Toxic Ingestion Research Articles

The feasibility of administration of activated charcoal with respect to current practice guidelines in emergency department patients

The American Academy of Clinical Toxicology, European Association of Poisons Centres, and Clinical Toxicologists recommend administration of activated charcoal (AC) within one-hour of an acute toxic ingestion [1]. Our poison control center periodically and upon request faxes an abbreviated protocol to hospital emergency departments, reminding physicians of these current AC recommendations. This study was conducted to describe how often patients present within the one-hour time frame and how often the guidelines in the above position statement are being followed. Following a brief training of systematic chart review, reviewers blinded to the purpose of the study completed a standardized data collection sheet. Three years after publication of these consensus statements, a period of 3 consecutive years of poison center patient encounters were reviewed. Recorded data included age, outcomes, and time to administration of charcoal. Approximately 150,000 reported toxic exposures were reviewed, of which 16,914 patients of acute ingestions presented to a health care facility. The mean age of the group that presented was 25 years [range 1 month-87 years]. A total of 2,700 (16%) patients that presented were within 60 minutes of an acute overdose and all were administered AC in accordance with the recommended guidelines. Interestingly, pre-hospital personnel administered AC within 60 minutes to 762 (28% of 2,700) patients. Correspondingly, 14,214 (84%) patients presented more than 60 minutes after an acute overdose. Of this latter group AC was withheld in 341 (2.4% of 14,214) patients, and 13,873 (97.6% of 14,214) patients received charcoal despite having arrived more than 60 minutes after ingestion. The mean time to the first administration of AC in this latter group was 225 minutes [range of 61-2160 minutes] following ingestion. Only a small percentage of patients treated for an acute overdose (16%) present within 60 minutes and are given charcoal according to the current guidelines. A large subset of these patients (28%) is given AC in a pre-hospital setting. Few patients presenting to a health care provider after an acute toxic ingestion are treated in accordance with the current recommendations for activated charcoal.

Are One or Two Dangerous? Calcium Channel Blocker Exposure in Toddlers

Unintentional pediatric ingestions of calcium channel blockers are increasing in frequency due to increased use of this antihypertensive class. Potential toxic effects include severe refractory hypotension and death; however, the true toxicity of unintentional pediatric ingestions of 1–2 pills is poorly defined. A literature review was conducted to more closely determine toxic and lethal dosages of calcium channel blockers in the pediatric population under 6 years of age. Results indicate that, although most accidental pediatric ingestions are asymptomatic, a small number do result in cardiovascular instability or even death. The dihydropyridines, particularly nifedipine, and the phenylalkylamine verapamil are most often implicated in symptomatic ingestions. There are no adequate data to identify which children are predisposed to illness, or to determine cutoffs for toxic dosages. However, ingestions of only one pill have been documented to cause severe symptoms, including death. Thus, emergency evaluation to assess potential toxicity is necessary, and gastrointestinal decontamination and in-hospital observation of at least 6 h after toxic ingestion for regular release medications, and 12–24 h after toxic ingestion for sustained release medications is recommended for all cases of unintentional calcium channel blocker ingestion in children younger than 6 years of age.

A Case of Methanol Poisoning

A 29‐year‐old male took about 300 ml industrial alcohol in a suicidal attempt. The industrial alcohol was later confirmed to be methanol. He presented to the emergency department 10 hours post‐ingestion with an anion gap metabolic acidosis and an osmol gap of 76.7 mOsm/kg. Ethanol infusion was started in the emergency department at 11 hours post‐ingestion before the availability of serum methanol level. The clinical diagnosis of toxic alcohol ingestion was based on the history, arterial blood gases results and the presence of a significant osmol gap. The patient was then admitted to the intensive care unit for ethanol therapy and haemodialysis. Prompt initiation of ethanol therapy and the subsequent intensive care prevented the development of life‐threatening complications of methanol poisoning in this case.

Superficial Hepatic Capsular Lesions in a Systemically Ill Young Woman

Superficial Hepatic Capsular Lesions in a Systemically Ill Young Woman

Poisoning due to raw Gyromitra esculenta (false morels) west of the Rockies

Vomiting with abdominal pain is a common presentation in the emergency department (ED). Without a careful history, unusual causes, such as toxic ingestion, may evade diagnosis. We report a case of an Asian couple who presented to the ED with vomiting and epigastric distress. They were discharged with no definite diagnosis, but on a return ED visit the following day were diagnosed with toxic ingestion of Gyromitra esculenta, commonly known as the western false morel. The patients were admitted and treated with intravenous hydration and pyridoxine. Both patients developed mild hepatotoxicity but went on to fully recover. This case demonstrates that the western false morel may cause significant toxicity and it highlights the importance of obtaining a complete history in patients who present with non-specific gastrointestinal symptoms.

Utility of urine drug screening: A Clinical audit

To assess requesting patterns and clinical utility of urine drug screens (UDS). All UDS requests received between March 2002 and October 2002 were identified. Two trained assessors reviewed case histories and categorized the utility of the UDS and gave a utility score using a Visual Analogue Scale. Of 171 UDS requested, 67.3% were men. Age range was 15-92 (mean 36) years. In total, 70.8% were received from accident and emergency centre (AEC). Clinical utility was identified in only 85 of 171 UDS. Sixty-one per cent of requests from AEC were defined as having no clinical utility. Twenty-four per cent of requests originating from other specialities were identified as having no clinical utility. Overall, a test was more likely to be of utility if it was requested from non-AEC than from AEC (Pearson's chi(2) two-sided t-test, P < 0.0001). Indications for UDS were toxic ingestion (33.3%), psychosis (15.2%), impaired consciousness (13.5%), behavioural disturbance (4.1%), confusion with HIV infection (3.5%), alleged adulteration (3.5%), seizure (9.4%), cardiac arrest (1.8%) and miscellaneous (15.8%). Our data show excessive requesting for UDS in routine overdose, contrary to international guidelines. Requests for UDS originating from AEC are more likely to have no utility than those from other specialities. Availability of point of care UDS might increase use of UDS, but cost-effectiveness and utility must be assessed.

A Retrospective Study of the Etiologies and Outcomes of Patients Admitted to a University Hospital with Presumed Acetaminophen Toxicity

We evaluated the characteristics and outcomes of patients admitted with presumed acetaminophen (APAP) toxicity in a large university hospital over a 3-year period. There were 128 adults (mean age, 36 + 12.5 y) and 51 pediatric patients (mean age, 14.3 + 4 y). Seventy-eight (60.9%) adult patients presented with intentional toxic ingestion, 47 (36.7%) unintentional toxic ingestion, and seven (5.5%) cases in whom the intent of APAP ingestion was unknown. Conversely, 42 (82.4%) of the pediatric cases were intentional ingestion ( P= 0.01 vs adults). Patients admitted with unintentional toxic ingestion had a greater degree of hepatic impairment; although, significant differences in serum chemistries were not seen in the pediatric patients. However, in the adult group, those with unintentional toxic ingestion had significantly greater peak serum concentrations of aspartame aminotransferase (AST), alanine aminotransferase (ALT), bilirubin, and prothrombin time (PT). There were 56 cases of unintentional toxic ingestion (47 adult, 9 pediatric). Acetaminophen was used for the treatment of pain in 37 adults (78.7%) and four children (44.4%); headache was the most frequent cause of pain (10 [27%] adult and three [75%] pediatric patients). Use of other potentially hepatotoxic medications was noted in 23 adult patients (62.2%), with hydrocodone/APAP (Vicodin) being used most frequently (51.4%). There were 31 patients who experienced fulminant hepatic failure. Eighteen (32%) patients developed fulminant hepatic failure following unintentional toxic APAP ingestion compared to 10 (8.3%) patients who had intentional toxic ingestion ( P&lt; 0.001) (see Table 4 ). Fulminant hepatic failure occurred most frequently in adults (26 patients, 93%) and in females (71%). The ubiquity of over-the-counter APAP and the ever increasing use of APAP prescription products have increased the risk in a population largely unaware of the potential toxicity. Health care providers need to document all medications that patients are ingesting and provide education to those who are at risk of APAP toxicity.

A Prospective Evaluation of Shortened Course Oral N-Acetylcysteine for the Treatment of Acute Acetaminophen Poisoning

Treatment with a shortened duration of oral N-acetylcysteine (20 to 48 hours) after acute acetaminophen poisoning is effective in the prevention of subsequent hepatic failure and death when administered to individuals meeting appropriate laboratory criteria. Individuals with a potentially toxic acetaminophen ingestion according to serum acetaminophen levels were identified prospectively using a large statewide poison control system database throughout a 12-month period. N-acetylcysteine was administered for a minimum of 6 doses (20 hours), after which laboratory studies were obtained. Discontinuation of N-acetylcysteine was recommended by the poison center when 2 criteria were met: serum acetaminophen was undetectable (<10 microg/mL) and liver test results were normal (serum aminotransferase, international normalized ratio). A follow-up questionnaire was administered to individuals treated with N-acetylcysteine for 48 hours or less to ascertain the presence of symptoms consistent with progressive hepatotoxicity. Of 205 acutely poisoned individuals treated with N-acetylcysteine for 48 hours or less, 195 were successfully contacted after discharge, and 187 of 195 (95.9%) reported no symptoms consistent with hepatic failure. Eight individuals (4.1%) reported abdominal pain or vomiting; however, none received further N-acetylcysteine treatment or additional hospitalization. A shortened duration of treatment with N-acetylcysteine (20 to 48 hours) may be an effective treatment option in individuals considered to be at no further risk of developing liver toxicity according to the fulfillment of appropriate laboratory criteria before N-acetylcysteine discontinuation.

Lithium use in special populations

Byline: E. Mohandas, V. Rajmohan Lithium, a monovalent cation, was first used for the treatment of mania in the 1940s. Half a century into its use, the drug continues to be the preeminent choice for bipolar disorder with antimanic, antidepressant (modest) and antisuicidal property. Lithium is the "gold standard" mood stabilizer against which potential mood stabilizer agents are judged. The therapeutic uses of lithium also include use as an augmenting agent in depression, schizoaffective disorder, aggression, impulse control disorder, eating disorders, attention deficit disorder and in certain subsets of alcoholism. Lithium has been used in many medical disorders, especially cluster headache and dermatological disorders (seborrheic dermatitis, eczematoid dermatitis, genital herpes).[sup] [1] The drug is however associated with neurologic, endocrine, cardiovascular, renal, dermatologic and gastrointestinal adverse effects and possible teratogenicity. History Lithium was first discovered and defined by Johan August Arfvedson in 1817 when he did an analysis of the mineral petalite [LiAl(Si2O5)2]. Petalite was first found by Brazilian scientist Jose Bonifacio Andrade e Silva in 1800. Lepidolite, spodumene, petalite and amblygonite are the more important minerals containing lithium. It was Arfwedson's laboratory chief John Jacob Berzelius who named this alkali metal "lithion." Arfvedson was never able to fully isolate lithium, and it wasn't until 1855 that it was isolated by William Thomas Brande. Brande and Sir Humphrey Davy earlier had done electrolysis on lithium oxide in 1818. Lithium was first produced commercially in 1923 by Metallgesellschaft AG.[sup] [2] The use of lithium for medicinal purposes can be traced back 1,800 years to the Greek physician Galen, who treated patients with mania by having them bathe in alkaline springs and drink the water, which probably contained lithium. In 1843 Alexander Ure introduced lithium into modern medicine, and he showed the in vitro reduction of weight of a uric acid bladder stone in a lithium carbonate solution. Sir Alfred Garrod later discovered that gouty uric acid deposits also were soluble in lithium solution. The view in that time was that uric acid imbalances caused a wide range of diseases, and Armand Trousseau and Alexander Haig proposed that mania and depression also may result from this imbalance and lithium may be effective in these conditions. In the 1840s, lithium was mixed with carbonate or citrate to form a salt and was used to treat gout, epilepsy, diabetes, cancer and insomnia. In the 1870s, the then American Surgeon General William Hammond had provided anecdotal evidence for the use of lithium bromide in the treatment of acute mania. In the 1880s and 1890s the Lange brothers Carl and Fritz used lithium in depression, and Carl Lange was the first to systematically use lithium in the acute and prophylactic treatment of depression.[sup] [2] The introduction of lithium preparations and tablets in the 1900s brought to the fore the toxic effects of the drug; and there were reports of weakness, tremor, diarrhea, vomiting and deaths. The drug disappeared from the British Pharmacopoeia by 1932, but later in the 1940s it was used as a sodium substitute in low sodium diets; but the reports of severe intoxication led to its removal from American markets in 1949. [sup] [1] The appearance in 1949 in the Medical Journal of Australia of a paper entitled "Lithium salts in the treatment of psychotic excitement" by John F. J. Cade was an unspectacular entry into a new era of psychiatry. Manic patients showed improvement, with the patient becoming calmer after four to five days. There was no improvement in the excited schizophrenic patients, though there was a calming effect. There was no improvement or deepening of depression. The paper also gave details of initial dosage, maintenance doses, appearance of toxic symptoms and warning about lithium over-dosage. …

Two Cases of Rapid Onset Parkinson's Syndrome Following Toxic Ingestion of Ethylene Glycol and Methanol

Ethylene glycol and methanol are toxic alcohols commonly found in a variety of commercial products. We report two cases, one associated with ethylene glycol and one with methanol poisoning, which both led to acute hemorrhagic necrosis of the basal ganglia and resulted in acute Parkinson's syndrome. It is unlikely that oxalate crystal deposition is the only mechanism for such basal ganglia necrosis, because similar findings were seen following methanol intoxication. We discuss other possible mechanisms that may contribute towards this unusual neurotoxicity. Both of our patients survived their toxic ingestions, but then developed acute Parkinson's syndrome within 10 days of the ingestion. However, the patient who ingested methanol developed respiratory muscle stiffness/weakness, which responded poorly to anti-Parkinsonian drug therapy. Treatment with carbidopa/levodopa improved cogwheel rigidity and bradykinesia in both patients. We conclude that acute Parkinsonism is one of the lesser-recognized devastating complications of both ethylene glycol and methanol poisoning.

Unexpectedly Dangerous Escargot Stew: Oleandrin Poisoning through the Alimentary Chain*

A female, aged 43 and a male, aged 66, experienced gastrointestinal and cardiovascular symptoms after a meal including snail stew. Twelve hours after the ingestion, they presented with nausea, vomiting, diarrhea, and cardiovascular symptoms typical of acute toxic digoxin ingestion and were hospitalized. The man's electrocardiogram was altered, and the woman's was normal. Serum digoxin levels, measured on a Roche COBAS Integra 800 with the Roche On-Line Digoxin reagent, were 1.14 and 1.00 nmol/L, respectively. Potassium levels were normal in both patients. The serum digoxin concentration decreased on the second day, and symptoms resolved on the third day with patients fully recovered (i.e., reversion to a normal sinus rhythm). Cardiac-glycoside-like intoxication symptoms follow the ingestion of leaves or flowers of Nerium oleander. The consumed snails were suspected to be responsible for the intoxication. In the homogenized snail tissue, the concentration expressed in digoxin equivalents was 0.282 nmol/g. The presence of oleandrin and oleandrigenin in the snails was confirmed by liquid chromatography-tandem mass spectrometry analysis, which was performed on a ionic-trap Finnigan LXQ instrument using an electrospray ionization interface. High-pressure liquid chromatographic separation was performed on a C18 column with a gradient of methanol/water. An extract of oleander leaves was used as reference.

Use of Single-dose Activated Charcoal Among Canadian Pediatric Emergency Physicians

Gastric decontamination with single-dose activated charcoal (SDAC) is a mainstay in emergency department (ED) treatment of ingestions. Guidelines updated in 2005 encourage practitioners to use SDAC only in toxic ingestions presenting within 1 hour. Despite these guidelines, adult studies demonstrate a significant lack of consensus. This study examined the proposed use of SDAC for gastric decontamination in common pediatric ingestion scenarios by emergency physicians working in Canadian pediatric EDs. A standardized survey consisting of 5 clinical scenarios was mailed to all physicians with a primary clinical appointment to the ED at 9 Canadian children's hospitals. One hundred thirty-one physicians were surveyed, and 95 (72%) responded. The majority of respondents were pediatricians (68.1%) with a mean of 15.0 years of experience (SD, 6.8 years). Of those surveyed; 91 (97.8%) would use SDAC for a toxic ingestion presenting in less than 1 hour; 35 (36.8%) would use SDAC for a toxic ingestion presenting after 3 hours; 61 (64.9%) would use SDAC for a nontoxic exploratory ingestion presenting in less than 1 hour; and 29 (30.5%) would use SDAC for a mildly symptomatic intentional ingestion presenting at an unknown time. Eleven (11.7%) would use SDAC for an ingestion of a substance that does not adsorb to SDAC. There is variation in the use of SDAC among emergency physicians working in Canadian pediatric EDs. This variation suggests that optimal management is not clear and that continued education and research are required.

Lung disease 35 years after aspiration of activated charcoal in combination with pulmonary lymphangioleiomyomatosis

Activated charcoal provides effective treatment for most toxic ingestions. Accidental aspiration of activated charcoal is rare. Previously, there have been a few single cases reported on charcoal-related pulmonary complications. We describe an unusual case of pulmonary lesions 35 years after accidental aspiration of activated charcoal. The 38-year-old female patient presented with recurrent pneumothorax. A routinely performed chest roentgenogram revealed pulmonary lesions, highly suggestive to lymphangioleiomyomatosis (LAM). Histopathological investigation of the lung tissue demonstrated some features of LAM but showed prominent pneumoconiotic lesions with cystic tissue destruction. The pneumoconiotic reaction was characterized by prominent black deposits accompanied by foreign-body granuloma formation and minimal fibrosis. Scanning electron microscopic investigation of these deposits showed particles measuring up to 300 microm in greatest diameter. Energy-dispersive X-ray spectra of these particles revealed carbon-rich material, presumably charcoal. The aspiration event was confirmed by the clinical history. To our knowledge, this is the first report not only on a long-term follow-up after aspiration of activated charcoal but also on charcoal-related pulmonary lesions in combination with LAM.

Homicidal Ethylene Glycol Intoxication

We report a case of a 75-year-old hypertensive, diabetic man who presented to the emergency room with symptoms and signs of nausea, acute intoxication, significant alteration in mental status with rapid neurologic deterioration, and blunt impact injuries sustained during a recent altercation with a 36-year-old female companion-caretaker. He denied a history of ethanol abuse or other recent toxic ingestion and had not been diagnosed with or treated for depression. Hospital laboratory tests revealed a metabolic acidosis and a negative urine toxicology screen. He was diagnosed with toxic encephalopathy with metabolic acidosis secondary to metformin. Despite treatments including hemodialysis, he expired after approximately 28 hours of hospitalization. A postmortem anatomic examination revealed recent blunt-impact injuries and cardiac and renal pathology. A subsequent histologic examination revealed the presence of calcium oxalate crystals in the kidneys and brain, in addition to cardiac and renal pathology. Comprehensive forensic toxicologic testing was performed on antemortem and postmortem samples and revealed lethal levels of ethylene glycol. The cause of death was as a result of acute intoxication by ethylene glycol with another condition of multiple blunt impacts to the head, trunk, and extremities. The manner of death was ruled as homicide. A trial by jury, involving the female companion-caretaker, resulted in her conviction, and she was sentenced to 23 years to life in prison. In this report, we present an unusual case of homicidal ethylene glycol intoxication in which legal proceedings have occurred.

Evolving Practices in Critical Care and Potential Implications for Management of Acute Kidney Injury

Acute kidney injury (AKI) is a common complication in hospitalized patients, with an incidence of 3 to 10% (1–4). In-hospital mortality rates that are associated with AKI remain high, in the range of 30 to 70% (5–8), despite significant improvements in dialytic technology as well as important advances in critical care, which have resulted in improved survival for other critical illnesses, including acute lung injury and sepsis (9). These improvements include continuous renal replacement therapies, which allow for continuous removal of solutes and fluid and may be tolerated better from a hemodynamic standpoint, and biocompatible dialysis membranes, which are associated with reduced complement and granulocyte activation. In general, indications for dialysis in the acute care setting have been extrapolated from those that are applied in chronic kidney disease, including volume overload that is refractory to diuretic therapy; electrolyte abnormalities (in particular hyperkalemia); uremic complications (pericarditis or pleuritis); severe acidosis (pH < 7.20); and selected toxic ingestions, such as methanol, ethylene glycol, and other water-soluble agents (10,11). However, the evidence base supporting specific dialysis practices in the acute care setting is limited. For example, several studies that were completed in the 1960s and 1970s compared “early” and “late” initiation of dialysis, using blood urea nitrogen (BUN) to define early and late (Table 1). These studies primarily were cohort studies that used historical controls, not randomized, clinical trials. The results of these investigations, along with extrapolation from the ESRD population, promoted recent practice patterns. Currently, many nephrologists often delay dialysis in the acute care setting until the patient has an impending complication of AKI, such as hyperkalemia leading to cardiac arrhythmias, acidosis resulting in hypotension, or oliguria leading to volume overload or hypoxemia, or until the BUN exceeds 100 mg/dl (18). Given differences in protein catabolism, …

Transient Blindness Due to Posterior Reversible Encephalopathy Syndrome Following Ephedra Overdose

Posterior reversible encephalopathy syndrome (PRES), also known as reversible posterior leukoencephalopathy syndrome (RPLS), is most often associated with hypertensive emergencies and is characterized by seizures, mental status changes and visual disturbances. We report a case of a previously healthy young man who developed multiorgan failure and transient cortical blindness following ingestion of a performance-enhancing ephedra-based supplement. Neuroimaging findings confirmed the clinical suspicion of PRES. Radiographic abnormalities and neurologic dysfunction subsequently resolved with correction of his systolic blood pressure. This case emphasizes the need for prompt treatment and consideration of toxic ingestions in patients presenting with hypertension-related end-organ dysfunction.

Acetadote (Intravenous Acetylcysteine): Adverse Effects More Significant Than With Oral Acetylcysteine

Acetaminophen has been reported to be the leading cause of toxic drug ingestion in the United States,1 and acetylcysteine has been used in the emergency department setting to prevent or lessen the resulting liver damage.

Ataxia de aparición aguda en la infancia: etiología, tratamiento y seguimiento

Acute childhood ataxia is a cause of referency to the pediatric emergency room. AIM. To characterize the etiology, clinical picture, management, and outcome of acute ataxia in our hospital. A prospective study was undertaken including 39 children with acute ataxia who were admitted between January 1, 2001 and December 31, 2003. During the study period 159,002 episodes were evaluated, 39 children (0.024%) with acute ataxia. The most common diagnoses were post-infectious ataxia (51.2%) and toxic exposure (25.6%). The mean age at presentation in post-infectious ataxia was 55 +/- 27.61 months, 60% females. A prodromal febrile illness was noted in 95%: varicella (10), nonspecific viral infection (6), mycoplasma, enterovirus, and Epstein-Barr virus. The latency from the prodromal illness to the onset of ataxia was 5.86 +/- 3.78 days. Lumbar punctures were altered in 11/17. All computed tomography scans performed were normal. At follow up, one boy presented asymmetric signs of cerebellar dysfunction secondary to hemicerebellitis. The media of the patient who showed full-gait recovery was 18 days, and was complete in all children, except one boy who presented hemophagocytic lymphohistiocytosis. Toxic ingestion was the second most common cause. Boys less than 6 years were more commonly affected. Acute childhood ataxia are an uncommon cause of presentation to our pediatric emergency room. Postinfectious ataxia and drug ingestion are the most common diagnosis, with a usually benign and self-limited process. A thorough history and neurology examination should be guided to etiology. Neuroimaging studies and hospitalization are needed only if atypical presentation, asymmetric neurologic examination and prolonged ataxia.

Diagnosis and Management of the Poisoned Child

Pediatric toxic ingestions are treated commonly by pediatricians and emergency physicians. Significant injury after these ingestions is infrequent, but identifying the dangerous ingestion is sometimes a difficult task. By performing a detailed history, focused physical examination, and directed laboratory evaluation, an estimation of risk can be developed. This article introduced the term "toxic triage" to describe this process. The toxic triage estimation allows the clinician to make thoughtful decontamination and treatment decisions. Familiarity with the literature supporting or refuting each decontamination method allows educated decisions to be made. Supportive care is an integral part of treatment for all poisonings, from asymptomatic to life-threatening. Most antidotes are used rarely in clinical practice, but familiarity with common antidotes benefits those patients with specific hazardous ingestions. Prevention efforts have the potential to decrease the incidence of pediatric poisonings. The universal poison control center number provided should be distributed and posted in homes, clinics, and emergency departments.

A 25-Year Retrospective Review of Deaths Due to Pediatric Neglect

Neglect, defined as the failure of a caregiver to adequately provide safety, food, clothing, shelter, education, protection, medical/dental care, and supervision for a child in his/her care, is a relatively uncommon but important cause of child mortality. A retrospective review of pediatric deaths (age 18 years or less) referred to the Medical University of South Carolina Forensic Pathology Office for autopsy over the past 25 years revealed 16 deaths due to some type of pediatric neglect. Cases were analyzed as to age, sex, race, cause and manner of death, autopsy findings, ancillary studies, past medical history, social/family history, and caregiver. Six cases of malnutrition/starvation and/or dehydration were identified, composing the most common cause of death in the neglect cases identified and the majority of the homicides due to neglect. Other deaths in which neglect contributed significantly included toxic ingestions (2 cases), hyper-/hypothermia (2 cases), unusual drowning/aspiration (4 cases), electrocution (1 case), and delayed/absent medical therapy (2 cases, including one of the previously mentioned ingestions). Of these additional cases, 7 were certified as accidental manner, 2 as natural, and 1 as a homicide. Cases which fell into a "gray zone" in which the appropriateness of invoking neglect was a matter of opinion or societal convention were excluded from the review; examples included conventional accidental drowning, choking on food or aspiration of foreign body, overlying/wedging during sleep, accidental hanging, and motor-vehicle traffic accidents (pedestrians, unrestrained passengers). The findings of this review reinforce the fact that malnutrition/starvation and dehydration compose the most common form of lethal pediatric neglect while highlighting less common forms of neglect and the difficulty of determining manner of death in cases in which neglect plays a more questionable role than in seemingly clear-cut malnutrition/starvation and dehydration cases. We demonstrate the typical victim and scenario that investigators will encounter in cases of fatal pediatric neglect, often a child under the age of 1 year who has been deprived of food and/or drink for some time, or an older, more independently mobile child who has not been adequately supervised. These children may or may not have a demonstrable prior history of maltreatment or (nonfatal) neglect, and review of medical records is an important part of the investigation. We additionally discuss key gross autopsy findings, appropriate specimen collection, helpful ancillary studies, microscopic findings of significance, potential mimickers of neglect, and other special considerations in cases of pediatric neglect.