A 24 year-old male with no reported medical history is transferred from jail for altered mental status. The patient had been in jail for two days and was noted to develop worsening confusion and agitation.

On arrival in the emergency department, the patient was agitated, moving wildly requiring physical restraints and speaking incomprehensibly. Initial vital signs were notable for tachycardia (HR 145bpm) and hypertension (BP 140/100mmmHg), afebrile core temperature. Examination revealed dilated pupils and dry skin. Point-of-care glucose measured 70mg/dL. Midazolam 5mg IV was administered due to his severe agitation and inability to cooperate with detailed evaluation.

After administration of midazolam, the patient became somewhat more lucid though he appeared to be hallucinating. He reported a history of alprazolam use. The patient was treated with nutritional supplementation and escalating doses of benzodiazepines. The patient remained persistently agitated after administration of midazolam 40mg IV as a single dose so phenobarbital was administered and the patient was intubated for airway protection and anticipated clinical course. The patient was started on a midazolam infusion at 40mg/hour after which he became more calm and vital signs normalized. Laboratory tests were unremarkable with the exception of elevated CK. Head imaging was negative for acute intracranial processes. The patient was admitted to the intensive care unit where he was transitioned to propofol and dexmedetomidine infusions. He was eventually extubated and discharged on hospital day #3 with a chlordiazepoxide taper.

Algorithm for the Management of Sedative-Hypnotic Withdrawal

References

Treatment Algorithms

1. Gold, J. A., Rimal, B., Nolan, A. & Nelson, L. S. A strategy of escalating doses of benzodiazepines and phenobarbital administration reduces the need for mechanical ventilation in delirium tremens Crit Care Med 35, 724–730 (2007).
2. Schmidt, K. J. et al. Treatment of Severe Alcohol Withdrawal. Ann Pharmacother 50, 389–401 (2016).
3. Santos, C., Olmedo, R. E. & Kim, J. Sedative-hypnotic drug withdrawal syndrome: recognition and treatment. Emerg Medicine Pract 19, S1–S2 (2017).

Gabapentin

1. Myrick, H. et al. A Double‐Blind Trial of Gabapentin Versus Lorazepam in the Treatment of Alcohol Withdrawal. Alcohol Clin Exp Res 33, 1582–1588 (2009).
2. Stock, C. J., Carpenter, L., Ying, J. & Greene, T. Gabapentin Versus Chlordiazepoxide for Outpatient Alcohol Detoxification Treatment. Ann Pharmacother 47, 961–969 (2013).

Barbiturates

1. Hendey, G. W., Dery, R. A., Barnes, R. L., Snowden, B. & Mentler, P. A prospective, randomized, trial of phenobarbital versus benzodiazepines for acute alcohol withdrawal. Am J Emerg Medicine 29, 382–385 (2011).
2. Rosenson, J. et al. Phenobarbital for Acute Alcohol Withdrawal: A Prospective Randomized Double-blind Placebo-controlled Study. J Emerg Medicine 44, 592-598.e2 (2013).

Textbook Chapters

1. Cohen, J. P. et al. Alcohols. in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e (McGraw-Hill Education, 2020).
2. Quan, D. et al. Benzodiazepines. in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e (McGraw-Hill Education, 2020).

Reviews

1. Mayo-Smith, M. F. Pharmacological Management of Alcohol Withdrawal: A Meta-analysis and Evidence-Based Practice Guideline. Jama 278, 144–151 (1997).
2. Mayo-Smith, M. F. et al. Management of Alcohol Withdrawal Delirium: An Evidence-Based Practice Guideline. Arch Intern Med 164, 1405–1412 (2004).
3. DeBellis, R., Smith, B. S., Choi, S. & Malloy, M. Management of Delirium Tremens. J Intensive Care Med 20, 164–173 (2005).
4. Amato, L., Minozzi, S., Vecchi, S. & Davoli, M. Benzodiazepines for alcohol withdrawal. Cochrane Db Syst Rev CD005063 (2010) doi:10.1002/14651858.cd005063.pub3.

The post Sedative-Hypnotic Withdrawal appeared first on Differential Diagnosis of.

A 20 year-old male with a history of polysubstance use, depression and seasonal allergies presents via ambulance for altered mental status. According to prehospital report, EMS were contacted by the patient’s roommate who noted that he had been acting strangely after being alone in his room for several hours. Vital signs are notable for fever (T 103.2°F) and tachycardia. The patient was confused, unable to follow commands – pupils were dilated.

The initial impression was concerning for sympathomimetic toxicity, the patient was treated with cooled intravenous fluids and required pharmacologic sedation and physical restraints to obtain blood samples. ECG, initial laboratory tests and urine toxicology screen were unremarkable. A non-contrast CT head was normal.

The patient remained altered and a repeat examination was performed which revealed multiple, opened blister packs of diphenhydramine and dry, flushed skin.

Anti-cholinergic toxicity was presumed, likely exacerbated by the administration of butyrophenones for sedation. He was treated with benzodiazepines, additional evaporative cooling measures and was admitted to the intensive care unit.

Case 2:

A 32 year-old female with a history of depression was brought to the emergency department by family members who were concerned about bizarre behavior and muscle stiffness. They note that the patient was recently started on a new antidepressant though they are unsure of the name. They describe occasional alcohol consumption but no illicit drug use.

In the emergency department, vital signs were notable for fever and hypertension. Examination demonstrated increased muscle tone and sustained clonus in bilateral lower extremities.

The patient’s presentation was concerning for serotonin syndrome, she was treated with benzodiazepines and intravenous fluids with gradual improvement in mental status and hypertonicity. Upon awakening, she reported doubling her medication dose recently due to persistent feelings of hopelessness as well as increased wine consumption.

An Algorithm for the Evaluation of Toxidromes

Diagnostic Tests

GI Decontamination

Activated charcoal

Activated charcoal (1g/kg) within 1-hour post-ingestion and if the patient is awake and cooperative (or via enteric tube if intubated).

Not recommended

1. Heavy metals
2. Ions (ex. lithium)
3. Corrosives
4. Hydrocarbons
5. Alcohols

Whole-bowel irrigation

Indicated for sustained-release formulations, expulsion of body packing materials, or ingestion of agent not absorbed by activated charcoal.

Serum alkalinization

For certain ingestions (salicylate, phenobarbital, methotrexate), serum alkalinization through infusion of sodium bicarbonate targeting serum pH 7.5 (and urine pH 8.0) may promote elimination.

Intralipid emulsion

May be useful for local anesthetic toxicity, b-blocker, and calcium channel blocker overdose.

Electrocardiographic Toxidromes

Gap-producing Toxidromes

Osmolar Gap

• Toxic alcohol
  • Ethanol
  • Methanol
  • Ethylene glycol
  • Isopropyl alcohol
• Drug stabilizing agents
  • Mannitol
  • Propylene glycol
  • Glycerol

Anion Gap

• Salicylate
• Iron
• Isoniazid
• Methanol
• Ethylene glycol
• Cyanide

References

1. Meehan, T. J. (2018). Approach to the Poisoned Patient. In Rosens emergency medicine: concepts and clinical practice (pp. 1813–1822). Philadelphia, PA: Elsevier.
2. Holstege, C., Borek, H. (2012). Toxidromes Critical Care Clinics 28(4), 479-498. https://dx.doi.org/10.1016/j.ccc.2012.07.008
3. Mégarbane, B. (2014). Toxidrome-based Approach to Common Poisonings Asia Pacific Journal of Medical Toxicology 3(1), 2-12. https://dx.doi.org/10.22038/apjmt.2014.2463
4. Rasimas, J., Sinclair, C. (2017). Assessment and Management of Toxidromes in the Critical Care Unit. Critical care clinics 33(3), 521-541. https://dx.doi.org/10.1016/j.ccc.2017.03.002
5. Thompson, T., Theobald, J., Lu, J., Erickson, T. (2014). The general approach to the poisoned patient Disease-a-Month 60(11), 509-524. https://dx.doi.org/10.1016/j.disamonth.2014.10.002

The post Toxidromes appeared first on Differential Diagnosis of.

A young male with unknown medical history is brought in by ambulance with altered mental status. EMS reports that the patient was agitated, requiring restraints for transportation. On arrival, the patient is agitated, uncooperative and unable to provide history. Vital signs are notable for tachycardia, tachypnea and hypertension. Physical examination demonstrates diaphoresis and mydriasis, as well as increased muscle tone – particularly in the lower extremities with ankle clonus. A core temperature is obtained and noted to be elevated at 41.5°C. Point-of-care glucose is normal.

Rapid external cooling measures were instituted and several doses of intravenous benzodiazepines were administered with improvement in agitation. Laboratory studies were notable for a modest leukocytosis (WBC 18.4 without immature forms), serum sodium was 135 without osmolar gap, creatine kinase was slightly elevated without renal dysfunction, and thyroid function tests were normal. Toxicology screen was negative. ECG revealed sinus tachycardia but was otherwise normal and non-contrast computed tomography of the head was normal.

After a brief admission in the intensive care unit, the patient’s mental status improved and he reported MDMA use on the evening of presentation, he also described a history of major depression and was taking paroxetine.

Evaluation of Elevated Temperature

The designation of 38°C as “suspicious” for fever dates to 1868 and the analysis of over one million (axillary) temperature measurements by Carl Wunderlich¹. Any cutoff is arbitrary and requires recognition of the clinical context and normal daily variations (with nadir in the morning and peak in evening) ^2,3. What is clear is that peripheral thermometry (unless demonstrating fever) is unreliable and a core temperature should be sought⁴.

Thermoregulation

Temperature homeostasis is a balance between heat production and dissipation maintained by the anterior hypothalamus. Heat production is a byproduct of normal metabolic processes and skeletal muscle activity. Conservation, maintenance or dissipation of heat is aided by cutaneous vasodilation, sweating, or behavioral responses.

Fever is caused by endogenous or exogenous pyrogens which alter the homeostatic set-point, inducing thermogenesis and elevating the body temperature. Precipitants of fever are usually infectious, however non-infectious processes (ex. malignancy, tissue ischemia/infarction, auto-immune disease) resulting in inflammation can provoke a similar response ^5-7.

There is no explicit temperature distinction to diagnose hyperthermia, instead the physiologic mechanism is different. In hyperthermia, the body’s homeostatic mechanisms are dysfunctional or overwhelmed due to heat exposure, excess production, ineffective dissipation or hypothalamic malfunction ⁸.

Algorithm for the Evaluation of Hyperthermia ^8-15

Implicated Agents in Drug-Induced Hyperthermic Syndromes ^9,10

Serotonin Syndrome

Neuroleptic Malignant Syndrome (NMS)

References:

1. Wunderlich CA. Das Verhalten Der Eigenwärme in Krankheiten. 1870.
2. Mackowiak PA, Wasserman SS, Levine MM. A critical appraisal of 98.6 degrees F, the upper limit of the normal body temperature, and other legacies of Carl Reinhold August Wunderlich. JAMA. 1992;268(12):1578-1580.
3. Lee-Chiong TL, Stitt JT. Disorders of temperature regulation. Compr Ther. 1995;21(12):697-704.
4. Niven DJ, Gaudet JE, Laupland KB, Mrklas KJ, Roberts DJ, Stelfox HT. Accuracy of peripheral thermometers for estimating temperature: a systematic review and meta-analysis. Ann Intern Med. 2015;163(10):768-777. doi:10.7326/M15-1150.
5. Dinarello CA. Infection, fever, and exogenous and endogenous pyrogens: some concepts have changed. J Endotoxin Res. 2004;10(4):201-222. doi:10.1179/096805104225006129.
6. Greisman LA, Mackowiak PA. Fever: beneficial and detrimental effects of antipyretics. Curr Opin Infect Dis. 2002;15(3):241-245.
7. Dinarello CA. Thermoregulation and the pathogenesis of fever. Infect Dis Clin North Am. 1996;10(2):433-449.
8. Simon HB. Hyperthermia. N Engl J Med. 1993;329(7):483-487. doi:10.1056/NEJM199308123290708.
9. Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med. 2005;352(11):1112-1120. doi:10.1056/NEJMra041867.
10. Berman BD. Neuroleptic malignant syndrome: a review for neurohospitalists. Neurohospitalist. 2011;1(1):41-47. doi:10.1177/1941875210386491.
11. Hayes BD, Martinez JP, Barrueto F. Drug-induced hyperthermic syndromes: part I. Hyperthermia in overdose. Emerg Med Clin North Am. 2013;31(4):1019-1033. doi:10.1016/j.emc.2013.07.004.
12. Oruch R, Pryme IF, Engelsen BA, Lund A. Neuroleptic malignant syndrome: an easily overlooked neurologic emergency. Neuropsychiatr Dis Treat. 2017;13:161-175. doi:10.2147/NDT.S118438.
13. Musselman ME, Saely S. Diagnosis and treatment of drug-induced hyperthermia. Am J Health Syst Pharm. 2013;70(1):34-42. doi:10.2146/ajhp110543.
14. Ahuja N, Cole AJ. Hyperthermia syndromes in psychiatry. Adv psychiatr treat (Print). 2018;15(03):181-191. doi:10.1192/apt.bp.107.005090.
15. Tomarken JL, Britt BA. Malignant hyperthermia. Ann Emerg Med. 1987;16(11):1253-1265. doi:10.1016/S0196-0644(87)80235-4.

The post Hyperthermia appeared first on Differential Diagnosis of.

Toxic Alcohols

• Overview
  • Toxic metabolites produced by alcohol dehydrogenase which can be inhibited by ethanol or fomepizole
  • Fomepizole: 15mg/kg loading dose, 10mg/kg q12h x4 doses then 15mg/kg q12h (stimulates own metabolism); if dialysis, q4h
• Diagnosis: osmolar gap (>14), 2Na + Glu/18 + BUN/2.8 + EtOH/4.6
• Treatment
  • ADH inhibition
  • HCO₃
  • Hemodialysis
  • Supportive care
  • Hypoglycemia: dextrose

Methanol

• Component of antifreeze, windshield washer fluid
• Metabolite formic acid which causes acidosis and blindness
• Can give folate

Ethylene glycol

• Component of antifreeze, automobile coolants, de-icing agents
• Metabolite oxalic acid which precipitates calcium oxalate crystals and causes acute renal failure
• Can give thiamine (100mg q6h), pyridoxine (500mg q6h), Mg

Isopropanol

• Component of rubbing alcohol
• Metabolite acetone which does not cause acidosis

Analgesics

Acetaminophen

• Metabolism: glucoronidation, CYP450
  • CYP450 pathway produces toxic metabolite when glucoronidation overwhelmed
  • In pediatrics, sulfation process protective
• Toxic dose: >150mg/kg, >3g/day
• Injury: liver (centrilobular necrosis), renal, pancreatic
• Increased risk: induced CYP450 (chronic EtOH, rifampin, anti-epileptics)
• Nomogram: applicable to single ingestion at 4-hours
• Labs: PT/INR, LFT, lipase, chemistry
• Management: NAC
  • PO: 140mg/kg, 70mg/kg q4h
  • IV: 150mg/kg, 50mg/kg over 4h, 100mg/kg over 16h

NSAID

• Symptoms
  • Acute: GI upset, low risk UGIB
  • Acute massive: acidosis, coma, seizures
  • Chronic: UGIB, nephropathy, agranulocytosis

Aspirin

• Signs: tachycardia, hyperthermia, tachypnea/hyperpnea
• Severe: cerebral and pulmonary edema, CNS hypoglycemia
• Labs: primary respiratory alkalosis with metabolic acidosis
• Management
  • Hypoglycemia (CNS) treatment
  • Bicarbonate infusion (urine pH > 8)
  • Hemodialysis for pulmonary edema, cerebral edema, renal failure, acidemia, level >100mg/dL (acute) or > 60mg/dL (chronic)

Opioids

• Symptoms: respiratory depression, miosis
• Management: naloxone 0.04mg, 0.4mg, 2mg
• Withdrawal: nausea/vomiting, diarrhea, abdominal pain, piloerection
  • Neonates: seizure, death
• Complications with specific agents:
  • Meperidine, tramadol: seizures
  • Methadone: QT prolongation

Anesthetics

Lidocaine

• Mechanism: Na-channel blockade
• Types:
  • Ester (one “i”): cocaine, procaine, benzocaine
  • Amide (two “i”): lidocaine, bupivacaine
• Toxicity
  • Dose: 4mg/kg, 7mg/kg with epinephrine
  • CNS: perioral numbness, slurred speech, seizure
  • CV: VT, VF, AV block
  • Methemoglobinemia: methylene blue
• Treatment
  • Seizure management
  • Bicarbonate for dysrhythmia
  • Intralipid

Anti-emetics

Phenothiazines

• Examples: compazine (prochlorperazine), phenergan (promethazine)
• MOA: DA-antagonist
• AE: sedation, dystonia, parkinsonism
• Toxicity: seizure, VT, hypotension (TCA-like)

5-HT3 antagonists

• Examples: zofran (ondansetron), granisetron
• Toxicity: QT-prolongation

Anti-hypertensives

Environmental

Carbon monoxide

• Source: combustion (gas heater, indoor barbeque)
• Toxicity
  • General: influenza-like, multiple proximate affected individuals
  • GI: abdominal pain, nausea
  • CNS: headache, dizziness, confusion, ataxia, seizure
  • CV: palpitations, arrhythmia, hypotension, MI
• Treatment
  • T½: RA 6h, NRB 1h, 3atm 0.5h
  • Hyperbaric: neuro deficit, syncope, pregnancy, CV toxicity

Cyanide

• Mechanism: inhibits oxidative phosphorylation
• Source: structural fire (wool, silk)
• Symptoms: syncope, seizure, coma, cardiovascular collapse
• Detection: severe lactic acidosis, “arterialization” of venous blood, “bitter almond” odor
• Treatment
  • Hydroxycobalamin (Cyanokit): 5g IV, may repeat x1
  • Sodium thiosulfate 12.5g IV

Methemoglobinemia

• Mechanism: Fe²⁺ converted to Fe³⁺, “functional anemia”
• Source: nitrite (food), topical/local anesthetics, pyridium, dapsone, reglan
• Detection: normal PaO2, SpO2 85% unresponsive to supplemental oxygen, ABG with co-oximetry
• Management: methylene blue 1-2mg/kg IV if symptomatic or MetHb >25%
  • Contraindicated in G6PD deficiency, treat with exchange transfusion or HBO

Hydrogen Sulfide

• Source: industrial, sulfur spring, sewer
• Detection: “rotten egg” odor
• Management: remove from source, supportive care

Hydrocarbon

• Source: huffing canisters
• Toxicity: VT/VF from myocardial sensitization
• Management: beta-blockade
• Complications: harmless if ingested, aspiration leads to ARDS

Hydrofluoric acid

• Source: rust remover, wheel cleaner, glass etching
• Symptoms: pain-out-of-proportion, delayed onset
• Toxicity: Hypocalcemia (QTc prolongation, VT/VF/TdP), hyperkalemia, hypomagnesemia
• Management: analgesia, topical calcium gluconate gel, intravenous calcium for large BSA involvement

Alkaline ingestion

• Symptoms: esophageal perforation, delayed stricture

Acid ingestion

• Symptoms: gastric perforation (rare), delayed gastric outlet obstruction
• Findings: metabolic acidosis

Botulism

• Sources
  • Adult: ingested preformed toxin
  • Infants: ingested spores (achlorhydric), in vivo toxin production
  • Wound: black tar heroin
• Symptoms: dysphagia, ptosis, diplopia, respiratory failure, descending paralysis
  • Infants: constipation, floppy
• Management: supportive care, intubation
  • Adults: Anti-toxin from CDC or local Department of Health
  • Infants: 100mg/kg IV x 1 dose (BabyBIG)

Heavy Metals

Iron

• Dose
  • Ferrous sulfate: 20% elemental iron
  • Toxic: >20mg/kg
  • Lethal: >60mg/kg (1 tablet 325mg ferrous sulfate per kilogram)
• Toxicity: corrosive, anti-coagulant, hepatotoxic
• Course
  • Stage I: GI effects, emesis with hematemesis
  • Stage II: Quiescent
  • Stage III: Systemic, multi-organ system dysfunction
  • Stage IV: Resolution, gastric scarring and outlet obstruction
• Workup
  • CBC/BMP
  • LFT
  • Lactate
  • Fe level
  • KUB (if positive consider WBI)
• Treatment
  • Decontamination: no activated charcoal, consider WBI
  • Deferoxamine: 15mg/kg/hr

Lead

• Source: paint, batteries
• Toxicity
  • Acute: headache, encephalopathy, seizure
  • Chronic: malaise, weight loss, arthralgia, anemia (basophilic stippling)
• Diagnosis: lead level, wrist drop
• Management: chelation (BAL, EDTA, DMSA) for level >50ug/dL or asymptomatic >70ug/dL

Lithium

• Source: iatrogenic, drug-drug interaction
• Symptoms
  • GI: nausea/vomiting, diarrhea
  • CNS: tremor, coma
  • CV: TWI, QT-prolongation
• Management
  • IVF, encourage renal elimination
  • Hemodialysis

Other Drugs

Disulfuram

• MOA: aldehyde dehydrogenase inhibitor
• Symptoms: increased acetaldehyde leads to flushing, headache, nausea/vomiting, tachycardia, hypotension
• Management: antihistamine, IVF, vasopressors
• Other agents causing disulfuram-like reaction: metronidazole, INH, sulfonylurea

Isoniazid

• Toxicity: seizure
• Management: pyridoxine 5g IV, repeat x1

Theophyline

• Toxicity: seizure
• Management
  • Decontamination: AC
  • Seizures: benzodiazepines
  • Tachyarrhythmia (commonly MAT): beta-blockade
  • Hemodialysis: acute > 100mg/L, chronic >30mg/L

Monoamine oxidase inhibitors

• Toxicity: food/drug interaction
• Symptoms: tachycardia, hypertension, hyperthermia, agitation
• Management: cooling, IVF, management of hyper/hypotension

Phenytoin

• Oral: cerebellar dysfunction (ataxia), CNS depression
• IV: hypotension (suspension contains propylene glycol)

Nutritional Supplements

• Fat-soluble vitamins
  • A: benign intracranial hypertension
  • D: hypercalcemia

Envenomations

Snake

• Crotalid (rattle), elapidae (coral)
• Symptoms
  • Local reaction: edema, hemorrhagic bullae
  • Systemic: perioral numbness, fasciculations
  • Severe: thrombocytopenia, decreased fibrinogen
• Management: Crofab 5 vials

Spider

• Black widow
  • Identification: hourglass on abdomen
  • Symptoms: painful bite, target-appearance, rarely “acute abdomen”
  • Management: analgesia, anti-venom, tetanus
• Brown recluse
  • Identification: violin shape on head
  • Geography: Southeast, Midwest
  • Symptoms: painless bite, local reaction, delayed healing with eschar
  • Rare: hemolysis, DIC, shock
  • Management: supportive care, antibiotics if superinfected, consider dapsone, tetanus

Scorpion (Centruroides)

• Geography: Arizona
• Symptoms
  • Autonomic: HTN, tachycardia, diaphoresis
  • CNS: opsoclonus, slurred speech, dysphagia
• Management: anti-venom, supportive care, analgesia, tetanus

Marine

• Ciguatera
  • Source: toxin bioconcentrated in fish
  • Symptoms: gastroenteritis, hot/cold-reversal, “loose teeth” sensation
  • Management: mannitol
• Scombroid
  • Source: poorly-refrigerated fish, histamine-like
  • Symptoms: flushing trunk/face (distinguish from allergic reaction), gastroenteritis
  • Management: supportive care, IVF, anti-histamine, bronchodilators if indicated
• Paralytic shellfish poisoning
  • Source: bivalve
  • Symptoms: gastroenteritis, paralysis
  • Management: supportive, intubation
• Jellyfish and Cnidaria
  • Source: nematocyst
  • Symptoms: burning pain, pruritus
  • Severe: Irakundji syndrome (HTN, pulmonary edema)
  • Management: supportive, analgesia, box jellyfish antidote, consider vinegar
• Stingray
  • Source: heat-labile toxin
  • Management: affected area in warm water, tetanus, ciprofloxacin (Vibrio)

Mushrooms

• Amanita: centrilobular necrosis, similar to acetaminophen
• Gyronatum: similar to INH (seizure and treatment), may cause methemoglobinemia
• Symptoms: muscarinic (SLUDGE)
  • Early onset generally benign, delayed onset (>6h) suggests more serious course
• Management: atropine, glycopyrrolate, IVF

Pesticides

• Organophosphate: irreversible
• Carbamate: reversible
• Symptoms: muscarinic (SLUDGE)
• Treatment: atropine 2-6mg IV double q5min to control secretions, pralidoxime (for organophosphates)

Strychnine

• Source: rodenticide
• Symptoms: myoclonus, opisthotonus, agitation
• Management: benzodiazepines, airway protection, paralysis

The post Toxicology appeared first on Differential Diagnosis of.

38M, unknown medical history, brought in after being found unresponsive next to an empty bottle of Seroquel. Presenting vital signs notable for blood pressure of 96/43, heart rate 103. Examination reveals tentatively protected airway (GCS E2 M5 V3, SpO2 100%, RR 14), normal pupil diameter and reactivity, dry mucous membranes with thick vomitus in oral cavity.

Laboratory evaluation was unremarkable, and there was no evidence of aspiration on chest radiography. ECG showed sinus tachycardia without QT prolongation. Blood pressure increased to normal range with fluid resuscitation. The patient’s mental status progressively improved and he was discharged after six hours of uneventful continuous cardiac monitoring.

Toxidrome Summary¹

Evaluation^1,2

• POC Glucose
• ECG (QT interval)
• Serum acetaminophen, salicylate, EtOH level
• Serum drug levels if known (anti-epileptics)
• Urine toxicology screen
• Chemistry (metabolic acidosis, electrolytes, renal function)
• LFT (hepatotoxicity)
• CK (rhabdomyolysis)
• Serum osmolarity (osmolar gap)
• UA with microscopy (crystals in ethylene glycol poisoning)
• ABG (carboxyhemoglobin, methemoglobin)

Pharmacology, Toxicity and Management of Second Generation Antipsychotic (SGA) Overdose³

References

1. Kulig, K. (2013). General Approach to the Poisoned Patient. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 1954-1959). Elsevier Health Sciences.
2. Wittler, M., & Lavonas, E. (2013). Antipsychotics. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 2047-2051). Elsevier Health Sciences.
3. Levine M, Ruha A-M. Overdose of atypical antipsychotics: clinical presentation, mechanisms of toxicity and management. CNS Drugs. 2012;26(7):601–611.
4. WikEM: Antipsychotic toxicity

The post Atypical Antipsychotic Overdose appeared first on Differential Diagnosis of.

“Gastosin” ingestion

HPI:

29F BIB family after patient was found down at home, near opened bottle of Gastosin in presumed suicide attempt. On arrival to ED, patient was awake, but unresponsive, groaning and clutching stomach. GCS  was E3-V2-M5, HR 110, BP 60/palp, RR 24.

ED Course:

Upon arrival, placed two large-bore IV w/rapid infusion of 2L NS and given DA 2g IV x2. NG tube placed, initiated lavage of gastric contents with NS. Patient’s mental status continued to deteriorate, became unresponsive.

PMH/PSH:

Unknown

SHx:

History of alcohol abuse and depression per family.

PE:

• VS: 110bpm, 60/palp, 24 R/min, no temp/O2sat available
• General: Ill-appearing female, laying on bed in considerable distress, groaning and clutching stomach, diaphoretic
• HEENT: NC/AT, PERRL (4-3mm), EOMI, MMM no lesions, no tongue lacerations, breath with foul odor, TM’s clear b/l.
• CV: RRR, normal S1/S2, tachycardia, faint heart sounds, JVP elevated though patient supine
• Lungs: CTAB, no crackles/wheezes
• Abdomen: +BS, soft, non-distended, no guarding, no ecchymosis
• GU: Normal external genitalia, loss of stool noted.
• Neuro: Patient confused, initially responsive to sternal rub, moving all 4 extremities spontaneously/equally, EOMI without nystagmus, gag reflex present, DTR 2+ and symmetric throughout with toes downgoing.
• Extremities: Cool, peripheral pulses 0 (radial, PT, DP), 1+ (femoral, brachial, carotid)¹, capillary refill 3sec
• Skin: No visible skin lesions

Assessment & Plan:

29F, unknown PMH, ċ ingestion of unknown amount of “Gastosin”. Patient presenting in likely cardiogenic shock given hypotension with reflex sympathetic activation (evidenced by peripheral vasoconstriction à cool extremities, diaphoresis) and no evidence of hemorrhage. Gastosin is a pesticide used in the storage of maize², and is well-known locally as a common agent in self-poisonings. Chemically composed of aluminum phosphide, and liberates phosphine gas on exposure to moisture which is rapidly absorbed by inhalation, transdermally or gastrointestinally. Toxicity results from free radical damage and inhibition of enzymes of metabolism (particularly affecting cardiac myocytes). Clinical features include vomiting, resistant hypotension and metabolic acidosis.³

Patient’s symptoms and presentation are consistent with cardiogenic shock secondary to Gastosin ingestion. Management included fluid resuscitation and inotropic support with dopamine, as well as gastric lavage. Resuscitation efforts were unsuccessful and patient remained hypotensive with worsening of mental status, and eventual death.

Differential Diagnosis for Shock:

A System for the Management of Aluminum Phosphide Poisoning:^4,5

The Glasgow Coma Scale:

References:

1. Hill RD, Smith RB III. Examination of the Extremities: Pulses, Bruits, and Phlebitis. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 30. Available from: http://www.ncbi.nlm.nih.gov/books/NBK350/
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