DP - 2003 Feb
TI - Valsartan-induced hepatotoxicity in a HBs-Ag-Positive patient.
SO - Am J Gastroenterol 2003 Feb;98(2):507.
DP - 2003 Mar
TI - Efficacy of Crotalidae polyvalent antivenin for the treatment of hognosed
viper (Porthidium nasutum) envenomation.
PG - 391-5
AB - Envenomation from pit vipers native to North America can be treated
successfully with either of the 2 commercially available antivenoms
licensed in the United States. However, envenomations from imported snakes
held in zoos or private collections often pose unique challenges to
management because of the lack of specific antivenom and the unclear
efficacy of the available licensed products. We report the case of a
37-year-old man who was envenomated on his left hand by his pet hognosed
viper (Porthidium nasutum ). He had swelling at the wound site that
progressively worsened over 3 to 4 hours. His symptom progression included
the structural motor impairment of his fingers and a sensory deficit.
Treatment with 8 vials of Antivenin (Crotalidae) polyvalent was associated
with a halt of extremity swelling and restoration of neurologic and motor
function of his hand. Limited experimental evidence provides support for
antigenic cross-reactivity between Antivenin (Crotalidae) polyvalent and P
nasutum venom.
AD - New York City Poison Control Center, 455 First Avenue, Room 123, New York,
SO - Ann Emerg Med 2003 Mar;41(3):391-5.
DP - 2003 Mar
TI - The frequency of complications associated with the use of multiple-dose
activated charcoal.
PG - 370-7
AB - STUDY OBJECTIVE: The objective of this study was to determine the
frequency of complications associated with the use of multiple-dose
activated charcoal. METHODS: The study population was drawn from 8
tertiary care hospitals in 4 North American cities. Medical records of all
inpatients between March 1993 and March 1998 with a discharge diagnosis of
poisoning (International Classification of Diseases, 9th edition, Clinical
Modification codes 960-989.9) were reviewed to select patients who had
received multiple-dose activated charcoal (defined as > or =2 doses
administered within 12 hours). Medical records of patients who received
multiple-dose activated charcoal were reviewed for patient demographics
and clinical information regarding the occurrence of pulmonary aspiration,
gastrointestinal obstruction, hypernatremia, hypermagnesemia, corneal
abrasion, and other complications associated with the use of multiple-dose
activated charcoal. RESULTS: We reviewed 6,258 medical records,
identifying 878 patients who received multiple-dose activated charcoal. We
judged 5 (0.6%; 95% confidence interval [CI] 0.1% to 1.1%) patients to
have had clinically significant pulmonary aspiration and none (0%; upper
95% CI 0.3%) to have had gastrointestinal obstruction. None of the
patients with pulmonary aspiration died or had residual sequelae recorded.
Hypernatremia (peak serum sodium >145 mEq/L [145 mmol/L]) was documented
in 53 (6.0%; 95% CI 4.4% to 7.6%) patients, of whom 5 (0.6%; 95% CI 0.1%
to 1.1%) had a serum sodium concentration of greater than 155 mEq/L (155
mmol/L). Hypermagnesemia (peak serum magnesium >2.5 mg/dL [1.0 mmol/L])
was documented in 27 (3.1%; 95% CI 2.0% to 4.2%) patients, of whom 3
(0.3%; 95% CI 0.1% to 1.0%) had peak values that were greater than 3.75
mg/dL (1.5 mmol/L). One patient had a corneal abrasion (0.1%; 95% CI 0% to
0.6%). No other complications were identified. CONCLUSION: Clinically
significant complications associated with the use of multiple-dose
activated charcoal occur infrequently.
SO - Ann Emerg Med 2003 Mar;41(3):370-7.
DP - 2003 Mar
TI - Antibiotic prophylaxis for Lyme disease: how the way of reporting a
clinical trial can alter the perception of effectiveness.
PG - 373-5
AD - Department of Dermatology, Clinica Plato, C/Plato 21, 08006 Barcelona,
Spain. 24998ugc@comb.es
SO - Arch Dermatol 2003 Mar;139(3):373-5.
DP - 2003 Mar 15
TI - Channelling new antidepressants to problem patients may be factor in fatal
toxicity.
SO - BMJ 2003 Mar 15;326(7389):600.
DP - 2003 Feb
TI - Severe heart failure in a young multiple sclerosis patient.
SO - J Neurol 2003 Feb;250(2):241-2.
DP - 2003
TI - Mercury vapor inhalation from Chinese red (Cinnabar).
PG - 75-8
AB - INTRODUCTION: Acute inhalation of mercury fumes or vapors is a rare but
frequently fatal cause of acute lung injury. This report describes a rare
cause of mercury inhalation from Chinese red. CASE REPORT: An 87-year-old
male inhaled the vapors from heating Chinese red (Cinnabar, mercury
sulphide) intended to treat his foot ulceration. He subsequently developed
acute lung injury (progressive dyspnea and acute respiratory failure) that
was treated with mechanical ventilation. DMPS
(2,3-Dimercapto-1-propanesulfonic acid) and penicillamine were used as
chelating agents, and methylprednisolone pulse therapy was used to treat
his pulmonary disease. Despite being extubated once, the patient
eventually died from profound hypoxemia. CONCLUSION: A rare case of
mercury intoxication was due to inappropriate use of an alternative
medicine, Chinese red. This case serves as a reminder of the toxicity of
the noxious gas from this substance and the importance of being familiar
with alternative medicines.
AD - Division of Pulmonary and Critical Care Medicine, Chang Gung Memorial
Hospital, Chang Gung University, Taipei, Taiwan.
SO - J Toxicol Clin Toxicol 2003;41(1):75-8.
DP - 2003
TI - Intoxication with foothill camas (Zigadenus paniculatus).
PG - 63-5
AB - Eight adults ingested foothill camas (Zigadenus paniculatus) bulbs in Juab
County, Utah, believing them to be nontoxic wild bulbs. All who ingested
the bulbs became ill, and three of them required admission for supportive
care. All patients had nausea; other findings included vomiting, abdominal
pain, dizziness, near syncope, hypotension, and bradycardia. No specific
antidote is available for intoxication with Zigadenus species. Supportive
care is indicated and atropine may benefit those with sympytomatic
bradycardia and hypotension.
AD - Nephi Medical Clinic, Nephi, Utah, USA mike.peterson@utahtelehealth.net
SO - J Toxicol Clin Toxicol 2003;41(1):63-5.
DP - 2003
TI - Repeated ingestion of 2-butoxyethanol: case report and literature review.
PG - 57-62
AB - BACKGROUND: Ethylene glycol monobutyl ether (2-butoxyethanol) is not
commonly associated with significant human poisoning. Exposures are
usually through occupational contact and typically involve inhalation
injury. Animal studies report severe hemolysis occurring in rats and mice.
Rare published human cases give varied descriptions of the clinical course
associated with 2-butoxyethanol poisoning including reports of metabolic
acidosis, ethylene glycol production, oxaluria, renal failure, and anemia.
We report a case of two separate ingestions (80 to 100 grams) of a glass
cleaner concentrate containing 22% 2-butoxyethanol, and its primary
metabolite butoxyacetic acid. CASE REPORT: An 18-year-old male ingested
360-480 mL of 22% 2-butoxyethanol on two separate occasions. Approximately
10hours after the first ingestion, the patient developed severe CNS
depression, metabolic acidosis, hematuria, and mild elevation of hepatic
enzymes. He was treated initially with ethanol therapy but continued to
deteriorate and was started on hemodialysis. Approximately 10 days after
discharge, the patient ingested 480 mL of the same product and received
ethanol and hemodialysis within four hours of ingestion. During his second
admission the patient did not develop the delayed severe CNS depression or
profound metabolic acidosis. Clinically significant hemolytic anemia,
oxaluria, ethylene glycol production, and renal failure were not noted in
either episode. The patient recovered on both occasions without sequelae.
CONCLUSION: Hemodialysis may be an effective treatment intervention for
managing severe acute 2-butoxyethanol intoxication, however, further
investigation is warranted.
AD - PROSAR-Intemational Poison Center, St. Paul, Minnesota, USA
SO - J Toxicol Clin Toxicol 2003;41(1):57-62.
DP - 2003
TI - Post-mortem toxicology: what the dead can and cannot tell us.
PG - 47-56
AB - The evaluation of postmortem laboratory assays of drugs needs to be
performed in a systematic manner. The condition of the body, drug
characteristics, matrix and site analysis are factors which need to be
considered in the proper interpretation of an autopsy specimen result.
AD - Evanston Northwestern Healthcare OMEGA, Glenbrook Hospital, Glenview,
Illinois, 60025, USA. Jleikin@enh.org
SO - J Toxicol Clin Toxicol 2003;41(1):47-56.
DP - 2003
TI - Copperhead envenomations in the Carolinas.
PG - 29-35
AB - INTRODUCTION: Although the copperhead (Akistrodon contortrix) is
responsible for most Crotaline envenomations in the Carolinas,
manifestations and treatment are poorly characterized. OBJECTIVE: We
sought to describe the clinical course after copperhead bites. METHOD:
Structured review of copperhead exposures reported to a regional poison
center from 1997-2000. Hospital records were reviewed when available.
Phone followup was attempted. RESULTS: A total of 178 cases were
identified. Of these 75% were males. The median age was 31 yr (range
2-93). The bite site included hand (52%), foot (36%), leg (7%), and arm
(5%). Classification included dry (7%), mild (48%), moderate (39%), and
severe (6%). The most common symptom was pain (93%). Local findings
included swelling (94%), fang marks (93%), ecchymosis (53%), erythema
(37%), bullae (13%), and tissue necrosis (8%). Eleven of 37 patients
developed abnormal PT and/or PTT. Two patients bled. Patients were treated
at a healthcare facility in 160 cases, with 79 patients admitted. Opioid
analgesics were the most common therapy (81%). Equine-derived antivenin
was given in 14 cases (range 2-30 vials). Antivenin reactions developed in
three. Two patients received blood products. Surgical treatment included
debridement (6), grafting (2), digit amputation (1), digit dermotomy (1),
and fasciotomy (1). No patients died. In followup, 18 patients reported
limb dysfunction ranging from 5-365 days. CONCLUSION: Copperhead bites
typically result in mild to moderate envenomation due to local tissue
effects. Significant systemic manifestations are rare. Limb dysfunction
can be prolonged.
AD - Carolinas Medical Center, Charlotte, North Carolina 28232-2861, USA
SO - J Toxicol Clin Toxicol 2003;41(1):29-35.
DP - 2003
TI - Australian tiger snake (Notechis scutatus) and mexican coral snake
(Micruris species) antivenoms prevent death from United States coral snake
(Micrurus fulvius fulvius) venom in a mouse model.
PG - 7-10
AB - BACKGROUND: Wyeth-Ayerst has discontinued production of Antivenin
(Micrurus fulvius). Currently, there is no other approved coral snake
antivenom available in the United States. METHODS: This study was a
randomized, placebo-controlled and blinded determination of the ability of
a Mexican Micrurus (coral snake) antivenom and an Australian Notechis
(tiger snake) antivenom to prevent lethality from a United States Micrurus
fulvius fulvius venom in a mouse model. Venom dosing was based on an LD50
determined for this experiment. Our comparison groups included: (1) M. f.
fulvius venom + Micrurus antivenom, (2) M. f. fulvius venom + Notechis
antivenom, (3) M. f. fulvius venom + protein control, (4) 0.9% normal
saline + protein control, (5) saline + Notechis antivenom, (6) saline +
Micrurus antivenom. Venom dose was 5 times the determined LD50. The
antivenom amounts were capable of neutralizing 10 times the venom injected
(50 times the LD50). RESULTS: The LD50 of M. f. fulvius venom was
determined to be 0.85 mg/kg. All mice in both antivenom test groups were
protected from lethality for the entire 24-hour observation period. Six of
the 7 mice in the venom test group died, with a survival time of 349 +/-
382 minutes (mean +/- s.d.) after the venom injection. All three groups of
control mice survived the entire 24-hour observation period. CONCLUSIONS:
Mexican Micrurus antivenom and Australian Notechis antivenom provide
protection from lethality in mice envenomated with a United States M. f.
filvius venom.
AD - Rocky Mountain Poison and Drug Center, Denver Health Authority, Denver,
Colorado 80230-6800, USA
SO - J Toxicol Clin Toxicol 2003;41(1):7-10.