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Biomedical subjects

A Graudins

Publications and source records attributed to A Graudins.

17 recordsLinked to original sources
PubMed2006

"Punk" rock can be bad for you: a case of surgical emphysema from a "punk" rocker's leather jacket.

Stab wounds to the thorax are seen in the emergency department (ED) and can be caused by a variety of mechanisms. This case highlights an unusual cause of injury: a leather jacket with spikes on the back of it. This type of jacket is often worn by "punks" as a fashion statement. We report that falling onto such a jacket may result in accidental thoracic injury leading to subcutaneous emphysema. A thorough clinical assessment is mandatory to exclude underlying lung injury or pneumothorax. In patients with subcutaneous emphysema and an otherwise normal chest radiograph, an in hospital observation period of 24 hours to check for any delayed complications is adequate if the patient remains clinically stable.

Adult↗
PubMed2002

Cross-reactivity of Sydney funnel-web spider antivenom: neutralization of the in vitro toxicity of other Australian funnel-web (Atrax and Hadronyche) spider venoms.

Australian funnel-web spiders are recognized as one of the most venomous spiders to humans world-wide. Funnel-web spider antivenom (FWS AV) reverses clinical effects of envenomation from the bite of Atrax robustus and a small number of related Hadronyche species. This study assessed the in vitro efficacy of FWS AV in neutralization of the effects of funnel-web spider venoms, collected from various locations along the eastern seaboard of Australia, in an isolated chick biventer cervicis nerve-muscle preparation. Venoms were separated by SDS-PAGE electrophoresis to compare protein composition and transblotted for Western blotting and incubation with FWS AV.SDS-PAGE of venoms revealed similar low and high molecular weight protein bands. Western blotting with FWS AV showed similar antivenom binding with protein bands in all the venoms tested. Male funnel-web spider venoms (7/7) and female venoms (5/10) produced muscle contracture and fasciculation when applied to the nerve-muscle preparation. Venom effects were reversed by subsequent application of FWS AV or prevented by pretreatment of the preparation with antivenom.FWS AV appears to reverse the in vitro toxicity of a number of funnel-web spider venoms from the eastern seaboard of Australia. FWS AV should be effective in the treatment of envenomation from most, if not all, species of Australian funnel-web spiders.

Antivenins↗
PubMed2001

Red-back spider (Latrodectus hasselti) antivenom prevents the toxicity of widow spider venoms.

STUDY OBJECTIVES: Widow spiders of the genus Latrodectus are found worldwide and produce similar clinical envenomation syndromes. In Australia, red-back spider antivenom (RBS-AV) is effective therapy for Latrodectus hasselti envenomation and it has been reported to reverse envenomation by other widow spiders. This study assessed the efficacy of RBS-AV in preventing in vitro and in vivo toxicity of widow spider venoms of North America and Europe. METHODS: The binding of RBS-AV to alpha-latrotoxin and Latrodectus venoms (Latrodectus spp mactans, hesperus, lugubris, tredecimguttatus, hasselti) was assayed using Western blotting. Prevention of in vitro toxicity to alpha-latrotoxin and the same venoms was tested by pretreating an isolated chick biventer cervicis nerve-muscle preparation with RBS-AV. Prevention of in vivo toxicity was determined by a lethality study in male Balb/c mice (2.5 to 5x median lethal dose [LD50]) or alpha-latrotoxin (10x LD50) preincubated with antivenom or without RBS-AV (control). RESULTS: In Western blots, RBS-AV bound to alpha-latrotoxin and similar widow spider proteins in all venoms tested, indicating antigenic similarity with proteins found in RBS venom. Antivenom prevented the typical in vitro muscle contracture and loss of twitch tension seen with alpha-latrotoxin and the venoms tested. Control mice rapidly developed signs of envenomation, but mice treated with RBS-AV remained free of signs of envenomation. CONCLUSION: RBS-AV prevented both in vitro and in vivo toxicity from Latrodectus venoms and alpha-latrotoxin in mice. These data suggest that RBS-AV may be clinically effective in the treatment of envenomation resulting from the bite of other widow spiders.

Animals↗
PubMed2000

A comparison of physostigmine and benzodiazepines for the treatment of anticholinergic poisoning.

STUDY OBJECTIVE: To compare the efficacy and safety of physostigmine with benzodiazepines for the treatment of agitation and delirium associated with anticholinergic poisoning. METHODS: We conducted a retrospective study of 52 consecutive patients referred to a university hospital toxicology consultation service who were treated with physostigmine, benzo-diazepines, or both for anticholinergic agitation and delirium. Patients treated with physostigmine were compared with those treated with benzodiazepines with respect to demographics, severity of poisoning, response to treatment, side effects of treatment, and complications. RESULTS: Physostigmine controlled agitation and reversed delirium in 96% and 87% of patients, respectively. Benzodiazepines controlled agitation in 24% of patients but were ineffective in reversing delirium. Initial treatment with physostigmine (n=30) resulted in a significant decrease in the incidence of agitation (P <.001) and level of central nervous system stimulation (P <.001), whereas initial treatment with benzodiazepines (n=22) did not (P =.03 and P =.05, respectively). Patients treated initially with physostigmine had a significantly lower incidence of complications (7% versus 46%; P <. 002) and a shorter time to recovery (median, 12 versus 24 hours; P =. 004) than those treated initially with benzodiazepines. There were no significant differences between these groups in the incidence of side effects (7% versus 14%; P =0.6) and length of stay (median, 32 versus 39 hours; P =.15). CONCLUSION: Results suggest that physostigmine is more effective and safer than benzodiazepines for the treatment of anticholinergic agitation and delirium. A prospective controlled study is necessary to confirm such findings.

Administration, Oral↗
PubMed1999

Triethylene glycol poisoning treated with intravenous ethanol infusion.

INTRODUCTION: Poisoning with triethylene glycol has been rarely reported in humans. Triethylene glycol is thought to be metabolized by alcohol dehydrogenase to acidic products resulting in the production of a metabolic acidemia. Triethylene glycol metabolism has previously been shown to be inhibited by fomepizole (4-methyl pyrazole) administration. We report a case of triethylene glycol ingestion, presenting with a metabolic acidemia, treated with intravenous ethanol administration. CASE REPORT: A 23-year-old female presented to the emergency department approximately 1-1.5 hours following ingestion of a gulp of triethylene glycol (99%) brake fluid with coma (GCS-3) and metabolic acidemia (pH 7.03, PCO2 44 mm Hg, Bicarbonate 11 mmol/L, anion gap 30 mmol/L, serum creatinine 90 mumol/L). She was intubated and given 100 mmol of intravenous sodium bicarbonate. An ethanol loading dose was administered followed by an infusion to maintain serum ethanol at 100 mg/dL. Acidemia gradually resolved over the next 8 hours and she was extubated 12 hours later. The ethanol infusion was continued for a total of 22 hours. There was no recurrence of acidemia. Serum ethanol, ethylene glycol, and methanol levels were nondetectable on presentation, as was serum salicylate. Urine drug of abuse screen and thin-layer chromatography revealed no other coingested substances. The patient was discharged to a psychiatric ward 36 hours postingestion. CONCLUSION: Pure triethylene glycol poisoning results in coma and metabolic acidemia and may be treated with alcohol dehydrogenase inhibitors such as ethanol.

Acidosis↗
PubMed1998

Serotonin syndrome resulting from drug interactions.

We describe six patients diagnosed with serotonin syndrome after exposure to drugs with serotonergic activity. Drug interactions occurred as a result of a combination of tricyclic antidepressants, selective serotonin reuptake inhibitors, selective noradrenaline reuptake inhibitors or monoamine oxidase inhibitors. Management included supportive care and the use of non-specific serotonin antagonists (cyproheptadine, benzodiazepines and chlorpromazine). All patients made uneventful recoveries.

Adolescent↗
PubMed1997

Treatment of methanol poisoning with intravenous 4-methylpyrazole.

Treatment of human methanol poisoning with the alcohol dehydrogenase inhibitor, 4-methylpyrazole (fomepizole), has not been previously described. We report the clinical and toxicokinetic data of a patient with methanol poisoning who was treated with fomepizole. Formic acid levels remained undetectable during fomepizole treatment, the toxic effects of methanol were prevented, and the patient made a full recovery.

Adult↗
PubMed1997

Regional intravenous infusion of calcium gluconate for hydrofluoric acid burns of the upper extremity.

STUDY OBJECTIVE: To describe regional intravenous infusion of calcium gluconate as a therapy for hydrofluoric acid (HF) burns of the forearm, hand, or digits. METHODS: This study describes seven patients with HF burns. Calcium gluconate, 10 mL of 10% solution with 30 to 40 mL normal saline solution, was injected intravenously into the affected limb using a Bier block technique. Ischemia was maintained for 20 to 25 minutes. Therapy was considered successful if significant reduction of pain and tenderness was noted after tourniquet release. RESULTS: Seven patients were treated. HF concentration varied from 5% to 49%. Exposure sites included the forearm (two cases), thenar eminence and digits (two cases), or digits only (three cases). Complete pain resolution occurred on tourniquet release in four patients (two with burns to the forearm, two with burns to digits only). One patient had partial relief (thenar but not digital exposure site), and two had no relief of symptoms. Intraarterial calcium gluconate perfusion was subsequently administered to the three patients with persistent subungual and pulp, or thenar pain. Recovery was complete in all cases. No adverse effects were noted. CONCLUSION: Regional intravenous infusion of calcium gluconate should be considered a therapeutic option in HF burns of the forearm, hand, or digits when topical therapy fails.

Adult↗
PubMed1997

Fluoxetine-induced cardiotoxicity with response to bicarbonate therapy.

This report describes a patient with an acute intentional fluoxetine exposure who developed unique cardiovascular and neurovascular toxicity. The patient presented with lethargy and cardiac conduction delays (QRS 110 msec, QTc 458 msec) and developed a delayed seizure. On admission, therapy with intravenous sodium bicarbonate promptly narrowed the QRS to 90 msec. A comprehensive toxicology screen demonstrated only a serum fluoxetine concentration of 901 ng/mL (therapeutic range, 37-301), a serum norfluoxetine concentration of 451 ng/mL (29-329) and a serum acetaminophen concentration of 174 mg/L. Tricyclic antidepresants were specifically noted to be absent. A self-limiting generalized seizure was witnessed 16 hours after ingestion. At this time the bicarbonate infusion had been ceased and the QRS interval was not prolonged. The patient improved over time and no other apparent causes for the observed clinical effects could be discovered. Emergency physicians need to be aware of the uncommon occurrence of fluoxetine-induced cardiotoxicity and the potential benefit of sodium bicarbonate therapy.

Adult↗
PubMed1996

Delayed peak serum valproic acid in massive divalproex overdose--treatment with charcoal hemoperfusion.

BACKGROUND: Increased clearance and apparent clinical improvement in valproic acid overdose has been reported following in-series hemodialysis/hemoperfusion therapy. We report a case of divalproex sodium and chlorpheniramine overdose treated with charcoal hemoperfusion and multiple-dose activated charcoal. CASE REPORT: A 32-year-old female presented alert three hours postingestion of her own medication. Serum valproic acid was 105 micrograms/mL. No anticholinergic toxicity was seen. Despite three doses of activated charcoal over 14 hours, serum valproic acid continued to rise. Whole bowel irrigation and multiple-dose activated charcoal were commenced 17 h postingestion when serum valproic acid was 1380 micrograms/mL. Charcoal hemoperfusion was instituted three hours later when serum valproic acid had not fallen and the patient remained obtunded. RESULTS: Initial extraction ratio of the hemoperfusion cartridge was 0.54 with plasma clearance of 54.5 mL/min. Valproic acid elimination half-life was 3 h during the 190 min hemoperfusion cycle. Posthemoperfusion elimination half-life was 4.8 h with continued multiple-dose activated charcoal dosing. The clinical condition improved during hemoperfusion. CONCLUSION: Enteric coated valproic acid preparations may cause delayed toxicity in overdose, particularly with coingested anticholinergic medications. In our case, charcoal hemoperfusion appeared to increase valproic acid clearance.

Adult↗
PubMed1985

The care of older children when a sibling is born.

This study into the care of a child when his/her mother is hospitalized has shown that most care is given by the father and the grandparents. However, about 10% of mothers do not feel or recognize their child's need to understand why she is not at home, where she is, nor to visit her in hospital.

Child Care↗
PubMedDate not supplied

Treatment of the serotonin syndrome with cyproheptadine.

The serotonin syndrome is the result of excess stimulation of central nervous 5-hydroxytryptamine (5HT)-1a and 5HT-2 receptors. The diagnosis requires a history of exposure to agents active at serotonin receptors and the presence of alterations in mental status, autonomic instability, and neuromuscular abnormalities such as tremor, hyperreflexia, or myoclonus. In this descriptive case series, five cases of serotonin syndrome are reported. All patients gave a history of recent exposure to one or more serotonergic medications, including moclobemide, paroxetine, sertraline, and venlafaxine, with clinical evidence of serotonin syndrome. All patients were administered cyproheptadine (4-8 mg orally) for serotonergic signs. Three had complete resolution of signs within 2 h of administration. Another two had a residual tremor or hyperreflexia following the first dose, which resolved following a repeat dose. There were no adverse outcomes from cyproheptadine use. The role of specific serotonin receptor antagonists such as cyproheptadine in the treatment of the serotonin syndrome remains to be delineated. Its use should be considered an adjunct to supportive care. Currently, it is unknown whether cyproheptadine modifies patient outcome.

1-Naphthylamine↗