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Biomedical subjects

William J Meggs

Publications and source records attributed to William J Meggs.

10 recordsLinked to original sources
PubMed2006

Heparin reverses anaphylactoid shock in a porcine model.

STUDY OBJECTIVE: Heparin binds histamine and has been advocated as a therapy for anaphylactic and anaphylactoid shock. The efficacy of heparin in treating anaphylactoid shock is compared with therapy with diphenhydramine and epinephrine, as well as sham treatment with saline. METHODS: This controlled study of 9 anesthetized, intubated pigs induced shock with intravenous calcium ionophore A23187 (5 mg/kg), which is known to degranulate mast cells in vitro. Serum histamine levels were measured using an enzyme-linked immunosorbent assay. Shock, defined as a greater than 20% decrease in mean arterial blood pressure, was treated with intravenous saline, epinephrine with diphenhydramine, or heparin. Data were analyzed using Wilcoxon rank sum and analysis of variance, as appropriate. RESULTS: All pigs developed anaphylactoid shock after injection with A23187, as evidenced by hypotension, flushing, and an increase in plasma histamine. Mean arterial blood pressure fell from a mean of 73 (SD 10) mm Hg to 28 (SD 16) mm Hg after injection (P<.001; 95% confidence interval [CI] of the difference in pressures 34 to 57 mm Hg). Mean serum histamine levels increased from 712 micromol/dL (SD 731) to 1,154 micromol/dL (SD 799) after injection (Z value -2.201; P=.0277; 95% CI of the difference -610 to -99). Both epinephrine with diphenhydramine and heparin but not saline reversed shock. CONCLUSION: A23187 induced anaphylactoid shock in all subjects. Therapy with intravenous epinephrine combined with diphenhydramine reversed shock. Heparin also rapidly reversed shock.

Adrenergic Agonists↗
PubMed2005

Sustained oxygenation without ventilation in paralyzed pigs with high-flow tracheal oxygen.

OBJECTIVES: It is generally assumed that ventilation is necessary for oxygenation. This study tested if paralyzed animals without respirations can maintain arterial oxygenation when administered high-flow oxygen delivered by a catheter in the trachea. METHODS DESIGN: Prospective observational study. SETTING: University research laboratory. PARTICIPANTS: 3 anesthetized/paralyzed swine weighing 29.5 +/- 4.2 kg. INTERVENTIONS/OBSERVATIONS: Pigs were intubated, anesthetized with intravenous tiletamine and a pentobarbital drip. A femoral arterial line was placed to record arterial blood gases and vital signs every 5 minutes. Respiratory paralysis was obtained with vecuronium 150 microg/kg and repeated at any sign of movement. A catheter was placed in the trachea to deliver oxygen at 15 L/min. Outflow gas from the endotracheal tube was analyzed for O2 and CO2. O2 was discontinued at 75 minutes. The institutional animal care and use committee approved the protocol. RESULTS: All pigs survived to 75 minutes. PaO2 was more than 100 mm Hg throughout the study period. Mean PaCO2 was 37.4 +/- 2.8 mm Hg at baseline, 146 +/- 59 at 30 minutes, then rose above 200 mm Hg in all pigs by 45 minutes. Mean arterial pH fell from 7.47 +/- 0.04 at onset to 6.75 +/- 0.06 at 75 minutes. When oxygen was terminated at 75 minutes, PaO2 fell to 16.5 +/- 7.6 mm Hg within 5 minutes, and all pigs were sacrificed within 10 minutes. For outflow gas, O2 was more than 98% and expired CO2 less than 1% throughout the study period. CONCLUSIONS: Paralyzed, unventilated pigs receiving high-flow oxygen via a tracheal catheter remained alive after 75 minutes, although a profound respiratory acidosis developed.

Animals↗
PubMed2005

Pressure-immobilization bandages delay toxicity in a porcine model of eastern coral snake (Micrurus fulvius fulvius) envenomation.

STUDY OBJECTIVES: Pressure-immobilization bandages are used in countries where neurotoxic snake envenomations are common. They impede lymphatic egress from the bite site and delay systemic venom toxicity. The effectiveness of these devices has not been evaluated in coral snake envenomations. We investigated the efficacy of pressure-immobilization bandages in delaying the onset of systemic toxicity in a porcine model of coral snake envenomation. METHODS: A randomized controlled trial of pressure-immobilization bandages was conducted in a university animal care center. Subjects were 12 anesthetized, spontaneously breathing pigs, ranging from 9.1 to 11.4 kg. After injection with 10 mg of Micrurus fulvius fulvius venom in the subcutaneous tissue of the distal foreleg, subjects were randomized to receive no treatment or application of a pressure-immobilization bandage at 1 minute after injection. Treated animals had elastic bandages applied to the extremity and splinting for immobilization. Vital signs and quality of respirations were recorded. Outcome was the onset of respiratory failure or survival to 8 hours. Necropsies and histologic analysis of the envenomation site was performed. RESULTS: One animal from each group was removed because of the discovery of pre-existing respiratory pathology. Four of 5 pigs in the treatment group survived to 8 hours, but none in the control group survived. Mean time to onset of respiratory compromise was 170.4 +/- 33.3 minutes in the control group. None of the pigs had histologic changes at the envenomation site consistent with ischemia or pressure-related injury. CONCLUSION: Pressure-immobilization bandages delayed the onset of systemic toxicity in our porcine model of M fulvius envenomation.

Animals↗
PubMed2004

The effect of calcium chloride in treating hyperkalemia due to acute digoxin toxicity in a porcine model.

BACKGROUND: The administration of intravenous (IV) calcium to treat hyperkalemia resulting from digoxin poisoning is considered potentially dangerous, based on a body of older literature which, in sum, reported increased cardiac glycoside toxicity with calcium administration (increased arrhythmias, higher rate of death). OBJECTIVE: This pilot study sought to determine if the administration of calcium chloride when compared to normal saline would affect time to death when given to hyperkalemic, digoxin toxic swine. METHODS: Digoxin IV at 0.25 mg/kg was determined to be appropriately toxic for this study. When arrhythmias consistent with hyperkalemia developed, animals were given either IV calcium chloride (CaCl) bolus (10 mg/kg, Group 1, n=6) or normal saline volume equivalent (Group 2, n=6). Three intervals were observed: Interval 1: time interval from digoxin administration (T0) to when ECG changes consistent with hyperkalemia developed (at which point calcium chloride or normal saline was administered); Interval 2: time interval from the development of ECG changes consistent with hyperkalemia to asystole; Interval 3: time interval from digoxin administration to asystole. Both groups were monitored for changes in heart rhythms, serum potassium levels, and time to asystole. RESULTS: The intravenous digoxin dose of 0.25 mg/kg induced hyperkalemia, arrhythmias, and death approximately 1 h after administration in all animals studied. Group 1: Interval 1 averaged 18.75 (S.D. +/-7.96) min, Interval 2 averaged 16.75 (S.D. +/-17.17) min, and Interval 3 averaged 35.5 (S.D. +/-14.49) min range; Group 2: average Interval 1 24.8 (S.D. +/-4.71) min, Interval 2 averaged 19.5 (S.D.+/-15.92), Interval 3 averaged 44.3 (S.D. +/-13.80) minutes. There was no statistically significant difference between the groups at any time interval, Interval 1 (p=0.43), Interval 2 (p=0.65), Interval 3 (p=0.40). There was no difference in serum potassium throughout the study period. CONCLUSION: The administration of intravenous CaCl in the setting of hyperkalemia from acute digoxin toxicity did not affect mortality or time to death at the dose administered.

Animals↗
PubMed2003

Permanent paralysis at sites of dermal exposure to chlorpyrifos.

OBJECTIVE: Poisoning with organophosphate pesticides can cause sensory and motor neuropathy with permanent paralysis. Paralysis at the site of dermal exposure has not been reported. CASE REPORT: A 61-year-old carpenter sprayed a nest of termites with an insecticide containing chlorpyrifos without protective equipment and with direct contact of pesticide solution to hands, lower arms, feet, and lower legs, as well as inhalation of vapors from spraying. After 30 min he became ill with nausea, abdominal cramping, arm and leg weakness, bilateral shoulder pain, chest pain, and numbness in the left hand and arm. At a hospital, he was treated with atropine 1 mg IV and pralidoxime Cl 2 g IV There was 0/5 strength in the hands and wrists and 3/5 elsewhere, a left peritoneal palsy, and urinary retention. He was transferred to a tertiary care hospital where paralysis persisted. Electromyogram studies documented widespread peripheral neuropathy. With continued progression of neuropathy, pralidoxime was repeated on the third day. By day 12, motor strength improved except for the hands and left lower leg. Right interosseous muscle strength was 1/5 and left was 0/5. Right-hand grip was 2/5, and left-hand grip was 0/5. He was transferred to a rehabilitation center. He never regained use of his hands and was disabled from employment as a carpenter. There was a disturbed gait, with inability to clear his left foot with walking. Urinary retention persisted and required self-catherization. CONCLUSION: Dermal exposure of the hands and feet to chlorpyrifos was associated with atrophy and permanent paralysis of exposed areas. The importance of protective equipment is emphasized.

Atropine↗
PubMed2003

Oral treatment of organophosphate poisoning in mice.

OBJECTIVE: Organophosphates are used as pesticides, herbicides, and chemical warfare agents. Treatment of organophosphate poisoning is with intravenous atropine and pralidoxime in addition to supportive care. This study determined the efficacy of oral agents in preventing death from organophosphate poisoning. METHODS: The organophosphate paraoxon (8 mg/kg) was used in a murine model with lethality at four and 24 hours as an end point. For oral treatment, 15 male Balbc mice were given either atropine sulfate (4 mg/kg), or a combination of atropine sulfate (4 mg/kg) with pralidoxime (100 mg/kg), by oral gavage. A control group of 22 mice received water by oral gavage. Chi-square analysis was used to compare results in the different groups. RESULTS: Of the control group, six of 22 survived to four hours after paraoxon exposure. Of the exposed animals treated with oral atropine, eight of 15 survived to four hours. Of the exposed animals treated with a combination of atropine and pralidoxime, 13 of 15 survived to four hours. All animals surviving to four hours survived to 24 hours. The increased survival of animals in the atropine group relative to the control group was not significant (p = 0.09). Survival was significant in the group treated with atropine and pralidoxime relative to atropine alone (p = 0.02) and to the control group (p = 0.0002). All treated mice surviving at four hours were alive at 24 hours. CONCLUSIONS: Both oral atropine and a combination of oral atropine and pralidoxime improved survival, and combination therapy achieved statistical significance. Generalization of this result to other organophosphate pesticides, other doses of paraoxon, and other species cannot be made without further investigations.

Animals↗
PubMed2002

Clearance of metformin by hemofiltration in overdose.

BACKGROUND: Metformin is prescribed with an increasing frequency for patients with Type II diabetes mellitus; the increasing availability increases the risk of intentional overdoses. Metformin may cause severe lactic acidosis in overdose, especially when accompanied by co-ingestants or other medical conditions that alter lactate handling or metformin elimination. Though the clearance of therapeutic metformin by hemodialysis is known, the clearance in the setting of a large overdose has not been reported. CASE REPORT: A 58-year-old man with a history of Type II diabetes, hypertension, bipolar disease, and decreased renal function presented after ingestion of approximately 40 500-mg metformin tablets and 20 240-mg diltiazem sustained-release tablets. Clinical manifestations of poisoning included somnolence, hypotension, bradycardia, severe lactic acidosis, and ultimately death. Gastric decontamination was attempted with gastric lavage, multiple dose activated charcoal, and whole bowel irrigation. Hemodynamic support was provided with pressors, glucagon, insulin, and intra-aortic balloon pump. Due to hypotension, continuous renal replacement therapy, rather than hemodialysis, was initiated. Continuous veno-venous hemodialysis was performed with a blood flow of 180 mL/min and dialysate flow of 2.5 L/h. A Multiflow 60 kidney (Cobe) on a Prisma (Cobe) continuous renal replacement therapy machine was used. The initial metformin level was 110 microg/mL (therapeutic range 1-2 microg/mL). By continuous veno-venous hemodialysis, an absolute clearance of 50.4 mL/min was obtained. CONCLUSION: Metformin was cleared by the continuous veno-venous hemodialysis modality of continuous renal replacement therapy in this metformin overdose. Although a fatal outcome occurred in this patient, its utility in other patients with metformin overdose should be investigated.

Antihypertensive Agents↗