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A case series of accidental ingestion of hand warmer
Abstract
The use of hand warmers in Hong Kong during cold weather has become increasingly popular. Iron powder is one of the ingredients. We report the first cases of ingestion of hand warmer contents. CARE REPORTS: Four elderly patients ingested the contents of hand warmers. All had no or mild symptoms, one had radiopaque particles in the stomach, two showed transiently increased serum iron concentrations (within the reference range), and all recovered with only supportive care.
These hand warmers contain a mixture of iron powder, activated charcoal, vermiculite, sodium chloride, and water. Iron powder accounts for about 50% of the weight (range 95-120 g). There are no reports of elemental iron or iron oxides ingestion causing iron toxicity and no published data on the absorption, elimination, adverse effects, or toxicities in humans after unintentional ingestion of hand warmer contents. A single oral dose toxicity test of hand warmer contents (2 g/kg) resulted in no toxicity or deaths in ten rats. Ingestions of one hand warmer packet or less can be treated with observation and supportive care as needed.
Although this case series is small, the lack of toxicity is consistent with animal studies. It appears unlikely that significant toxicity will occur after the ingestion of one hand warmer packet. The ingestion of larger amounts might lead to iron-related toxicity and may justify more aggressive management. Proper labeling by local distributors may prevent further unintentional ingestions of these non-food products.
... Their active ingredient is reduced iron—an amorphous powder without crystals prepared by reduction of iron oxide by hydrogen [1]. Reduced iron oxidizes when exposed to oxygen; this exothermic reaction produces the desired heating effect [2]. Classic teaching is that reduced iron is not expected to cause significant toxicity when ingested orally [1, 3]. ...
... Classic teaching is that reduced iron is not expected to cause significant toxicity when ingested orally [1, 3]. This supposition, however, is based on a very limited number of human cases [2]. We report a case of accidental heating pad ingestion visible on abdominal plain films that resulted in significantly elevated serum iron levels. ...
... Reduced iron has been reported to cause little to minimal effects123 .There have been reports of accidental ingestions of reduced iron with minimal elevations of serum iron; however, the elevated levels all returned to normal range within the first 24 h [2]. The authors in this series noted a theoretical risk of iron poisoning; mechanistically, this is possible as the iron oxides may react with hydrochloric acid in the stomach to produce the more easily absorbed iron chloride [4]. ...
Disposable heating pads are commonly used products, with reduced iron as their active ingredient. Reduced iron is not expected to cause significant toxicity when ingested orally. We report a case of accidental heating pad ingestion seen on abdominal plain films that resulted in significantly elevated serum iron concentrations.
... To the best of our knowledge, this is the first documented case of iron intoxication following ingestion of ironcontaining oxygen scavengers. Reported sources of unintentional iron intoxication in humans and animals include prenatal vitamins, multi-vitamins with iron, iron supplements (prescription or OTC), or, less commonly ferric chloride, parenteral iron, iron-based slug bait and fertilizers, and reduced-iron containing products such as instant hand/ foot warmers234. Reduced iron, the active ingredient believed to be in iron-based oxygen scavengers, is reported to have poor solubility in water and weak acids, which likely results in low oral bioavailability. ...
... Reduced iron, the active ingredient believed to be in iron-based oxygen scavengers, is reported to have poor solubility in water and weak acids, which likely results in low oral bioavailability. Until recently, the reduced iron contained in products such as oxygen absorbers or instant hand/foot warmers was not deemed to be of toxicological significance [3, 5]. However, the particle size of reduced iron is critically important to determine the bioavailability ; the smaller the iron particle, the greater its bioavailability [6]. ...
Oxygen absorbers are commonly used in packages of dried or dehydrated foods (e.g., beef jerky, dried fruit) to prolong shelf life and protect food from discoloration and decomposition. They usually contain reduced iron as the active ingredient although this is rarely stated on the external packaging. Although reduced iron typically has minimal oral bioavailability, such products are potential sources of iron poisoning in companion animals and children. We present a case of canine ingestion of an oxygen absorber from a bag of dog treats that resulted in iron intoxication necessitating chelation therapy. A 7-month-old female Jack Russell terrier presented for evaluation of vomiting and melena 8-12 h after ingesting 1-2 oxygen absorber sachets from a package of dog treats. Serum iron concentration and ALT were elevated. The dog was treated with deferoxamine and supportive care. Clinical signs resolved 14 h following treatment, but the ALT remained elevated at the 3-month recheck. The ingestion of reduced iron in humans has been reported to cause mild elevation of serum iron concentration with minimal clinical effects. To our knowledge, no cases of iron intoxication following the ingestion of oxygen absorbers have been reported. The lack of ingredient information on the packaging prompted analysis of contents of oxygen absorber sachets. Results indicate the contents contained 50-70% total iron. This case demonstrates that iron intoxication can occur following the ingestion of such products. Human and veterinary medical personnel need to be aware of this effect and monitor serum iron concentrations as chelation may be necessary.
... The hand warmer is a commodity that includes heat materials in a non-woven fabric bag and can expel cold, retain warmth, and promote the microcirculation of the body to relieve pain and detumescence [17,18]. The heating material is the main exothermic fraction of the hand warmer and is made up of iron powder, vermiculite, activated carbon, and salt. ...
In this study, an innovative method for RhB (Rhodamine B) degradation in a persulfate (PS) and hand warmer heterogeneous activation system was investigated. The hand warmer showed better catalytic performance and excellent reusability in terms of PS activation. The reaction rate constants of RhB removal in the hand warmer/PS process (0.354 min−1) were much faster than those in other PS- and Fe-related processes (0.010–0.233 min−1) at pH 7. The iron in the hand warmer is the main active ingredient to catalyze PS, and activated carbon, salt, and H+/OH− accelerate the activated reaction due to the formation of micro-batteries in the solution. Moreover, the catalyst of the hand warmer showed excellent stability and reusability with a low level of iron leaching. This new, effective, inexpensive, repeatable, and environmentally friendly catalyst combined with PS has promising prospects for the removal of dyes from industrial wastewater.
An 86-year-old man presented to the emergency room with vomiting and melena. The patient was hemodynamically stable and remained alert and orientated. According to his family, ingestion of a pack of disposable hand warmers, which he mistook for black sesame powder, occurred 17 h prior to admission. Before ingestion, he mixed the powder with warm water. Physical examination revealed no thermal injury of the oral mucosa with no abdominal pain or tenderness. An abdominal plain film showed multiple scattered radiopaque material with zonal distribution over the right abdomen. An intravenous 500-mg deferoxamine challenge test showed no vin rosé urine discoloration. Serial serum iron levels remained within the normal range. The patient remained clinically stable with no medical complications. He was discharged 3 days after admission. The hand warmers consisted of iron powder (50% w/w), sodium chloride, activated charcoal, and nontoxic vermiculite: a potential risk for intestinal thermal injury. In this case, the water added beforehand rapidly terminated the iron oxidation reaction. This explained the lack of thermal injury. Ferric oxide is poorly absorbed by the digestive tract and explained the absence of iron intoxication. Therefore, clinicians should clarify the method of ingestion. If a hand warmer has been premixed with water, less mucosa injury can be expected with a lower risk of iron intoxication. This report also provided evidence that abdominal plain films can be used to confirm the ingestion of iron and monitor its elimination.
Metabolic syndrome (MetS, i.e., type 2 diabetes and obesity) is often associated with dysbiosis, inflammation, and leaky gut syndrome, which increase the content of oxygen and reactive oxygen species (ROS) in the gastrointestinal (GI) tract. Using near-infrared fluorescent, in situ imaging of ROS, we evaluated the effects of oral administration of elemental iron powder (Fe⁰) on luminal ROS in the GI tract and related these changes to glucose metabolism and the gut microbiome. C57Bl/6J mice fed low-fat or high-fat diets and gavaged with Fe⁰ (2.5 g per kg), in both single- and repeat-doses, demonstrated decreased levels of luminal ROS. Fourteen days of repeated Fe⁰ administration reduced hyperglycemia and improved glucose tolerance in the obese and hyperglycemic animals compared to the untreated obese controls and reduced the relative amount of iron oxides in the feces, which indicated an increased redox environment of the GI tract. We determined that Fe⁰ administration can also be used as a diagnostic assay to assess the GI microenvironment. Improved metabolic outcomes and decreased gastrointestinal ROS in Fe⁰-treated, high-fat diet-fed animals correlated with the increase in a co-abundance group of beneficial bacteria, including Lactobacillus, and the suppression of detrimental populations, including Oscillibacter, Peptococcus, and Intestinimonas. Daily Fe⁰ treatment also increased the relative abundance of amplicon sequence variants that lacked functional enzymatic antioxidant systems, which is consistent with the ability of Fe⁰ to scavenge ROS and oxygen in the GI, thus favoring the growth of oxygen-sensitive bacteria. These findings delineate a functional role for antioxidants in modification of the GI microenvironment and subsequent reversal of metabolic dysfunction.
For individuals who work outdoors in the winter or play winter sports, chemical hand warmers are becoming increasingly more commonplace because of their convenience and effectiveness. A 32-year-old woman with a history of chronic pain and bipolar disorder presented to the emergency department complaining of a “warm sensation” in her mouth and epigastrium after reportedly ingesting the partial contents of a chemical hand warmer packet containing between 5 and 8 g of elemental iron. She had been complaining of abdominal pain for approximately 1 month and was prescribed unknown antibiotics the previous day. The patient denied ingestion of any other product or medication other than what was prescribed. A serum iron level obtained approximately 6 hours after ingestion measured 235 micrograms/dL (reference range 40–180 micrograms/dL). As the patient demonstrated no new abdominal complaints and no evidence of systemic iron toxicity, she was discharged uneventfully after education. However, the potential for significant iron toxicity exists depending on the extent of exposure to this or similar products. Treatment for severe iron toxicity may include fluid resuscitation, whole bowel irrigation, and iron chelation therapy with deferoxamine. Physicians should become aware of the toxicity associated with ingestion of commercially available hand warmers. Consultation with a medical toxicologist is recommended.
Acute exogenous lipoid pneumonia is an uncommon condition caused by aspiration of oil-based substances, occurring mainly in children. Here, we report the case of an 83-year-old patient with Alzheimer's disease who presented with coughing and hypoxia. The diagnosis of acute exogenous lipoid pneumonia caused by accidental kerosene ingestion was made on the basis of the patient's clinical history, and typical radiological and cytological findings. The patient's cognitive impairment and an unsafe environment, in which the patient's 91-year-old husband stored kerosene in an old shochu bottle, were responsible for the accidental ingestion. Acute exogenous lipoid pneumonia should be considered in the differential diagnosis for acute respiratory disorders in the rapidly aging population. Geriatr Gerontol Int 2013; 13: 222-225.
Corrosive injury of the esophagus and stomach is never been reported after intoxication of hand warmers. Herein we reported a case that had grade IIA corrosive injury found by endoscopic examination.
An 84 year-old woman with a history of dementia ingested the contents of hand warmers. She had radiopaque patches in the stomach and duodenum. Upper endooscopic examination revealed corrosive injury of the esophagus and stomach. She recovered with the use of deferoxamine and proton pump inhibitor (PPI).
The hand warmer contains activated charcoal, salt, and vermiculite, and 50% of iron powder. In previous literature, ingestions of one hand warmer packet or less are considered less toxic. But in our case, corrosive injury of the esophagus and stomach is obvious.
It appears that significant toxicity will occur after ingestion of one hand warmer packet. Appropriate gastrointestinal decontamination and aggressive management are needed for all patients who are hand warmers intoxicated.
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.
A prospective laboratory investigation.
A certified regional poison control center.
Six healthy adult male volunteers.
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.
Twenty mg/kg of elemental iron caused clinical toxicity in this study, and after iron overload the colorimetric TIBC increased by unknown mechanisms.
Death from ferric chloride poisoning has never been reported in Taiwan. We report a fatality from the suicidal ingestion of ferric chloride solution used as an etching agent for printed circuitry. A 25-y-old woman presented with vomiting after ingestion of 200 ml ferric chloride solution (pH 1.0). She had hypoxemia and severe metabolic acidosis with respiratory alkalosis initially. Three hours after her ingestion she presented with drowsy consciousness, tachycardia, tachypnea and protracted vomiting. Laboratory studies showed leukocytosis, elevated glucose, aspartate aminotransferase, amylase, lactate dehydrogenase, and total bilirubin, coagulation defect and hemolysis. Aspiration pneumonia and vision loss were also noted. Four hours after ingestion cardiopulmonary arrest suddenly occurred after severe vomiting and she expired. Toxicological studies showed marked elevation of serum iron (2440 micrograms/dl); the estimated oral dose of ferric chloride was equivalent to 11.52 g (230 mg/kg) of elemental iron. This patient did not receive deferoxamine due to rapid deterioration and a late diagnosis. Deferoxamine should be given in any symptomatic patient or in the presence of anion gap metabolic acidosis with a history of ferric chloride ingestion.
Iron is a unique poison because it is not a xenobiotic. It is an essential element and highly reactive. Because of the critical dependence upon iron and its potential to damage tissues, elaborate mechanisms have evolved for its efficient absorption, transport, cellular uptake, storage and conservation. These are incompletely understood with even less being known after the ingestion of an overdose. Thus little is known of iron's toxicokinetics. Less is known regarding its absorption. A saturable active receptor mediated mechanism has been described, however, a passive mechanism is speculated to exist. After overdose, the amount absorbed is unknown but is likely in the order of 10%. Transferrin capacity is saturated after the absorption of a toxic dose resulting in much of the circulating iron being hydrated ferric ion. The liver clears most of the circulating iron and the plasma half-life after overdose is similar to the 4-6 h observed after therapeutic dosing. There is no mechanism for iron excretion. The toxicodynamics are a consequence of the chief mechanism for iron-induced tissue damage, free radical production with resultant lipid peroxidation. Therefore target organs and tissues are those exposed to high concentrations of iron and have a high metabolic activity. These are the gastrointestinal epithelium, cardiovascular system and the liver. Five distinct clinical phases are recognized: Gastrointestinal Toxicity, Relative Stability, Circulatory Shock and Acidosis, Hepatotoxicity and Gastrointestinal Scarring. Rational treatment of iron poisoning requires a thorough understanding of its toxicokinetics and toxicodynamics.
Sir.—Although the review of iron poisoning offered by Drs Robotham and Lietman (Journal 1980;134:875-879) was comprehensive and thoughtful, several points regarding deferoxamine mesylate and lavage solutions deserve closer consideration. The authors suggest that "all patients arriving with a history of iron ingestion" be treated immediately with 2 g of intramuscular (IM) deferoxamine me-sylate. In cases with a reliable history of ingestion of less than 50 mg/kg of iron, animal data1 suggest a limited toxic potential. We have found this quantity to be a useful guide to identify those patients requiring early aggressive treatment in the absence of symptoms or other indications. For patients requiring deferoxamine, large fluid losses and poor tissue perfusion are common. In such a situation, treatment with IM deferoxamine would seem irrational. Intravenous administration is a more reasonable and reliable route for deferoxamine when it is clearly indicated.
The authors have supported the oral
Severe acute iron poisoning developed in a 1 1/2-year-old child who had eaten an iron preparation that resembles a popular chocolate candy. Tablets containing iron, with and without vitamins, and the sugar-coated candy of similar appearance, were radiographed with human gastric juice in vitro. Times of dissolution of the radiopaque tablets were noted, to assess the value of abdominal radiographs in the diagnosis and management of acute iron poisoning.
An 11-month-old, 11-kg infant presented to the emergency department after ingesting 130 to 150 mg/kg of elemental iron. Emesis was induced twice and the child was lavaged throughout a 4-hour period with some tablet return. An abdominal radiograph after gastrointestinal decontamination showed at least 16 whole iron tablets remaining in the stomach. Serum iron drawn 2 hours postingestion was 46.7 mumol/L. Blood glucose was 7.7 mmol/L and white blood count was 21,800 mm3. Despite a second lavage 8 hours postingestion, a large number of whole tablets were visualized in the stomach per radiograph. Whole bowel irrigation with polyethylene glycol electrolyte lavage solution (Golytely, Braintree Laboratories, Inc, Braintree, MA) was begun via nasogastric tube 14 hours after the ingestion. Serial abdominal radiographs showed tablet movement out of the stomach within 4 hours after initiating whole bowel irrigation. This case demonstrates the safety and efficacy of WBI in an infant when conventional gastrointestinal decontamination has failed.
Even though ingestion of chewable iron preparations is much more common, treatment recommendations for iron overdose are usually based on experience with nonchewable preparations. To determine the optimal time to measure serum iron concentrations, five volunteers were given chewable iron in 5 mg/kg and 10 mg/kg doses and their serum iron concentrations monitored. Peak levels occurred at 4.2 and 4.5 hours, respectively, after ingestion, and levels drawn at 3 hours were within 90% of the peak. Nausea and headache were experienced by all volunteers, and serum iron exceeded baseline total iron binding capacity in two subjects at the 10 mg/kg dose. In minor iron overdose resulting from the ingestion of chewable vitamins, serum iron concentrations measured between 3 and 7 hours (95% confidence level of peak concentrations) may be adequate in assessing the peak serum iron concentration.
Iron poisoning continues to be a major toxicologic problem, with major impact on the gastrointestinal and circulatory systems. Failure to recognize the severity of iron intoxication may result in an inappropriate level of intervention. By using estimates of the total body burden of iron, clinical symptoms, and the serum iron concentration, an appropriate decision can be made to initiate aggressive chelation therapy with deferoxamine. In severe intoxication, the use of intravenous deferoxamine is indicated, along with supportive care, with particular attention to maintaining the intravascular volume. Other important measures include correction of acidosis and disorders of coagulation and replacement of blood components when there is evidence of gastrointestinal hemorrhage. Under rare circumstances in which large numbers of iron tablets are present in the gastrointestinal tract, surgical removal may be indicated. In addition, measures such as hemodialysis and exchange transfusion should be reserved for those unusual poisonings in which more conservative therapy is unsuccessful. In rare cases of iron intoxication, late sequelae such as hepatic necrosis and gastrointestinal scarring with obstruction may occur. The prompt recognition and initiation of management of children with acute iron poisoning is the single most critical element in decreasing the morbidity and mortality associated with these products.
Acute iron poisoning is most common in children below the age of 5 years. While there is no doubt that it may be fatal, recent surveys show that death occurs in only a very small percentage of cases and that iron salts are responsible for a small minority of fatalities due to overdosage with drugs. Similarly, the proportion of severe cases seems to have fallen over the last thirty years, possibly due to earlier and more aggressive treatment but more probably due to an increase in the number of minor exposures reported.
Iron salts are directly toxic to the gastrointestinal tract causing vomiting, diarrhoea, abdominal pain and occasionally significant blood loss. They also cause metabolic acidosis by interfering with intermediary metabolism and producing shock and reduced tissue perfusion.
The clinical course of acute iron poisoning is divided into 4 phases. Features of acute gastrointestinal irritation dominate the period up to 6 hours after ingestion and most patients do not develop other features or progress beyond this stage. Rarely, blood loss may be sufficient to cause hypotension. Severe poisoning is characterised by impairment of consciousness, convulsions and metabolic acidosis. The second phase, 6 to 12 hours after ingestion, is one of remission of features. Phase 3 comprises the period 12 to 48 hours from ingestion and is reached only by a small minority of patients. Recurrence or development of shock, and metabolic acidosis are usual and renal failure and features of extensive hepatocellular necrosis may develop. The last (fourth) phase, 2 to 6 weeks after ingestion, is only likely to develop in young children and is characterised by recurrence of vomiting due to gastric or duodenal stenosis caused by healing of iron-induced mucosal ulcers.
Acute iron poisoning in humans has not been adequately studied and is unlikely to be so now because of the infrequent and sporadic occurrence of cases. The evidence for many conventional aspects of management is therefore unsatisfactory. Assessment of severity of poisoning is an essential prerequisite to optimum management but is difficult. The amount of elemental iron ingested is unacceptable since it is seldom known with accuracy and absorption is unpredictable because of vomiting and diarrhoea. The commonly encountered clinical features are also unreliable although it is generally accepted that coma, shock and metabolic acidosis indicate severe poisoning. Measurement of the serum iron concentration is the most satisfactory method with levels above the predicted serum iron binding capacity (i.e. > 70 μmol/L or 375 μg/dl) indicating circulating free iron and the risk of serious toxicity. Emergency serum iron measurements should be available round-the-clock to obviate the need to use indirect methods based upon urine colour change in response to intramuscular desferrioxamine (deferoxamine) [the desferrioxamine challenge test].
Treatment of the majority of patients poisoned with iron salts requires no more than decisions about gastric emptying and the need for administration of the specific chelating agent, desferrioxamine. Immediately the patient presents, blood should be taken for urgent measurement of the serum iron concentration and gastric emptying carried out, if indicated, while waiting for the result. An important exception to this guideline are patients who are in shock, coma or who have metabolic acidosis who should be started on intravenous desferrioxamine at a rate of 15 mg/kg/hour without waiting for the result of the serum iron concentration.
The stomach should be emptied if >10 mg/kg bodyweight of elemental iron has been ingested within the preceding 4 hours. Gastric lavage is preferable to induced emesis and tepid tap water is probably as adequate as any other solution for the purpose and is safer than some. Desferrioxamine (10g) should be left in the stomach at the end of lavage, although its efficacy in preventing iron absorption is uncertain.
Patients whose serum iron concentrations are greater than their expected iron binding capacity should be given desferrioxamine 15 mg/kg/hour intravenously and observed for adverse effects such as rashes, hypotension and, rarely, anaphylaxis. The rate of administration should be reduced to 5 mg/kg/hour as soon as clinical improvement has occurred (which will usually be within 4 hours) and stopped when the serum iron has fallen below the expected total iron binding capacity. The total dose of desferrioxamine should not exceed 80 mg/kg per 24 hours.
Iron overdosage in pregnancy should be managed in the same manner. The limited evidence available indicates that desferrioxamine protects the mother and appears to have no adverse effects on the fetus.
In addition to these measures, severe poisoning may require blood transfusion, correction of metabolic acidosis with intravenous sodium bicarbonate, supportive treatment for hypotension and maintenance of a clear airway and adequate ventilation. Renal and hepatic function must be monitored in symptomatic patients and failure treated conventionally.
Emesis and lavage often are ineffective in providing complete emptying of the stomach after an ingestion. With a locally corrosive and systemically toxic agent such as iron, surgical intervention with emergency gastrotomy may be required. We recently treated a 19-year-old man in the ED and in the departments of surgery and medicine who required a gastrotomy to remove a large amount of elemental iron inaccessible to removal by emesis, lavage, or gastroscopy. At gastrotomy the stomach showed full-thickness inflammation; the entire mucosal surface was hemorrhagic in nature. Gastrotomy was successful in allowing the removal of a large amount of the retained corrosive material. The severity of the findings at gastrotomy and the dramatic clinical improvement and recovery in our patient strongly support this approach if traditional methods fail.
ACCIDENTAL poisoning by iron compounds continues to be a common pediatric problem.1 2 3 This brief review includes the current thoughts on the pathophysiology of iron poisoning, the results of treatment with a new chelating agent, deferoxamine, in 6 previously published cases and 5 new cases treated by us, including a detailed case report. Information is given regarding availability of the drug for clinical use in the treatment of acute iron poisoning. Clinical Features The clinical features of iron intoxication are summarized in Table 1. The patient ingesting an overdose of iron may proceed through four stages.4 Stage 1 occurs from immediately to . . .
Reduced iron, B.P. 1932, an old form of medicinal metallic iron powder, was given by mouth to albino rats. Measurable toxic effects were not produced until the dose reached 10 g./kg. body weight, which is 10 times the LD(50) of iron similarly given as ferrous sulfate. Death occurred at three days and after from doses of 60 to 100 g./kg. and was due to hemoconcentration and vascular congestion of the liver and kidneys resulting from absorption of iron through an inflamed gastrointestinal mucosa. Larger doses produced death in one to three days from bowel obstruction due to impaction of iron in the stomach and intestines. The results suggest that reduced iron is the least toxic of all iron medicinal preparations and that re-investigation of its therapeutic value is warranted.
A 15-month-old girl who ingested an estimated 80 mg/kg to 100 mg/kg of elemental iron was treated in the emergency department for acute iron poisoning. Attempts to evacuate the stomach using emesis and gastric lavage were ineffective. Abdominal radiographs confirmed the presence of large, iron-containing aggregates in the stomach. An emergency gastrotomy was required to remove this potentially lethal dose of iron. During surgery the iron was noted to be embedded in the gastric mucosa, explaining its previous resistance to conventional stomach-emptying methods.
Acute iron overdose is a serious cause of morbidity and mortality, however, optimal gastric decontamination procedures in iron overdose are unclear. In order to determine the effectiveness of oral deferoxamine mesylate solution in humans to prevent the absorption of iron in acute exposures, the following prospective case control crossover study was designed. Seven informed adult human volunteers were given an oral dose of 5 mg/kg elemental iron alone in a control phase and again in an experimental phase followed by a single equimolar dose of oral buffered deferoxamine solution. Plasma iron concentrations were determined spectrophotometrically for eight hours following administration of iron alone and following doses of iron with deferoxamine. There was no significant difference in peak iron concentration, time to peak iron concentration or area-under-the-curve between the two groups. Based on our results, equimolar doses of oral deferoxamine do not appear to decrease the absorption of low doses of oral iron in humans.
We describe the successful treatment of a severely iron-poisoned adult patient in week 26 of gestation with 10.2 g deferoxamine administered iv over 14 h and whole bowel irrigation (2 L/h of polyethylene glycol-electrolyte solution/nasogastric tube for 12 h) with a good maternal outcome and no adverse effects on the fetus.
The maximum duration and volume of polyethylene glycol electrolyte solution (PEG-ELS) that can be safely administered during whole-bowel irrigation of the poisoned patient are poorly defined. We present a case of a 33-month-old boy who ingested at least 160 mg/kg elemental iron and received 44.3 L of PEG-ELS (2,953 ml/kg) over 5 days because of the persistence of iron tablets in teh gastrointestinal tract. The child remained clinically well after initiation of PEG-ELS therapy, and further significant iron absorption did not appear to occur. The rectal effluent cleared within 2 days of the start of PEG-ELS therapy despite the persistence of iron in the gastrointestinal tract as shown on radiography. No adverse effects resulted from teh large volume or duration of the PEG-ELS therapy. This is the greatest reported volume of PEG-ELS to be used for whole-bowel irrigation in the treatment of a toxic ingestion.
To determine whether leukocytosis, hyperglycemia, vomiting, and opacities in abdominal radiographs are indicators of a serum iron concentration of > 300 micrograms/dL in adult iron overdose patients, a retrospective medical record review was undertaken at a university medical center of all patients older than 12 years of age for whom clinical data were collected before deferoxamine therapy and within 6 hours of iron ingestion. Forty-three patients met the inclusion criteria; 37 were female. The mean and range serum iron concentrations were 382 micrograms/dL and 58 to 710 micrograms/dL, with 34 patients having values of > 300 micrograms/dL. There were no statistically significant relationships between iron concentration of > 300 microgram/dL and leukocytosis, hyperglycemia, vomiting, and opacities in abdominal radiographs (P > .05). Sensitivities, specificities, and positive and negative predictive values indicate poor performance of these parameters as clinical predictors of serum iron concentration of > 300 micrograms/dL. Leukocytosis, hyperglycemia, vomiting, or the presence of opacities in abdominal X-rays are not indicators of a serum iron concentration of > 300 micrograms/dL in adults. These parameters should not be used to assess the severity of iron overdose or to guide its management.
Ingestion of iron-containing tablets ranks high as a cause of poisoning in children in the United States. In spite of various therapeutic regimens, the mortality rate approaches 50 per cent (1). As little as one gram may be fatal to a child (5). In children with iron intoxication vomiting, diarrhea, drowsiness, shock, and acidosis usually develop within thirty to sixty minutes after ingestion. Death follows within the first six hours in 20 per cent of the patients. In the remainder there is either gradual recovery or a period of apparent recovery lasting eight to sixteen hours, followed by shock, coma, convulsions, and death. One to two months later scarring of the stomach or bowel may cause obstruction (2). Abdominal roentgenograms have been recommended to establish the presence of iron in the gastrointestinal tract (3) and to determine the effectiveness of measures employed to remove it from the stomach and colon (3, 4). The following studies were undertaken to ascertain the roentgenographic appearance ...
Vomiting frequently complicates the administration of activated charcoal. The incidence of such vomiting is not defined precisely in the pediatric population. Little is known about the patient-, poison-, or procedure-specific factors that contribute to emesis of charcoal. This study aimed to estimate the incidence of vomiting subsequent to therapeutic administration of charcoal to poisoned children < or =18 years of age and to examine the relative contributions of several risk factors to the occurrence of vomiting.
Data were collected on a prospective cohort of 275 consecutive children who were treated with activated charcoal for acute poisoning exposure. The study was set in the emergency department of an urban, tertiary-care children's hospital. Sorbitol content of the charcoal was alternately assigned. Potential risk factors for vomiting were recorded prospectively, and the occurrence of vomiting within 2 hours of charcoal administration was measured.
A total of 56 (20.4%) of 275 patients vomited. Median time to vomiting was 10 minutes. Previous vomiting (relative risk: 3.41; 95% CI: 1.48-7.85) and nasogastric tube administration (relative risk: 2.40; 95% CI: 1.13-5.09) were found to be the most significant independent risk factors for vomiting. The increased risk among children >12 years of age, compared with younger children, approached significance. Sorbitol content, large charcoal volumes, or fast administration rates did not increase vomiting risk significantly.
One of every 5 children who are given activated charcoal within our pediatric emergency department vomited. Children with previous vomiting or nasogastric tube administration were at highest risk, and these factors should be accounted for in future investigation of antiemetic strategies. Sorbitol content of charcoal was not a significant risk factor for emesis.
The rise in the total ironbinding capacity after iron overdose Clinical Toxicology Downloaded from informahealthcare.com by 202
- Kk Burkhart
- Kw Kulig
- Hammond
Burkhart KK, Kulig KW, Hammond KB. The rise in the total ironbinding capacity after iron overdose. Ann Emerg Med 1991; 20:532–535. Clinical Toxicology Downloaded from informahealthcare.com by 202.98.123.126 on 05/20/14 For personal use only.
Iron poisoning: assessment of radiography in diagnosis and management
- Rcw Ng
- K Perry
- D J Martin
Ng RCW, Perry K, Martin DJ. Iron poisoning: assessment of radiography in diagnosis and management. Clin Pediatr 1979; 18:614-616.
Use of whole-bowel irrigation in an infant following iron overdose
- Gw Everson
- Jo O Bertaccini
- Leary