal vital signs. Arterial blood gas analysis revealed mild respiratory alkalosis. Despite supportive care, she developed confusion 4 hours later and her spontaneous respiration deteriorated. She also developed hypotension (BP 60/40 mm Hg). Seizure activity (tonic-clonic) developed on day 2. By day 3, her vital signs and mental status had started to clinically improve. However, she developed a new onset of ventricular tachycardia on day 7 and died (Lee et al, 2009).

a) Bradycardia with hypotension and seizures has been reported on the second day following a suicidal ingestion (Ishizawa et al, 1992).
b) CASE REPORT: A 41-year-old woman intentionally ingested 30 to 50 mL of a herbicide containing 14% glufosinate. Somnolence and bradycardia (40 beats/min) developed 17 hours after ingestion. The patient's condition continued to deteriorate, necessitating intubation 32 hours after admission, and bradycardia persisted with rates of 40 to 45 beats/min. A self-limiting episode of ventricular tachycardia occurred 60 hours postingestion. She was extubated 48 hours after intubation and made a full recovery, but sinus bradycardia (less than 60 beats/min) persisted through day 8 (Lluis et al, 2008).

a) No change in blood pressure or heart rate was reported when glufosinate ammonium was fed to anesthetized rats. In contrast, when high doses of the anionic surfactant contained in Basta(R) was administered to rats, a decrease in blood pressure and marked drop in heart rate was reported (Koyama et al, 1997).

a) Respiratory failure, developing 8 to 32 hours after ingestion, is reported as a delayed effect of glufosinate poisoning (Park et al, 2013; Lluis et al, 2008; Bergmann et al, 2000; Koyama et al, 2000; Tanaka et al, 1998; Koyama, 1995; Koyama et al, 1994; Koyama, 1993; Kubo et al, 1993; Hirose et al, 1992; Ishizawa et al, 1992).
b) CASE SERIES: In a retrospective observational case series of 16 adults with an intentional glufosinate only ingestions, patients that developed severe effects were more likely to be associated with 2 or more positive SIRS (systemic inflammatory response syndrome) criteria. The criteria consists of the following: elevated body temperature, increased heart rate and respirations or a PaCO2 of less than 32 mm Hg; a white blood cell count of greater than 12000 cu mm or less than 4000/cu mm or 10% immature bands. In the case of respiratory events, a low P/F ratio (PaO2/FiO2) was significantly associated with severe respiratory complications. A P/F ratio of 300 or less, but more than 200 were consistent with mild respiratory distress; 200 or less, but more than 100 was equal to moderate distress; and less than or equal to 100 was equal to severe respiratory distress. Of the 8 patients that developed severe respiratory distress, 8 had a median P/F ratio of 287.5 (range 71 to 523) compared to the non-severe group with a P/F ratio of 409 (range, 216 to 533) (Inoue et al, 2013).
c) CASE REPORT: A 34-year-old man presented to the ED after intentionally ingesting 150 mL of glufosinate ammonium. Gastric lavage was performed 1 hour after ingestion and about 5 hours after ingestion hemodialysis was performed for 2 hours. Despite these interventions, 11 hours after exposure the patient became stuporous and was transferred to a higher level of care. Initial vital signs and diagnostic and laboratory studies were normal. Twelve hours after ingestion, the patient developed a sudden increase in bronchial secretions, hypoxia and CO2 retention requiring immediate intubation and mechanical ventilation. Lipid emulsion therapy (a loading dose followed by an infusion) was initiated. By day 2, the patient remained drowsy. Hemoperfusion was added for ongoing management. During the same day, the patient developed tonic-type seizure activity and was treated with lorazepam. By day 5, the patient was successfully extubated and had a new complaint of double vision; ophthalmologic examination revealed evidence of bilateral sixth cranial nerve palsy. Diplopia and nystagmus gradually improved over several days. The patient was discharged on day 11 without any ophthalmologic abnormalities and no permanent sequelae (Park et al, 2013).
d) CASE REPORT: Respiratory failure, developing several hours after ingesting glufosinate, occurred in a 44-year-old woman. Respirations improved after 2 days of intubation with controlled ventilation (Yoshida, 1997).
e) CASE REPORT: Transient respiratory arrest was reported in a 59-year-old woman about 9 hours following ingestion of glufosinate. Artificial ventilation was begun, and she was extubated on the eighth day (Koyama et al, 1994).
f) CASE SERIES: Respiratory failure, requiring intubation, along with neurotoxicity, seizures and hyperammonemia, developed in 7 of 13 patients from acute ingestion of glufosinate-ammonium herbicide(Kyong et al, 2011)
g) CASE SERIES: Two of 4 patients ingesting over 100 mL of Basta(R), experienced sudden respiratory suppression requiring assisted ventilation about 20 hours after the ingestion (Hirose et al, 1996).
h) CASE REPORT: Respiratory failure and hypotension developed suddenly 27 hours postingestion of an herbicide containing glufosinate in a 66-year-old woman (Hashimoto et al, 1994).
i) CASE REPORT: Respiratory arrest was reported at 10 hours postingestion of 500 mL of an herbicide containing 18.5% glufosinate in an adult (Shinohara et al, 1997).

a) Lingual and laryngeal edema, sufficient to prevent endotracheal intubation, have been reported after ingestion (Koyama, 1995).

a) Decreased levels of consciousness are common shortly following ingestions. Following a latent period of 8 to 30 hours, coma may rapidly develop (Park et al, 2013; Mao et al, 2011; Koyama et al, 2000; Watanabe & Sano, 1998; Shinohara et al, 1997; Yoshida, 1997; Koyama, 1995; Koyama, 1993; Hirose et al, 1992; Ishizawa et al, 1992). Coma may persist for several days (Shinohara et al, 1997).
b) CASE REPORT: A 34-year-old man presented to the ED after intentionally ingesting 150 mL of glufosinate ammonium. Gastric lavage was performed 1 hour after ingestion and about 5 hours after ingestion hemodialysis was performed for 2 hours. Despite these interventions, 11 hours after exposure the patient became stuporous and was transferred to a higher level of care. Initial vital signs and diagnostic and laboratory studies were normal. Twelve hours after ingestion, the patient developed a sudden increase in bronchial secretions, hypoxia and CO2 retention requiring immediate intubation and mechanical ventilation. Lipid emulsion therapy (a loading dose followed by an infusion) was initiated. By day 2, the patient remained drowsy. Hemoperfusion was added for ongoing management. During the same day, the patient developed tonic-type seizure activity and was treated with lorazepam. By day 5, the patient was successfully extubated and had a new complaint of double vision; ophthalmologic examination revealed evidence of bilateral sixth cranial nerve palsy. Diplopia and nystagmus gradually improved over several days. The patient was discharged on day 11 without any ophthalmologic abnormalities and no permanent sequelae (Park et al, 2013).
c) CASE REPORT: Yoshida et al (1997) reported a 44-year-old woman whose level of consciousness deteriorated into coma several hours after ingesting about 200 mL of a glufosinate ammonium-containing herbicide (Yoshida, 1997).
d) CASE REPORT: A 64-year-old man was admitted to the ED 2 hours after ingestion of about 33.3 g glufosinate, with impaired consciousness. He was assessed on the Glasgow Coma Scale as 11 points (Watanabe & Sano, 1998).
e) CASE REPORT: Nine hours after ingestion of 500 mL of Basta(R), a 59-year-old woman was in a deep coma with general cyanosis (Koyama et al, 1994).
f) CASE SERIES: Hyperammonemia developed in 7 of 13 patients following acute ingestion of a glufosinate-ammonia herbicide. Severe neurotoxicity, including coma and amnesia during the recovery period, was delayed and lasted between 10 to 24 hours after ingestion. Patients also experienced severe respiratory failure and seizures. Four of the 7 patients had generalized tonic-clonic seizures (Kyong et al, 2011).

a) Coma may be associated with an abnormal EEG following an overdose (Koyama, 1993).
b) CASE REPORT: A 45-year-old woman, who developed coma about 15 hours after a toxic ingestion, was reported to have an EEG that showed high amplitude, slow waves of 4 to 5 and 6 to 8 Hz with no alpha wave. By the seventh day, the EEG showed slightly slower continuous alpha waves of about 9 Hz with low amplitude. By the 46th day, her EEG was normal (Koyama, 1993).

a) Generalized seizures and tremors are common neurological effects generally occurring after a latent period of 8 to 48 hours (Park et al, 2013; Mao et al, 2011; Lee et al, 2009; Koyama et al, 2000; Watanabe & Sano, 1998; Shinohara et al, 1997; Kubo et al, 1993; Hirose et al, 1992; Ishizawa et al, 1992), although not all poisoned patients will develop seizures (Koyama et al, 1994). Three out of 4 cases discussed by Hashimoto et al (1994) first experienced seizures after blood glufosinate levels had decreased below detectable limits.
b) CASE REPORT: A 34-year-old man presented to the ED after intentionally ingesting 150 mL of glufosinate ammonium. Gastric lavage was performed 1 hour after ingestion and about 5 hours after ingestion hemodialysis was performed for 2 hours. Despite these interventions, 11 hours after exposure the patient became stuporous and was transferred to a higher level of care. Initial vital signs and diagnostic and laboratory studies were normal. Twelve hours after ingestion, the patient developed a sudden increase in bronchial secretions, hypoxia and CO2 retention requiring immediate intubation and mechanical ventilation. Lipid emulsion therapy (a loading dose followed by an infusion) was initiated. By day 2, the patient remained drowsy. Hemoperfusion was added for ongoing management. During the same day, the patient developed tonic-type seizure activity and was treated with lorazepam. By day 5, the patient was successfully extubated and had a new complaint of double vision; ophthalmologic examination revealed evidence of bilateral sixth cranial nerve palsy. Diplopia and nystagmus gradually improved over several days. The patient was discharged on day 11 without any ophthalmologic abnormalities and no permanent sequelae (Park et al, 2013).
c) CASE REPORT: Generalized seizures of the entire body and frequent tremors were reported on the second day following an ingestion. The first seizure was noted about 29 hours after ingestion. After 6 hours of direct hemophoresis and administration of thiopental and diazepam, the seizures slowly resolved (Watanabe & Sano, 1998).
d) CASE REPORT: Seizures, treated with diazepam, were reported on the second hospital day in a 44-year-old woman after ingesting about 200 mL of Basta(R). Concurrently, she also experienced coma and respiratory failure (Yoshida, 1997).
e) CASE SERIES: 3 of 4 patients experienced sudden seizures after their blood glufosinate levels were not detectable (Hirose et al, 1996).
f) CASE REPORT: A 39-year-old woman developed generalized seizures, disturbance of consciousness, and respiratory depression 23 hours after ingestion of approximately 55 g of glufosinate (Hirose et al, 1992).
g) CASE REPORTS: Delayed onset of seizures was reported in 2 patients following ingestions of glufosinate. A 69-year-old woman developed seizures 8.5 hours after ingestion, despite gastrointestinal decontamination and hemodialysis and hemoperfusion being performed. An 87-year-old man experienced generalized seizures over 30 hours after the ingestion, and after his blood concentration of glufosinate had decreased from 1.56 mcg/mL to 0.68 mcg/mL (Tanaka et al, 1998). Both patients had recurrent seizures over the next several days.

a) Retrograde and anterograde amnesia (loss of short-term memory) has commonly been reported following overdoses and symptoms may persist (Mao et al, 2011; Ohtake et al, 2001; Bergmann et al, 2000; Watanabe & Sano, 1998; Koyama et al, 1994; Koyama, 1993; Ishizawa et al, 1992).
b) CASE REPORT: A 64-year-old man experienced retrograde and anterograde amnesia, beginning the day after ingestion of approximately 33.3 g, and lasting about 1 week, and accompanied by confabulation (Watanabe & Sano, 1998).
c) CASE REPORT: A 59-year-old woman was reported to have retrograde partial amnesia for the last 5 years following an ingestion (Koyama et al, 1994).
d) CASE REPORT: A 24-year-old man developed nausea, vomiting, mild metabolic acidosis, confusion, and mild irritability after drinking glufosinate ammonium. Following gastric lavage and activated charcoal, his symptoms improved and he was discharged on day 7. Ten days later, he complained of memory loss. A brain MRI showed symmetrically increased signal intensity in the hippocampus and parahippocampal gyrus bilaterally on T2-weighted and fluid-attenuated inversion recovery images. Six months later, a follow-up MRI revealed significant disappearance of the hippocampal lesions (Park et al, 2006).
e) CASE REPORTS: A 39-year-old woman intentionally ingested 300 mL of Basta(R) (a glufosinate containing herbicide) and received gastric lavage and activated charcoal shortly after exposure. Initially, the patient was stable with a normal ECG, vital signs and laboratory studies. Drowsiness occurred about 23 hours after exposure and her Glasgow Coma Scale (GCS) declined to 9. An arterial blood gas analysis showed acidosis (pH 7.27, PaCO2 63.7 mm Hg, PaO2 156 mm Hg) along with an ammonia level of 171 mcg/dL (normal, 5 to 69 mcg/dL). Thirty hours after exposure, the patient became unresponsive. Supportive measures included intubation and ventilation and hemodialysis (6 hours of therapy). Her blood gases improved and the ammonia level decreased to 133 mcg/dL. A repeat session of hemodialysis was performed about 50 hours post-ingestion. By day 3, she was more awake, but the following day she had a loss of recall. She was diagnosed with persistent amnesia that was present almost 2 years later (Mao et al, 2011).

a) VASOGENIC EDEMA/CASE REPORT: A 58-year-old woman intentionally ingested 250 mL of Basta(R) (18.5% GLA, 30% sodium polyoxyethylene alkylether sulfate (as a surfactant)) and initially developed irritability and vomiting. Upon admission (5 hours after ingestion), the patient was alert with normal vital signs. During the same day, she developed a sudden onset of hypotension (BP 60/40 mm Hg) and loss of respirations. Seizure activity (tonic-clonic) was observed the following day. By day 3, patient was gradually improving and her vital signs were stable. A MRI of the brain was performed on day 5 that showed evidence of hyperintense lesions in the hippocampus and striatum (basal ganglia), that were consistent with cytotoxic edema and vasogenic edema, respectively. On hospital day 7, the patient developed a new onset of ventricular tachycardia and died (Lee et al, 2009).

a) Nausea, vomiting, abdominal pain, and diarrhea are early signs (within 2 hours) of glufosinate poisoning. Gastric erosions are late signs of toxicity.
b) An early and common sign of glufosinate poisoning is nausea, vomiting, and often diarrhea. These effects tend to remit within a few hours (Park et al, 2006; Watanabe & Sano, 1998; Hashimoto et al, 1994; Koyama et al, 1994; Koyama, 1993; Kubo et al, 1993). Some of the early gastric effects may be attributable to the anionic surfactant contained in many of the glufosinate herbicides (Hashimoto et al, 1994).
c) CASE REPORT: A 64-year-old man was discovered about 2 hours after he ingested approximately 33.3 g of glufosinate ammonium with vomiting and diarrhea (Watanabe & Sano, 1998).

a) Gastric mucosal erosions may occur as a latent effect (several days) of glufosinate ingestions (Koyama et al, 1994).

a) Elevations of serum transaminases is a common glufosinate poisoning effect and may occur within the first 24 hours(Watanabe & Sano, 1998; Koyama et al, 1994).
b) CASE REPORT: Koyama et al (1995) report of a 59-year-old woman admitted to the ED following ingestion of 500 mL Basta(R). On day 6, the maximum serum hepatic enzyme levels were GOT 243 International Units/L; GPT 295 International Units/L; and LDH 762 International Units/L on day 7 (Koyama, 1995).

a) Other than slightly increased kidney weights, no signs of renal toxicity were reported in chronic toxicity studies in male and female rats (Ebert et al, 1990).

a) Circulatory failure and resultant metabolic acidosis may occur within 24 hours of glufosinate poisoning (Watanabe & Sano, 1998; Koyama, 1993).
b) CASE REPORT: Mild metabolic acidosis was reported in a 64-year-old man after an ingestion of about 33.3 grams. He was also experiencing circulatory failure (Watanabe & Sano, 1998).
c) CASE REPORT: A 24-year-old man developed mild metabolic acidosis (pH 7.33, PO2 82.6 mm Hg, PCO2 31.8 mmHg, and HCO3 16.6 mM/dL) after drinking glufosinate ammonium (Park et al, 2006).

a) Elevation of leukocyte counts, occurring within the first 24 hours, has been reported in several cases of glufosinate poisonings (Watanabe & Sano, 1998; Koyama et al, 1994) .
b) CASE REPORT: Watanabe et al (1998) report of a 64-year-old man with blood leukocyte levels of 13.4 x 10(3)/mm(3) on day 1 and increasing to 18.4 x 10(3)/mm(3) on day 3. Levels returned to normal by day 19 (Watanabe & Sano, 1998).

a) When exposed to glufosinate ammonium as a 50% aqueous solution for 6 hours 3 times weekly under an occluded patch, rabbits demonstrated a lack of skin sensitization (Ebert et al, 1990).

a) Rhabdomyolysis may develop following ingestions, especially when repeated seizures have occurred. Tanaka et al (1998) reported peak serum CPK levels of 24,900 International Units/L on the third day of admission in a 69-year-old woman who experienced generalized seizures 8.5 hours following an ingestion and then had 13 more seizures on the second day (Tanaka et al, 1998).

a) Transient diabetes insipidus associated with ingestion of an herbicide containing glufosinate has been reported. A 60-year-old man developed impaired consciousness, seizures, respiratory distress, and increased urine output (7885 mL/day) with elevated serum sodium (167 mEq/L), elevated plasma osmolality (332 mOsm/kg), and a decrease in both urine osmolality (200 mOsm/kg) and urine specific gravity (1003), suggesting development of diabetes insipidus. Antidiuretic hormone plasma level remained normal (1.3 pg/mL) despite high plasma osmolality. The patient improved following administration of vasopressin. Glufosinate may have influenced neuronal regulators of pituitary gland function (Takahashi et al, 2000).

a) No teratogenic effects were found in rats or rabbits (FAO, 1991; (Ebert et al, 1990).

a) Embryotoxicity was demonstrated by more frequent distension of the renal pelvis and ureter, and retarded ossification in fetuses of rat dams fed 50 or 250 mg/kg/day (Ebert et al, 1990).
b) Watanabe & Iwase (1996) reported in vitro embryotoxicity in mouse embryo cultures, with growth retardation and increased embryolethality. Specific morphological defects included hypoplasia of the prosencephalon and visceral arches, cleft lips and numerous cell death present throughout the neuroepithelium in the brain vesicle and neural tube.

a) Case reports suggest that mild depression of cholinesterase levels may occur with glufosinate poisoning, however cholinergic effects are not a predominant part of the clinical syndrome after exposure. The clinical utility of monitoring cholinesterase levels is unclear.

a) Patients with shock should have a pulmonary artery catheter inserted to assist in evaluating fluid balance and prevent fluid overload.

a) CYTOTOXIC AND VASOGENIC EDEMA/CASE REPORT: A 58-year-old woman intentionally ingested 250 mL of Basta(R) (18.5% GLA, 30% sodium polyoxyethylene alkylether sulfate (as a surfactant)). She was alert and oriented upon admission with normal vital signs. Shortly after admission, she developed hypotension and a sudden absence of respirations; a tonic-clonic seizure occurred on day 2. By day 3, the patient was gradually improving. A MRI of the brain was performed on day 5 that showed evidence of hyperintense lesions in the hippocampus and striatum (basal ganglia) that were consistent with cytotoxic edema and vasogenic edema, respectively. Diffusion weighted imaging showed a high-signal intensity lesion in the left hippocampus and both striata. Despite clinical improvement, the patient developed sudden ventricular tachycardia on hospital day 7 and died (Lee et al, 2009).

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.

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).
b) ADVERSE EFFECTS/CONTRAINDICATIONS

a) Treatment of mild to moderate toxicity consists of predominantly symptomatic and supportive care with IV fluid hydration and close monitoring.

a) Severe toxicity may require intubation for respiratory failure, IV fluids and vasopressors for hypotension and benzodiazepines for seizures. Persistent amnesia has been reported in some patients following exposure. Treatment is predominantly symptomatic and supportive care.

a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).

a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .

a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).

a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).

a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).

a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):

a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.

a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).

a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
b) DOSE

a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)

a) These recommendations apply to patients with MINOR chemical burns (FIRST DEGREE; SECOND DEGREE: less than 15% body surface area in adults; less than 10% body surface area in children; THIRD DEGREE: less than 2% body surface area). Consultation with a clinician experienced in burn therapy or a burn unit should be obtained if larger area or more severe burns are present. Neutralizing agents should NOT be used.

a) After initial flushing with large volumes of water to remove any residual chemical material, clean wounds with a mild disinfectant soap and water.
b) DEVITALIZED SKIN: Loose, nonviable tissue should be removed by gentle cleansing with surgical soap or formal skin debridement (Moylan, 1980; Haynes, 1981). Intravenous analgesia may be required (Roberts, 1988).
c) BLISTERS: Removal and debridement of closed blisters is controversial. Current consensus is that intact blisters prevent pain and dehydration, promote healing, and allow motion; therefore, blisters should be left intact until they rupture spontaneously or healing is well underway, unless they are extremely large or inhibit motion (Roberts, 1988; Carvajal & Stewart, 1987).

a) TOPICAL ANTIBIOTICS: Prophylactic topical antibiotic therapy with silver sulfadiazine is recommended for all burns except superficial partial thickness (first-degree) burns (Roberts, 1988). For first-degree burns bacitracin may be used, but effectiveness is not documented (Roberts, 1988).
b) SYSTEMIC ANTIBIOTICS: Systemic antibiotics are generally not indicated unless infection is present or the burn involves the hands, feet, or perineum.
c) WOUND DRESSING:
d) DRESSING CHANGES:
e) Analgesics such as acetaminophen with codeine may be used for pain relief if needed.

a) The patient's tetanus immunization status should be determined. Tetanus toxoid 0.5 milliliter intramuscularly or other indicated tetanus prophylaxis should be administered if required.

a) Approximately 2 to 3 hours after ingestion of 500 mL Basta(R) (containing 18.5% glufosinate), the serum level of glufosinate was measured at 179 mg/dL (Shinohara et al, 1997).
b) Koyama (1995) reported a serum concentration of glufosinate of 31.7 ppm approximately 4 hours after an ingestion (Koyama, 1995).
c) Serum level at 3 hours after ingestion of 60 grams was reported to be 440.0 mcg/mL, which decreased by a bi-exponential curve up to 42 hours after the ingestion (Hirose et al, 1999).
d) Koyama et al (2000) determined that serum glufosinate levels taken immediately on hospital admission could predict severity of poisoning while the patient was still in the latent period in order to guide further therapy. Severe cases had serum levels above 200 ppm at 2 hours post-ingestion and above 15 ppm at 8 hours post-ingestion. Non-severe cases were those with serum levels below 70 ppm at 2 hours post-ingestion and below 5 ppm at 8 hours post-ingestion. Severe cases were defined as those who developed at least one of the following: coma, apnea and/or generalized seizures.

a) 436 mg/kg

a) 83 mg/kg

a) 1660 mg/kg

a) Greater than 2 gm/kg

a) 61 mg/kg