Friday, May 7, 2021

Poisoning Case File

Posted By: Medical Group - 5/07/2021 Post Author : Medical Group Post Date : Friday, May 7, 2021 Post Time : 5/07/2021
Poisoning Case File
Eugene C. Toy, MD, Manuel Suarez, MD, FACCP, Terrence H. Liu, MD, MPH

Case 37
A  46-year-old man was brought to the hospital because family members have noted that he appears lethargic and complains of abdominal pain. The patient has a history of chronic low back pain and has been under the care of a physician for the past several  weeks. He has been prescribed acetaminophen/hydrocodone (Vicodin) and has been supplementing this medication with extra-strength
acetaminophen (500 mg tablets). His family members reported that they found several empty medication bottles at home. His laboratory studies from the emergency  department revealed normal white blood cell count, hemoglobin, hematocrit, and platelet counts. His serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) are 1300 IU/L and 1700 IU/L, respectively.

 What is the most likely cause of the patient's current condition? 
 What is the best next step in management? 
 How is this disease process staged?



Summary: This patient is a 46-year-old man with lethargy and abdominal pain, found to have elevated liver transaminase enzymes in the setting of significant acetaminophen ingestion. His presentation to the emergency department is consistent with hepatotoxicity secondary to acetaminophen overdose. 
  • Likely cause of current condition: Acetaminophen overdose. 
  • Next step in management: Gastric lavage following massive ingestions may be effective in retrieving undigested pills or pill fragments 30 to 60 minutes after the ingestion. Activated charcoal that absorbs most toxins (due to its large surface area) should only be administered to awake patients or to comatose patients after appropriate airway protection. The dose is 1 g/kg orally or via gastric tube, with the goal of a 10:1 (charcoal:toxin) ratio. 
  • Disease stages: There are 4 distinct stages of acetaminophen-induced hepatotoxicity: (1) preclinical toxic effects (no lab abnormalities); (2) hepatic injury (elevated transaminase enzymes); (3) hepatic failure; and (4) recovery. Each stage has a different prognosis and management strategy. This patient would appear to be stage 2 based on his initial evaluations.


  1. To learn the clinical manifestations, management, and outcome of acetaminophen, salicylate, tricyclic antidepressants, alcohol, oral hypoglycemics, cyanide, and propofol.
  2. To learn when activate charcoal is indicated in the management of substance ingestion/overdose.
  3. To recognize the importance of airway, breathing, and circulation management in patients with substance ingestion/overdose.
This 46-year-old patient was given a prescription for acetaminophen/hydrocodone (Vicodin) and was supplementing this medication with extra-strength acetaminophen to treat his back pain. The additional over-the-counter acetaminophen is sufficient to exceed the liver's ability to metabolize acetaminophen safely. Significant hepatic injury is evident by the patient's elevated transaminase enzymes. Due to the potential for decreased GI motility from opiates, such as hydrocodone, the acetaminophen toxicity could be potentiated because the compound would remain in the patient's system over a prolonged period of time.

Assess the patient's airway, with careful attention to the patient's airway-protective reflexes. The most common factor contributing to increased morbidity related to drug overdose is airway compromise caused by a flaccid tongue, aspiration of gastric content, or apnea from respiratory depression. Securing the patient's airway with endotracheal intubation is necessary if the patient's level of consciousness is compromised. Cardiac monitoring and assessment of respiratory rate and functions may give clues to other potential co-ingestants. Continued monitoring of the patient's level of alertness and assessment of serum glucose are important, as the patient may have also ingested other substances in addition to those mentioned by the family. After stabilization of the patient's airway, breathing, and circulation, the acetaminophen level and time of ingestion will be used in concert with the liver enzyme levels and coagulation studies to determine the course of treatment and the extent of hepatic injury. Additional tests to evaluate for concomitant ingestion of other substances include salicylate level, alcohol level, serum electrolytes, serum osmolality, urine toxicology screens (to screen for drugs of abuse), lactate, serum ketones, and an ECG.

Additional History
Approach all poisoned patients as if they have potentially life-threatening polysubstance intoxication (ingestion of multiple substances). Additional history is always helpful to determine which other substances the patient could have accessed. Family members, emergency medical personnel (paramedics, fire department), and the patient's primary doctor are often helpful in providing additional insight. The timing of ingestion and dosage of medication is also of extreme importance and will help guide treatments. In this situation, it will be helpful to have a family member retrieve the additional empty pill bottles that were found in the patient's home. It is always helpful to consult your local poison control center for assistance with patient management, once all the suspected or confirmed ingested toxic substances are identified.

The technique for decontamination will largely depend on the timing, amount, and type of substance ingested. Gastrointestinal decontamination may involve gastric lavage, activated charcoal administration, or whole bowel irrigation depending on the circumstance. There is little clinical evidence to support gastric lavage, but it is currently used for massive ingestions of extremely toxic substances. The aim is retrieving undigested pills or pill fragments, usually most effective when begun within 30 to 60 minutes after the ingestion. Activated charcoal is a highly effective absorbent that functions to absorb most toxins (due to its large surface area) , and should be administered to awake patients or to comatose patients with secured airways. The dose is 1 g/kg orally or via gastric tube, with the goal of a 10:1 (charcoal:toxin) ratio. Repeat doses of charcoal may enhance elimination of substances. Iron, lithium, and heavy metals are poorly absorbed by activated charcoal. Whole bowel irrigation utilizes nonabsorbable surgical bowel cleansing solutions at high flow rates to force intestinal contents out by way of large volume force. This technique is indicated with ingestion of: (1) substances not absorbed by charcoal, (2) drug-filled condoms or packets, (3) sustained-release tablets. Hemodialysis and antidotes may also hasten the elimination of specific substances.

Psychiatric Evaluation
All poisoned patients must be assessed for suicidal ideation, risk factors for depression, prior history of suicide attempts, and prior psychiatric illnesses. This information can be obtained by the patient, if possible, and corroborated by the family. The potential for accidental overdose exists, particularly in the pediatric, elderly, and disabled populations. Therefore, the need for further evaluation by a psychiatrist should be considered after medical stabilization.

Approach To:


The American Association of Poison Control Centers estimated that acetaminophen was responsible for over 70,000 visits to health-care facilities and 300 deaths in 2005. Acetaminophen poisoning can be due to ingestion of a single overdose (typically with suicide attempts) or ingestions of excessive repetitive doses or too frequent dosages, with therapeutic intent.

Pathophysiology of Acetaminophen Toxicity
Acetaminophen is normally metabolized by the liver, primarily via glucuronidation and sulfation into nontoxic metabolites. However, approximately 5% of acetaminophen is metabolized via cytochrome P-450 2E1 to N-acetyl-p-benzoquinone imine (NAPQI), which is extremely toxic to the liver. When acetaminophen is taken in therapeutic doses, NAPQI is rapidly detoxified by glutathione to form nontoxic metabolites (cysteine and mercapturic conjugates). However, in an acetaminophen overdose, NAPQI depletes glutathione reserves and this toxic metabolite inter, acts with hepatic macromolecules to cause liver injury.

There are 4 distinct stages of acetaminophen-induced hepatotoxicity: (1) preclinical toxic effects (no lab abnormalities); (2) hepatic injury (elevated transaminase enzymes); (3) hepatic failure; and (4) recovery. Each stage has a different prognosis and management strategy. Patients with frank hepatic failure have a mortality rate of 20% to 40%.

Clinical Assessment
The initial assessment of any patient with a potential overdose should focus on evaluating the airway, breathing, circulation, disability, and decontamination. Early in acute acetaminophen ingestions, the majority of patients remains asymptomatic, or will complain of nausea, vomiting, and anorexia. However, 24 to 48 hours postingestion, patients begin to show signs of liver injury and liver failure.

After stabilization of the airway, breathing, and circulation, the acetaminophen level and time of ingestion will be used in concert with the liver enzyme levels and coagulation studies to determine the extent of injury and course of treatment.

Additional history to pinpoint the time of ingestion is critical in guiding the therapy. Activated charcoal administration should be considered. Perhaps one of the greatest contributions to the management of patients with acetaminophen overdose is the Rumack-Matthew nomogram (Figure 3 7-1). The nomogram, which was first published in 1975 , was developed from the acetaminophen levels of untreated

Acetaminophen plasma concentration

Figure 37-1. Rumack-Matthew acetaminophen nomogram. (Reproduced, with permission, from Tintinalli JE, Stapczynski JS, Ma OJ, et al. Tintinalli's Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York, NY: McGraw-Hill Education; 2011. Figure 184-2.) 

patients, and describes the mathematic relationship between acetaminophen level, time of ingestion, and the potential for hepatic injury. The upper line of the nomogram defines the toxic level likely to be associated with acute overdose; it is also known as the "200 line," since any level of 200 mcg/mL or greater within 4 hours of ingestion requires antidote treatment. The lower line ("150 line") on the nomogram, defines serum levels 25% below those expected to cause hepatotoxicity, and was instituted by the FDA to better improve clinical outcomes with antidote treatment. The nomogram helps the clinician interpret the acetaminophen level. Any acetaminophen level obtained prior to 4 hours post-ingestion is unable to predict the likelihood of hepatotoxicity, but it is able to confirm acetaminophen ingestion.

Acetaminophen levels obtained 4 to 24 hours after ingestion can be plotted on the nomogram to determine the probability of hepatic injury. If the levels plot above the lower line on the nomogram, antidote treatment should be initiated. Any elevated acetaminophen level detected 24 hours after ingestion should be considered toxic and warrants antidote treatment. The majority of poisoned patients present after polypharmacy ingestions. When the 4-hour acetaminophen level is nontoxic, an 8-hour level should be drawn in patients who have taken co- ingestants that may delay GI absorption (ie, extended release acetaminophen preparations, opiates, or anticholinergics). Treatment is still guided by the nomogram in these circumstances. The nomogram is not valid in cases of chronic ingestions.

N-acetylcysteine (NAC) is the FDA-approved antidote for acetaminophen toxicity, and functions to aid in glutathione repletion. Glutathione is synthesized from amino acids glutamate, glycine, and cysteine (cysteine availability is the ratelimiting step in production). N-aetylcysteine is readily absorbed and hydrolyzed to cysteine, which provides the substrate for glutathione synthesis. Glutathione functions to convert N-acetyl-p-benzoquinone (NAPQI) to a nontoxic metabolite that is easily eliminated from the body via renal clearance. NAPQI is capable of causing liver injury by 2 separate mechanisms. First, NAPQI can bind covalently to intracellular proteins and cause hepatocellular necrosis. Second, high rate of NAPQI formation can cause depletion of intrahepatic glutathione stores and cause increased liver toxicity. NAC is of maximal benefit if given within 8 to 10 hours of ingestion, since this is usually prior to NAPQI accumulation. Although the benefit of NAC diminishes after 12 hours, treatment should not be withheld despite a delay of 24 hours or more. Mortality reduction with NAC treatment has been shown in cases where hepatic failure has already developed.

NAC can be given orally, with a loading dose of 140 mg/kg, followed by a maintenance dose of 70 mg/kg every 4 hours. Uncomplicated cases with no evidence of hepatic injury may be treated for 20 hours with 5 maintenance doses. However, if there is evidence of hepatic injury, NAC treatment should be continued until liver function tests have improved. Intravenous NAC is indicated if the patient is unable to tolerate the oral formulation, such as those with decreased level of consciousness, vomiting, or ileus. NAC can be given intravenously with a loading dose of 150 mg/kg over 15 minutes, followed by 50 mg/kg over 4 hours, and then 100 mg/kg over 16 hours. Liver enzymes, as well as coagulation studies are monitored until 36 hours post-ingestion. If evidence of liver injury develops, intravenous NAC treatment is continued until liver improvement in function tests occurs.

pain medications

Management of Salicylate Toxicity 
Salicylates are  commonly used for their anti-inflammatory and analgesic proper­ties and can be found in Aspirin, Pep to-Bismol, over-the-counter cold medicines, and topical muscle and joint preparations (Aspercreme, Bayer Joint Cream, Icy Hot Cream). The daily therapeutic dose ranges from 40 to 60 mg/kg/d. Mild toxicity can be seen with doses of 150 to 200 mg/kg/d with marked toxicity at 300 to  500 mg/kg/d.

Toxicity from salicylate occurs via 2 main mechanisms: (1) respiratory alkalosis and (2) metabolic acidosis. Salicylates may directly stimulate the central respiratory centers causing hyperventilation, which leads to respiratory alkalosis and a compensatory metabolic acidosis. This metabolic acidosis is further exacerbated by the interruption of glucose and fatty acid metabolism, leading to increased carbon dioxide production. Mild salicylate toxicity may result in respiratory alkalosis with compensatory metabolic acidosis as bicarbonate excreted in the urine. However, with moderate to severe toxicity, the respiratory alkalosis is accompanied by a high anion gap metabolic acidosis, as the kidneys deplete sodium bicarbonate and potassium.

Patients typically present with nausea, vomiting, tinnitus, tachypnea, and lethargy. Pulmonary edema, coma, and cardiovascular collapse can occur with severe toxicity. Management is aimed at supporting the patient's airway, breathing, and circulation with close attention to ensure adequate ventilation to allow the compensatory mechanisms to maintain a suitable arterial pH. Activated charcoal administration should be considered. Laboratory tests of significance include a salicylate level, electrolytes (to calculate the anion gap), arterial blood gas, and ECG (evidence of hypokalemia). Treatment is aimed at enhancing the elimination of salicylates by the kidneys, which is dependent on hydrogen ion gradients. Therefore, the treatment of choice remains sodium bicarbonate, which functions to treat the metabolic acidosis and enhance renal clearance. Sodium bicarbonate is given as a continuous infusion with a targeted urine pH of 7.5 to 8.0. Potassium supplementation should be added to IV fluids as potassium is rapidly depleted in salicylate toxicity. Hemodialysis should be considered in acute intoxication with serum salicylate levels of 100 mg/dL in association with severe acidosis.

Tricyclic Antidepressant Toxicity
Tricyclic antidepressants (TCAs) were traditionally used to treat depression, but they are currently more commonly used to treat chronic pain syndromes and migraine prophylaxis in adults, and enuresis, attention deficit disorder, and obsessive- compulsive disorder in children. TCAs have a narrow therapeutic window, and have anticholinergic properties that may delay GI absorption. TCAs also have α-adrenergic blockade effects and can cause hypotension and contribute to acidemia along with respiratory depression from CNS effects. However, the most serious complications are its cardiovascular and CNS effects. Conduction defects occur as a result of the membrane-depressant qualities due to myocardial fast sodium channel blockade, leading to prolonged PR, QRS, and QT intervals. Hypotension may occur from α-adrenergic blockade. Anticholinergic properties may cause tachycardia. CNS effects mainly manifest a s lethargy and coma (due to the anticholinergic
properties), in addition to seizures (attributed to central CNS activity).

Supportive care should b e immediately initiated t o stabilize the airway and support breathing. Intravenous fluids and cardiac monitoring should be instituted for circulatory support. Decontamination with activated charcoal should be considered. Sodium bicarbonate should be administered for patients with QRS prolongation or hypotension. Sodium bicarbonate is believed to reverse the sodium blockade and subsequent myocardial suppressant effects of TCAs. Sodium bicarbonate may also be utilized for serum alkalinization with a goal of achieving serum pH of 7.45 to 7.55, which has been shown t o elevate blood pressure and shorten the QRS interval.

Alcohol Toxicity
A variety of alcohols can be found commercially available in liquor, cold medicines, mouthwash, food extracts, colognes, after-shave solutions, antifreeze, and rubbing alcohol. Up to 15% of the US population is considered to be at risk for alcohol dependence. Alcohol dehydrogenase is the primary enzyme that metabolizes ethanol, isopropyl alcohol, methanol, and ethylene glycol. The genetic polymorphisms of alcohol dehydrogenase will determine the rate of alcohol metabolism. Patients with alcohol toxicity are typically grossly inebriated, with evidence of slurred speech, ataxia, impaired judgment, and lack of coordination. Severe toxicity may present with progressive CNS depression and coma. Methanol toxicities typically cause changes in vision in addition to inebriation. Isopropyl alcohol and ethylene glycol typically present gross intoxication similar to that associated with ethanol toxicity.

Ethanol toxicity typically causes CNS depression, which is additive when in combination with benzodiazipines, barbituates, or opiods. Hypoglycemia occurs commonly due to impaired gluconeogenesis along with poor nutrition in patients with history of chronic alcohol abuse. Occult head injury, hypoxemia, aspiration, and underlying metabolic disturbance must also be considered in all intoxicated patients. Treatment is mainly supportive with intravenous fluids, glucose, and thiamine. In cases of alcoholic ketoacidosis (defined by anion gap metabolic acidosis and elevated β-hydroxybutyrate) , supplemental glucose and volume replacement are essential. There is no specific antidote for ethanol or isopropyl alcohol intoxication. However, methanol and ethylene glycol toxicity should be treated with fomepizole or ethanol to saturate the alcohol dehydrogenase enzyme and prevent further production of toxic metabolites. Methanol may also be eliminated by hemodialysis in cases of severe toxicity.

Hypogylcemic Agent Toxicity
There are several oral agents used to lower serum glucose in the treatment of type 2 diabetes mellitus. Typically, these medications are divided into 2 categories: hypoglycemics and antihyperglycemics. Agents referred to as antihyperglycemics work to reduce glucose levels, but rarely cause hypoglycemia, even when used in excess; these agents include metformin (glucophage), alpha-glucosidase inhibitors, and glitazones. The aforementioned agents work by reducing hepatic glucose production (metformin and glitazones), as well as decreasing intestinal glucose absorption (metformin and a-glucosidase inhibitors). On the other hand, hypoglycemics, namely sulfonylureas, typically cause hypoglycemia in cases of overdose or decreased elimination. Sulfonylurea lowers blood glucose by increasing insulin release from the pancreas and enhancing peripheral sensitivity to insulin.

Sulfonylurea toxicity may cause hypoglycemia, which presents as diaphoresis, delirium, progressive decreased level of consciousness, syncope, or coma. The method of toxicity may be an intentional or unintentional overdose, or decreased elimination secondary to renal insufficiency. The duration of action for many sulfonylureas exceeds 24 hours. Therefore, patients are typically admitted to the hospital and treated with dextrose-containing intravenous fluids in addition to close glucose monitoring. Patients may require intravenous octreotide when they are unresponsive to intravenous dextrose. Octreotide is a synthetic somatostatin analog, which suppresses pancreatic insulin release. Adjunctive therapy for patients with sulfonylurea overdose includes alkalinization of the urine to increase renal elimination of sulfonylureas.

Although antihyperglycemics rarely cause hypoglycemia at toxic levels, these agents do exhibit toxicity through other mechanisms. For instance, metformin is known to cause lactic acidosis with overdose and with renal insufficiency. Severe cases of acidosis may warrant hemodialysis.

Cyanide Toxicity
Cyanide toxicity is most commonly encountered in victims of smoke inhalation from industrial or residential fires. It is caused by the formation of gaseous hydrogen cyanide from burning plastics. Cyanide toxicity can also occur in the ICU as a result of high-dose or prolonged nitroprusside infusions. Nitroprusside releases cyanide during metabolism, and is normally converted to a nontoxic metabolite in the liver. However, cyanide may accumulate with prolonged use or high dosages. A rare cause of cyanide toxicity in the United States is the ingestion of cyanide-containing foods, such as cassava, apricot seeds, apple seeds, and spinach.

Cyanide uncouples oxidative phosphorylation, which causes cellular metabolism to switch from aerobic to anaerobic processes, resulting in lactic acidosis. Patients typically present with malaise, headache, confusion, and generalized weakness. Cardiovascular collapse, syncope, and coma may occur with severe toxicity. The safest antidote for cyanide toxicity is intravenous hydroxocobalamin, which combines with cyanide to form cyanocobalamin (vitamin B12), which is subsequently excreted by the kidneys. The cyanide antidote kit should be used if hydroxocobalamin is not accessible. The cyanide antidote kit consists of amyl nitrites, sodium nitrites, and sodium thiosulfate. Amyl nitrite pearls and intravenous sodium nitrite are capable of inducing methemoglobinemia in cells, which binds cyanide. However, nitrites should be avoided in cases of smoke inhalation, where carboxyhemoglobinemia may coexist. Instead, if hydroxocobalamin is not available, sodium thiosulfate should be administered intravenously, which enhances the conversion of cyanide to thiocyanate that is also excreted by the kidneys.

Propofol Toxicity
Propofol is a lipid-soluble, sedative-hypnotic agent, and is commonly used in surgical and critical care units. It is metabolized by the liver via oxidation by CYP-450 2B6, excreted b y the kidneys. Its primary site of action is a t the GABA-A receptors. Due to its rapid onset of action and quick metabolism (mean duration of action is 3-5 minutes for a single bolus), propofol is used with increasing frequency in the ICU in patients on mechanical ventilation. It is contraindicated in patients with egg or soybean allergies because of the additives in the formulation of the emulsion in which it is administered. Standard dosing of propofol for sedation is 25-75 μg/kg/ min (or 1.5-3 mg/kg/h).

Adverse effects with use of propofol range from pain at the site of injection to death. Patients may experience hypotension, arrhythmias (both bradycardia and supraventricular tachyarrhythmias have been described), acute pancreatitis secondary to hypertriglyceridemia, and/or bronchospasm as a result of propofol administration. Propofol infusion syndrome includes rhabdomyolysis, acute renal failure, lactic acidosis, and hemodynamic instability as a result of prolonged (>48 hours), high-dose infusion (> 5 mg/kg/h) of propofol. There is n o specific antidote for propofol toxicity. The treatment is immediate discontinuation of the propofol infusion followed by supportive care. Supportive care may include administration of IV fluids, vasopressor, or antiarrhythmic agents.

  • See also Case 23 (Acute Kidney Injury), Case 24 (Acid-Base Abnormali­ties 1), and Case 25 (Acid-Base Abnormalities II).


7.1  A 25-year-old woman is admitted to the ICU for altered level of consciousness after a polypharmacy ingestion. He was noted to have an acetaminophen level of 80 μ/dL, obtained 12 hours after the ingestion. After stabilization of the patient's airway, breathing, and circulation, the ICU team discussed antidote treatment with liver function tests pending. Which statement is most accurate regarding the next step of management for this patient?
A. Sodium bicarbonate infusion should be initiated with a goal serum pH 7.45 to 7.55.
B . N-acetylcysteine treatment should not b e considered until the liver function tests are available.
C. Octreotide can be considered if the patient does not respond to IV dextrose administration.
D. N-acetylcysteine treatment should be started and serial liver function tests should be monitored during treatment.
E. Initiate NG lavage of gastric contents.

37.2  A 54-year-old man is admitted to the burn ICU with confusion and decreased level of consciousness, along with several third-degree burns throughout his body at an industrial fire. The patient was intubated for airway protection after soot in the posterior pharynx and airway edema were noted upon arrival. Cyanide toxicity is suspected. What is the best treatment method for cyanide toxicity in this patient?
A. Sodium bicarbonate infusion should be initiated with a goal serum pH 7.45 to 7.55.
B . Amyl nitrite pearls and intravenous sodium nitrite should b e administered.
C. Hydroxocobalamin should be administered intravenously.
D. Methemoglobinemia should be the goal of treatment.
E. Nitroprusside should be administered.

37.3  A 33-year-old man was admitted to the ICU after having been found comatose in his home with a suicide note and an empty bottle of aspirin (30 count). His salicylate level returns at 111 mg/dL and his serum pH is 7.01. What is the best treatment plan for this patient?
A. Octreotide can be considered if the patient does not respond to IV dextrose administration.
B. Sodium bicarbonate infusion should be initiated w ith a goal serum pH 7.45 to 7.55.
C . Hemodialysis should be initiated to enhance elimination and correct the acidosis.
D. N-acetylcysteine treatment should be started and serial liver function should be monitored during the treatment.
E. Potassium supplementation in intravenous fluid.

37.4  A 40-year-old woman with diabetes mellitus was admitted to the emergency department for acute kidney injury with creatinine 3.2 mg/dL. The patient was prescribed a sulfonylurea agent. She was found to have persistent hypoglycemia (glucose initially noted to be 30 mg/dL). Which of the following therapies is the first-line treatment?
A . Intravenous dextrose infusion with close glucose monitoring.
B. Fomepizole therapy should be initiated immediately.
C. Intravenous octreotide should be administered immediately.
D. Sodium bicarbonate infusion should be initiated with a goal urine pH 7.5 to 8.0.
E. Administer calcium chloride.


37.1  D. The patient's alcohol level is clearly past the line indicating probable hepatic toxicity when plotted on the nomogram for 12 hours after ingestion. Therefore, NAC therapy is warranted. Remember that the nomogram functions to assist the medical team with the decision on whether or not to initiate NAC therapy. Serial liver function tests are followed while the patient is receiving NAC therapy, to help determine the length of therapy. Gastric lavage may be of value when initiated within 30 to 60 minutes following ingestion to help evacuate pill fragments. Sodium bicarbonate and octreotide are not indicated for the treatment of acetaminophen toxicity.

37.2  C. Hydroxocobalamin (Cyanokit) is the preferred treatment for cyanide toxicity, especially in the setting of smoke inhalation. Amyl nitrites and sodium nitrite should be avoided with smoke inhalation exposures, as carbon monoxide toxicity is also common with these types of exposures. Since amyl
nitrite and sodium nitrite function by inducing methemoglobinemia, this may be detrimental to the patient's oxygen-carrying capacity with concomitant carboxyhemoglobinemia. If hydroxocobalamin is unavailable in these situations, treating with thiosulfate is the next best option for cyanide toxicity
from smoke inhalation exposures. Sodium bicarbonate is not indicated in the treatment of cyanide toxicity. Nitroprusside administration in high doses or prolonged fashion can contribute to cyanide toxicity, and its administration has no role in treatment of inhalation-related cyanide toxicity.

37.3  C. Hemodialysis is indicated in salicylate toxicity with a serum level above 100 mg/dL with profound acidosis. Sodium bicarbonate is the mainstay of treatment with salicylate toxicity; however, the goal of treatment is to alkalinize the urine to enhance salicylate elimination. Therefore, the goal of sodium bicarbonate therapy is to maintain a urinary pH of 7.5 to 8.0. Octreotide and N-acetylcysteine are not indicated in salicylate toxicity. Potassium supplementation is helpful during treatment of salicylate toxicity as depletion often occurs; however, replacement of potassium does not actually address the salicylate toxicity.

37.4  A. The mainstay of treatment for sulfonylurea- induced hypoglycemia is the administration of dextrose-containing IV fluids and close monitoring for > 24 hours. Octreotide is warranted only after patients display that they are unresponsive to dextrose-containing IV fluids. Fomepizole is used for ethylene glycol poisoning. Sodium bicarbonate can be applied as an adjunctive measure to facilitate the elimination of sulfonylurea in the treatment of sulfonylurea toxicity, if the patient's renal functions are adequate. In this patient with a serum creatinine of 3.2 and acute kidney injury, alkalinization most likely does not work. Calcium chloride does not have any therapeutic benefits in a patient with sulfonyurea poisoning.

 Gastric lavage following massive ingestions may be effective in retrieving undigested pill fragments 30 to 60 minute after ingestion. 
 The most common factor contributing to mordity related to drug over­dose is airway compromise, aspiration from gastric contents, or respiratory depression. 
 Activated charcoal  is an effective absorbent but should be administered to awake patients, or to comatose patients with secured airways. 
 NAC is the FDA-approved medication for patients with acetamino­phen toxicity, and it is of maximal benefit when administered within 8 to 10 hours after ingestion. Benefits may be seen even when adminis­tered after 24 hours after ingestion. 
 Acute ethanol ingestion may serve a  protective role against acetamino­phen toxicity by occupying the cytochrome P-450 2E1 system and decreas­ing the metabolism of acetaminophen to NAPQI. 
 Chronic ethanol ingestion up-regulates  cytochrome P-450 2E1 system and increases the conversion of acetaminophen to the toxic metabolite NAPQI. 
 Patients with salicylate poisoning may have a respiratory alkalosis and met­abolic acidosis. Sodium bicarbonate corrects the  acidosis and enhances renal excretion of the salicylate. Severe cases may require dialysis. 
 Sulfonyurea overdoses may lead to profound hypoglycemia. If dextrose treatment is ineffective, IV octreotide may be helpful. 
 Propofol infusion syndrome includes rhabdomyolysis, acute  renal failure, lactic acidosis, and hemodynamic  instability. This syndrome may be the result of prolonged (>48 hours) high-dose infusion (>5 mg/kg/h) of propofol.


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Olson K. Poisoning and Drug Overdose. 5th ed. San Francisco, CA: McGraw Hill; 2004. 

Stolbach A, Goldfrank LR. Toxicology. In: Gabrielli A, Layon AJ, Yu M, eds. Civetta, Tay lor, and Kirby's Critical Care. Philadelphia PA: Linppincott Williams & Wilkins; 2009:987-1014.


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