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Biomedical subjects

K W Kulig

Publications and source records attributed to K W Kulig.

At least 19 recordsLinked to original sources
PubMed1991

Acetaminophen overdose: a 48-hour intravenous N-acetylcysteine treatment protocol.

STUDY OBJECTIVE: To determine the safety and efficacy of a 48-hour IV N-acetylcysteine (IV NAC) treatment protocol for acute acetaminophen overdose. DESIGN: Nonrandomized trial open to all eligible patients. SETTING: Multicenter; hospitals included moderate- and high-volume private, university, and municipal hospitals in urban and suburban settings. TYPE OF PARTICIPANTS: Two hundred twenty-three patients were entered. Of these, 179 met inclusion criteria: acute acetaminophen overdose, plasma acetaminophen concentration above the treatment nomogram line, treatment with IV NAC according to the protocol, and sufficient data to determine outcome. INTERVENTIONS: IV NAC treatment consisted of a loading dose of 140 mg/kg followed by 12 doses of 70 mg/kg every four hours. MEASUREMENTS AND MAIN RESULTS: Patients were grouped for analysis according to risk group based on the initial plasma acetaminophen concentration. Hepatotoxicity (aspartate aminotransferase or alanine aminotransferase of more than 1,000 IU/L) developed in 10% (five of 50) of patients at "probable risk" when IV NAC was started within ten hours of acetaminophen ingestion and in 27.1% (23 of 85) when therapy was begun after ten to 24 hours. Among "high-risk" patients first treated 16 to 24 hours after overdose, hepatotoxicity occurred in 57.9% (11 of 19). There were two deaths (two of 179, 1.1%). Adverse reactions resulting from NAC occurred in 32 of 223 cases (14.3%), consisting in 29 of 32 patients (91% of reactions) of transient, patchy, skin erythema or mild urticaria during the loading dose that did not require discontinuation of therapy. CONCLUSION: This 48-hour IV NAC protocol is safe and effective antidotal therapy for acetaminophen overdose. Based on available data, it is equal to 72-hour oral and 20-hour IV treatment protocols when started early and superior to the 20-hour IV regimen when treatment is delayed. Further study will be required to determine its relative efficacy in the high-risk patient treated very late.

Acetaminophen↗
PubMed1991

The rise in the total iron-binding capacity after iron overdose.

STUDY OBJECTIVES: To determine if and to what extent the total iron-binding capacity (TIBC) would increase following an iron overload, and to identify specific iron-binding proteins that might be responsible for the increased TIBC. DESIGN: A prospective laboratory investigation. SETTING: A certified regional poison control center. PARTICIPANTS: Six healthy adult male volunteers. MEASUREMENTS AND MAIN RESULTS: All volunteers ingested 20 mg/kg of elemental iron. Blood samples were drawn at hourly intervals for eight hours and analyzed for serum iron, TIBC, transferrin, ferritin, lactoferrin, glucose, bicarbonate, and WBC. Within two hours of ingestion, subjects developed symptoms of toxicity, including nausea, lightheadedness, vomiting, severe crampy abdominal pain, and voluminous diarrhea. The TIBC was statistically significantly increased at all points measured from one to six hours. Despite rising above 300 micrograms/dL in five of six subjects, the serum iron never exceeded the TIBC in any subject. Transferrin and ferritin did not increase to account for the increased TIBC. The lactoferrin levels did increase, but they did not correlate with significant increases in the TIBC. CONCLUSIONS: Twenty mg/kg of elemental iron caused clinical toxicity in this study, and after iron overload the colorimetric TIBC increased by unknown mechanisms.

Adult↗
PubMed1991

Fluoride ingestion in children: a review of 87 cases.

All cases of fluoride ingestion in children younger than 12 years old reported to the Rocky Mountain Poison Center between January 1 and December 31, 1986, were retrospectively reviewed. Eighty-seven cases were identified. Eighty-four cases involved accidental ingestion of dental fluoride products in the home (tablets, drops, rinses) in children 8 months to 6 years old. Two older children (8 and 9 years old) became symptomatic after fluoride treatment by a dentist. A 13-month-old child died after ingesting an unknown amount of sodium fluoride insecticide, the only insecticide exposure in our series. Postmortem total serum calcium value was 4.8 mg/dL (normal 8.8 to 10.3). No other patients had serious symptoms or sequelae. Twenty-six (30%) of 87 became symptomatic, with gastrointestinal symptoms (nausea, vomiting, diarrhea, abdominal pain) in 25 patients and drowsiness in 1. Only 3 patients became symptomatic later than 1 hour after ingestion. Analysis of data from 70 cases with sufficient information revealed that as the amount of fluoride ingested increased, the percentage of patients with symptoms increased. Not including the fatal case, 6 patients had serum calcium levels measured, and all were normal. Children who ingested up to 8.4 mg/kg of elemental fluoride in dental products had mild and self-limited symptoms, mostly gastrointestinal.

Accidents↗
PubMed1990

Whole-bowel irrigation as treatment for zinc sulfate overdose.

A 16-year-old boy ingested approximately 50 zinc sulfate tablets (ZnSO4; 500-mg tablets). After spontaneous emesis, ipecac-induced emesis, and orogastric lavage, an abdominal radiograph performed four hours after ingestion still demonstrated approximately 50 ZnSO4 tablets within the stomach and three pills within the colon. Whole-bowel irrigation was begun with a polyethylene glycol lavage solution (PEG; Golytely) that was administered through a nasogastric tube; within one hour, the patient began producing a rectal effluent that contained pills. The patient remained asymptomatic throughout whole-bowel irrigation. Stool guaiac tests were negative. The serum chloride, however, increased from 105 to 127 mEq/L. Follow-up kidney, ureter, and bladder studies demonstrated the clearance of the zinc tablets from the gastrointestinal tract during the next 24 hours.

Administration, Rectal↗
PubMed1990

The diagnostic utility of flumazenil (a benzodiazepine antagonist) in coma of unknown etiology.

The use of flumazenil, a benzodiazepine antagonist, was studied in two patients with coma of unknown etiology. One patient ingested 20.5 mg alprazolam before crashing his truck into parked automobiles. The patient was awakened by flumazenil administration, and the severity of his injuries was evaluated reliably. A second patient ingested 7.5 mg triazolam and attempted suicide with carbon monoxide from car exhaust. His coma resolved completely after the administration of the double-blind study drug, obviating treatment with hyperbaric oxygen. Flumazenil had a clear diagnostic and therapeutic role in the treatment of these patients and should be a useful tool for emergency physicians and toxicologists.

Adult↗
PubMed1990

The other alcohols. Methanol, ethylene glycol, and isopropanol.

The alcoholic patient, in an attempt to maintain an altered mental status, may ingest ethanol substitutes containing methanol, ethylene glycol, or isopropanol. The subsequent clinical presentation in the Emergency Department is highly variable and depends on the ethanol substitute ingested, the time since ingestion, and concomitant ethanol abuse. This article describes the clinical features of intoxication by the ethanol substitutes. Early diagnosis and therapeutic intervention may prevent irreversible sequelae. The rationale for treatment interventions is discussed.

1-Propanol↗
PubMed1990

Formate levels following a formalin ingestion.

Although formalin ingestions have previously been reported in the literature, technology has only recently been developed to measure both formaldehyde and formate levels in plasma. Methanol, formaldehyde, and formate levels were followed in the case reported here until the patient's death approximately 13 h after the ingestion. The clinical course was marked by an initial profound CNS depression followed by an apparent clinically quiescent period. Severe abdominal pain and retching preceded the development of seizures, DIC, severe hypotension, and cardiac arrest. Methanol levels rose throughout this 13-h course. Formate and formaldehyde levels increased until bicarbonate and ethanol therapy were instituted. The "fixing" of the stomach by formaldehyde may have produced delayed absorption following formalin ingestion. Therapeutic implications are discussed.

Central Nervous System↗
PubMed1989

Superwarfarin poisoning in children: a prospective study.

This prospective study was undertaken to determine the incidence, severity, time of onset, and duration of coagulopathy in children following accidental ingestion of long-acting anticoagulant rodenticides, often called "superwarfarins." Of 110 children, who ingested superwarfarins and in whom one or more prothrombin time values were obtained, 8 had a prothrombin time ratio (patient to control) of greater than or equal to 1.2, indicative of anticoagulation. Prothrombin time values obtained 48 hours after ingestion were more likely to be prolonged (6/34, 17.6%) than values obtained 24 hours after ingestion (2/104, 1.9%) (P less than .005). The occurrence of an abnormal prothrombin time could not be predicted based on the history of amount ingested or on the presence of the characteristic green-blue product dye in or around the child's mouth. Acute toxicity was evidenced by transient abdominal pain, vomiting, and heme positive stools in 2 patients. The duration of prothrombin time prolongation could not be determined because of the few values obtained after 48 hours. To detect all possible abnormal prothrombin time values, 24- and 48-hour determinations are recommended after a child has ingested a superwarfarin.

4-Hydroxycoumarins↗
PubMed1988

Efficacy of oral N-acetylcysteine in the treatment of acetaminophen overdose. Analysis of the national multicenter study (1976 to 1985)

During the investigational use of oral N-acetylcysteine as an antidote for poisoning with acetaminophen, 11,195 cases of suspected acetaminophen overdose were reported. We describe the outcomes of 2540 patients with acetaminophen ingestions treated with a loading dose of 140 mg of oral N-acetylcysteine per kilogram of body weight, followed four hours later by 70 mg per kilogram given every four hours for an additional 17 doses. Patients were categorized for analysis on the basis of initial plasma acetaminophen concentrations and the interval between ingestion and treatment. Hepatotoxicity developed in 6.1 percent of patients at probable risk when N-acetylcysteine was started within 10 hours of acetaminophen ingestion and in 26.4 percent of such patients when therapy was begun 10 to 24 hours after ingestion. Among patients at high risk who were treated 16 to 24 hours after an acetaminophen overdose, hepatotoxicity developed in 41 percent--a rate lower than that among historical controls. When given within eight hours of acetaminophen ingestion, N-acetylcysteine was protective regardless of the initial plasma acetaminophen concentration. There was no difference in outcome whether N-acetylcysteine was started zero to four or four to eight hours after ingestion, but efficacy decreased with further delay. There were 11 deaths among the 2540 patients (0.43 percent); in the nine fatal cases in which aminotransferase was measured before treatment, values were elevated before N-acetylcysteine was started. No deaths were clearly caused by acetaminophen among patients in whom N-acetylcysteine therapy was begun within 16 hours. We conclude that N-acetylcysteine treatment should be started within eight hours of an acetaminophen overdose, but that treatment is still indicated at least as late as 24 hours after ingestion. On the basis of available data, the 72-hour regimen of oral N-acetylcysteine is as effective as the 20-hour intravenous regimen described previously, and it may be superior when treatment is delayed.

Acetaminophen↗
PubMed1988

Captopril overdose resulting in hypotension.

We present a case in which a patient took an overdose of captopril (Capoten) and alprazolam (Xanax) in a suicide attempt. The patient presented with hypotension (systolic blood pressure of 80 mm Hg) and drowsiness. The hypotension initially responded to administration of intravenous fluids and dopamine; however, it recurred twice at 18.5 and 24.5 hours after ingestion. These episodes again responded to administration of fluids and dopamine. A plasma captopril level of 27,391.1 nmol/L (5982 ng/mL) was documented, as well as a depressed level of angiotensin converting enzyme. Captopril is an angiotensin converting enzyme inhibitor used in the management of hypertension and ventricular failure; to our knowledge, this is the first case of an acute captopril overdose reported in the English-language literature. The role of captopril in inducing hypotension is discussed herein.

Adult↗
PubMed1988

Ethyl alcohol (ethanol)-containing cologne, perfume, and after-shave ingestions in children.

Colognes, perfumes, and after-shaves containing ethyl alcohol (ethanol) are frequently ingested by children. These products may contain from 50% to 99% ethanol. To determine if ingestion of colognes, perfumes, or after-shaves by children results in serious ethanol toxic reactions, this retrospective study was performed. One hundred twenty-three cases of children younger than 6 years old who ingested these products were reviewed. The cases were arbitrarily divided into three groups based on the amount ingested by history. Group 1 included children in whom less than 30 mL was ingested; group 2, 30 to 60 mL was ingested; and group 3, more than 60 to 105 mL was ingested. Of the 102 patients in group 1, no children experienced symptoms or signs. One of 17 children in group 2 was described by parents as sleepy but was asymptomatic one hour later. Two of four children in group 3 behaved as if intoxicated, yet blood ethanol levels were undetectable within 2 1/2 hours after ingestion. Based on our study, asymptomatic children who ingested by history less than 105 mL of a cologne, perfume, or after-shave and remain asymptomatic can be safely watched at home. All children with symptoms of intoxication need health care facility referral.

Alcoholic Intoxication↗
PubMed1988

Magnesium levels after magnesium-containing cathartics.

To determine the effect on serum Mg++ levels of oral Magnesium-containing cathartics (MgCC) used in the treatment of suspected drug overdose, a prospective, non-randomized study of 24 cases of suspected drug overdose was conducted. Ten cases admitted to the observation unit were assigned to the single dose MgCC group. Fourteen cases admitted to either the ICU or the observation unit were assigned to the multiple dose MgCC group. Single dose cases received 30 gm of magnesium sulfate (MgSO4) at 0 hours. Multiple dose cases received 3 30 gm doses of MgSO4 at 0, 4, and 8 hours. Mg++ levels were measured prior to each MgSO4 dose and 1 and 4 hours after the final dose in both groups. In the single dose group, there was no difference between baseline Mg++ levels and post MgSO4 levels, and only 2/10 developed slightly elevated levels (2.2, 2.3 mEq/L). In the multiple dose group, levels increased and remained significantly higher than baseline after the second MgSO4 dose, and 9/14 developed elevated levels (2.2 to 5.0 mEq/L). All patients who developed elevated Mg++ levels had normal BUN and creatinine values. When the single and multiple dose groups were compared, baseline Mg++ levels were no different (1.68 +/- 0.21 vs 1.69 +/- 0.24, p = 0.952), but peak Mg++ levels were significantly higher in the multiple dose group (1.80 +/- 0.31 vs 2.61 +/- 0.86, p = 0.004). Cases that developed hypermagnesemia had slightly higher baseline Mg++ levels (1.78 +/- 0.22 vs 1.60 +/- 0.19 mEq/L, p = 0.041). In the multiple dose group, higher peak Mg++ levels were noted in cases involving ingestions of anticholinergic or opioid drugs (2.83 vs 1.98, p = 0.025). Hypermagnesemia developed in some cases with normal renal function, blood pressure, and urine output. We conclude that significant hypermagnesemia can occur rapidly after use of multiple dose Mg++ cathartics in standard doses in patients with normal renal function.

Administration, Oral↗
PubMed1988

Ibuprofen overdose--a prospective study.

Of 61 cases of ibuprofen overdosage reported consecutively to the Rocky Mountain Poison and Drug Center from September 1985 through April 1986, 16 were excluded because of incomplete follow-up or concurrent medication ingestion. A toxic reaction developed in 7 (16%) of the remaining 45 patients. Nausea, vomiting, abdominal cramps, mild central nervous system depression, coma, tachycardia, apnea, metabolic acidosis with or without respiratory alkalosis, hematemesis, and oliguric renal failure were noted. Two of six adults had a toxic reaction, and one died. Among pediatric patients, 5/39 (13%) had a toxic reaction. Of patients whose ibuprofen ingestion was less than 104 mg per kg, none became ill. All patients in whom the time of ingestion was known (six of seven) and who had a toxic reaction did so within four hours of ingestion. An ibuprofen overdose, although usually benign, can occasionally produce serious toxicity.

Adolescent↗
PubMed1987

Clinical effects of accidental levothyroxine ingestion in children.

Forty-one children, aged 1 to 5 years, who accidentally ingested levothyroxine sodium were studied. Symptoms possibly associated with the ingestion occurred in 11 patients (27%). These symptoms (tachycardia, hyperactive behavior, fever, vomiting, diarrhea, diaphoresis, and flushing) were categorized as minor and all resolved without treatment. Because observed effects were generally mild and often unrelated to either estimated amounts of hormone consumed or serum thyroxine levels, a conservative approach to patient treatment is recommended in cases of levothyroxine ingestion in children.

Administration, Oral↗