Annals of B-Pod: Caustic Ingestions

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History of Present illness

The patient is a female in her late 40s who presents via EMS with altered mental status. Per EMS and family, the patient has been unusually somnolent and lethargic for the past two hours. A similar event occurred approximately two weeks prior after the patient consumed an unknown quantity of laundry detergent pods. The family is now concerned that the patient has ingested laundry detergent again. The patient herself is unable to provide further history.

    Past Medical History: 

    1. Multiple sclerosis
    2. Psychogenic nonepileptic seizures
    3. Anxiety
    4. Endometriosis
    5. Scleroderma
    6. Depression

    Past Surgical History:

    1. Caesarean section x2
    2. Tonsillectomy
    3. Antrectomy with Roux-en-Y gastrojejunostomy

    Medications:

    1. Amitriptyline
    2. Baclofen
    3. Dextroamphetamine-amphetamine
    4. Diazepam
    5. Ergocalciferol
    6. Fluoxetine
    7. Furosemide
    8. Interferon beta-1a
    9. Lisdexamfetamine
    10. Omeprazole
    11. Prochlorperazine
    12. Quetiapine
    13. Sumatriptan

     

      Vital Signs:  T 36.6°C  BP 121/76  P 87  RR 25  SaO2 95% on room air

      Physical Exam:Well-nourished, well-developed adult woman in no acute distress. Normocephalic with intact extraocular movements and no nystagmus. Pupils equally round and reactive to light. Cardiac exam reveals a regular rhythm and rate with intact peripheral pulses. Lungs clear to auscultation bilaterally with normal work of breathing and no respiratory distress. Her abdomen is soft, non-tender, with no rebound or guarding. Genitourinary exam shows normal female external genitalia with no hemorrhoids, fissures, or masses; normal rectal tone with guaiac-negative stool. Neurologic exam is notable for a depressed mental status although she is arousable to verbal stimuli. The patient follows commands with notable diffuse weakness in all four extremities. Normal deep tendon reflexes without clonus. No obvious sensory deficits. Speech is slurred. Grossly depressed mood but no obvious suicidal ideation. Patient's skin is warm and dry.

      Diagnostics

      WBC: 17.4  Hgb: 9.2  Platelets: 771

      Urinalysis:  Unremarkable   Urine hCG: Negative   Urine Drug Screen: Positive for tricyclic antidepressants

      CT head:  No definite interval changes in patient's demyelinating disease.

      CT abdomen and pelvis: Marked gastric distention with abnormal gastric debris in the setting of prior antrectomy.

      Hospital Course

      Given the patient's significantly depressed mental status in the context of known neurologic disease, neurology was consulted in the emergency department. The neurology team independently evaluated the patient, but had a low concern for neuraxial pathology as the primary cause of the patient's somnolence. Neurology recommended EEG to rule out atypical seizures causing the patient’s altered mental status in addition to further observation pending improvement in her cognition. 

      Psychiatry was consulted the following day (hospital day one) to evaluate the patient and provide recommendations. On their examination, the patient's mental status had improved dramatically. Furthermore, the patient adamantly denied any self-injurious intent or suicidal ideation. As such, psychiatry felt that there were no significant safety concerns at the time and that patient could safely be discharged home with a slight reduction in her quetiapine dose pending medical clearance.

      The patient was subsequently discharged from the hospital on hospital day two. As the patient's mental status had improved spontaneously, more aggressive diagnostic and therapeutic interventions - such as endoscopy - were not pursued. Instead, the patient was counseled on the risks of ingesting caustic agents and was instructed to follow-up with her neurologist as an outpatient for further evaluation and titration of her medications.

      Discussion

      Ingestion of detergent agents, whether intentional or accidental, can cause serious and potentially life-threatening toxicologic disease. While ingestion in the adult population often stems from psychiatric disease or self-injurious behaviors, the advent of water-soluble laundry detergent pods has led to a significant increase in the number of pediatric poisonings, due in part to their bright coloration and pleasant smell.[1] This article will discuss the various manifestations of toxic exposure, pathogenesis, and evidence-based management of detergent poisonings in both the pediatric and adult populations.
       
      The exact mechanism by which detergent causes injury has not been fully elucidated but is presumed to be multimodal in nature. Detergents are composed of a complex mixture of various chemical entities, including caustic alkali agents (such as sodium carbonate or sodium silicate), surfactants, anti-redeposition agents, fragrances, opacifiers, and many other non-toxic ingredients.[2] These compositions are specially formulated to loosen, solubilize, and emulsify debris while simultaneously chelating inorganic solutes and prevent redeposition.[2] While the caustic alkaline agents are typically viewed as the culprit pathological entity, the other chemical constituents of detergents likely contribute to or exacerbate these injuries.
       
      In-vitro histological studies and case reports indicate that caustic alkaline substances may rapidly induce liquefactive necrosis of exposed mucosal structures. Esophageal mucosa may develop transmural injuries after only one second of exposure to 30% sodium hypochlorite solution.[3] This is not to be confused with household bleach which is composed of only 5.25% sodium hypochlorite. On initial exposure, mucosal tissues quickly become inflamed and edematous before progressing to frank necrosis within minutes to hours. The hours to days following an ingestion are characterized by progressive inflammation and local superficial thrombosis, with evidence of wound granulation by day 10.[4] During this period, the nascent wound is at increased risk of perforation. By three weeks, however, fibrin deposition and recollagenization mechanisms have progressed, producing a mature, stable wound similar to normal tissue. More severe or extensive injuries may eventually progress to scarring and stricture formation around three weeks to one month.

      Pharyngoesophageal insults occur most frequently given their relative position in the aerodigestive axis. Gastric injuries are also common but tend to be less severe due to partial neutralization of the caustic substances in the acidic medium of the stomach. Injuries of the duodenum and more distal enteric structures are less common. This is likely due to dilution of the offending agent. However, more distal injuries are often associated with significant morbidity, such as visceral perforation and peritonitis.[5] Additionally, regurgitation and aspiration may lead to inhalation of the caustic entity into the tracheobronchial tree, potentially leading to respiratory compromise.
       
      Serious mucosal injuries following ingestion of detergents and other caustic household products tends to be rare and correlate with the concentration of the agent as well as the volume imbibed.[6,7] A grading scale has been developed to categorize the severity of esophageal injury and likelihood of long-term sequelae based on endoscopic appearance (Figure 1).[8] Higher grade injuries (>2B) have been shown to correlate with increased risk of serious pathology, such as gastric or esophageal cicatrization, necessitating surgical or endoscopic intervention, while low grade injuries often require no further diagnostic or therapeutic intervention. The utility of this grading scale is limited in the emergency department, however, by the need for formal fiberoptic endoscopy and the lack of reliable symptomatic predictors.[9]  Nonetheless, urgent endoscopic evaluation should at least be considered in all possible cases of caustic ingestion in order to identify the extent of mucosal injury. 

      fIGURE 1.  eNDOSCOPIC GRADING SYSTEM FOR CAUSTIC INJURIES.

      Clinical manifestations of caustic ingestions are varied, but often present with severe oropharyngeal, chest and/or abdominal pain, and dysphagia/odynophagia. Hematemesis is suggestive of gastric involvement, while abdominal distention, rigidity, and objective fevers may indicate visceral perforation causing pneumoperitoneum and/or -mediastinum. While clinical symptoms have not been shown to correlate with the severity of injury, vital sign abnormalities (such as fever and hypotension) and clinical evidence of peritonitis should warrant urgent endoscopic evaluation. Coughing, drooling, hoarseness, and respiratory distress are suggestive of laryngeal exposure and glottic edema, and should prompt emergency providers to strongly consider establishing a definitive airway early in the patient's course given the potential for progressive disease causing respiratory compromise.
       
      On arrival to the emergency department, providers should assess for evidence of oropharyngeal injuries and respiratory distress, including tachypnea, stridor, pooled secretions, and accessory muscle use, as these may indicate the need for laryngoscopy and endotracheal intubation. Objective fever or hypotension in conjunction with severe chest pain or signs of peritonitis (e.g., distended abdominal, exquisite pain to palpation) should raise concern for a perforated viscus and should prompt emergent surgical consultation. Even well-appearing, hemodynamically stable patients warrant a discussion with an endoscopic specialist urgently, given the aforementioned lack of correlation between symptom severity, degree of injury, and potential need for esophagogastroduodenoscopy. Emergency physicians may consider concomitantly contacting a local poison control center to discuss the case with a medical toxicologist, who may provide further guidance in developing a treatment plan and disposition for the patient.
       
      Fiberoptic endoscopy remains the definitive diagnostic tool, though its use is contraindicated in patients with findings concerning for perforation. While lacking sensitivity, plain chest radiographs provide a cost-effective and quick method of assessing for free sub-diaphragmatic or mediastinal air as well as possible pneumonitis. Esophagography with water-soluble contrast is another viable modality to assess for gross dysmotility and perforation, though it lacks the ability to categorize mucosal changes or the extent of an exposure. Modern high-resolution computed tomography may demonstrate inflammation in exposed mucosal tissue as well as evidence of free air within the mediastinum or peritoneum. Recent studies have validated the use of cross-sectional imaging of the chest and abdomen as a decision tool in evaluating the need for emergent esophagectomy in patients with high grade injuries.[10] These studies can often be readily obtained in the emergency department, and may help to guide further diagnostic and therapeutic decision-making. Given the lack of correlation between symptoms and extent of injury, all suspected cases of caustic ingestion may benefit from cross-sectional imaging in the emergency department.

      The management of most caustic substance exposures in the emergency department is largely supportive. Providers should consider administering intravenous opioid agents for analgesia and crystalloid fluids for resuscitation. Current guidelines recommend against the use of emetics to expel the caustic substance or neutralizing xenobiotics due to the risk of potentially exacerbating the injury or causing an aspiration event. The use of prophylactic antibiotics is common practice, though there is not robust evidence for their use. In patients with symptoms concerning for viscus perforation and consequent mediastinitis or peritonitis, however, empiric treatment with a third generation cephalosporin is recommended. Corticosteroid use following ingestion remains controversial, with some studies showing a decreased incidence of strictures and others showing no significant benefit.[11,12] Expert opinion suggests that the empiric use of systemic glucocorticoids (e.g., dexamethasone 10 mg IV) is justified in patients with evidence of airway involvement to reduce edema and the risk of cardiopulmonary collapse.[9] Proton pump inhibitors are sometimes used to de-acidify the gastric contents and are thought to reduce the likelihood of gastric ulceration or reflux, though their efficacy in reducing morbidity has not been demonstrated.[13]
       
      Toxicologists recommend against the routine use of activated charcoal as it does not readily absorb high pH substances and itself carries the risk of aspiration and chemical pneumonitis. Similarly, the placement of blind nasogastric tubes is cautioned against due to the potential of perforating through injured, friable mucosa.
       
      Ultimately, emergent surgical resection remains the definitive treatment of severe transmural, circumferential, or perforating injuries. Patients with severe injuries and damage to the swallowing apparatus may require prolonged parenteral nutrition; in these cases, nasogastric feeding tubes should be placed intraoperatively under direct visualization to reduce the risk of perforation.

      While long-term sequelae are uncommon for mild injuries (grade 1), more serious injuries are associated with various late complications. The most common delayed complication is stricture formation. Up to one-third of patients with esophageal burns (and virtually all patients with injuries of grade 2B or worse) will develop strictures.[8] While not necessarily life-threatening, strictures may be associated with esophageal dysmotility, dysphagia, and gastric outlet obstruction depending on the location of the injury. Severely symptomatic patients may require endoscopic dilation. Strictures are prone to recurrence, however, and symptomatic relief from dilation is often temporary. More alarmingly, patients with severe injuries have increased risk of esophageal malignancy, with the incidence of esophageal neoplasms roughly 1000-3000 times higher than that of the general population.[13]
       
      Though the ultimate cause of the above patient’s altered mental status was never fully elucidated, the concern for possible caustic ingestion highlights a unique pathology with which emergency providers must be familiar. Recognizing the hazards of and knowing the management of caustic ingestions are both essential parts of an emergency physician’s repertoire.

      Authored and posted by matthew scanlon, m.d.

      References

      1. Bonney, A. G., Mazor, S., & Goldman, R. D. (2013). Laundry detergent capsules and pediatric poisoning. Canadian Family Physician, 59(12), 1295–1296.
      2. Bajpai, D. & Tyagi, V.K. (2007) Laundry Detergents: An overview. Journal of Oleo Science 56(7), 327-340.
      3. Kennetz, B. F. (1992). Ingestion of strong corrosive alkalis: Spectrum of injury to upper gastrointestinal tract and natural history. The Journal of Emergency Medicine,10(6), 780.
      4. Dafoe, C. S., & Ross, C. A. (1969). Acute corrosive oesophagitis. Thorax, 24(3), 291-294.
      5. Leape, L. L., Ashcraft, K. W., Scarpelli, D. G., & Holder, T. M. (1971). Hazard to Health — Liquid Lye. New England Journal of Medicine, 284(11), 578-581.
      6. Mühlendahl, K. E., Oberdisse, U., & Krienke, E. G. (1978). Local injuries by accidental ingestion of corrosive substances by children. Archives of Toxicology, 39(4), 299-314.
      7. Mattos, G. M., Lopes, D. D., Mamede, R. C., Ricz, H., Mello-Filho, F. V., & Neto, J. B. (2006). Effects of Time of Contact and Concentration of Caustic Agent on Generation of Injuries. The Laryngoscope, 116(3), 456-460.
      8. Zargar, S. A., Kochhar, R., Mehta, S., & Mehta, S. K. (1991). The role of fiberoptic endoscopy in the management of corrosive ingestion and modified endoscopic classification of burns. Gastrointestinal Endoscopy, 37(2), 165-169.
      9. Goldfrank, L. R., & Flomenbaum, N. (2006). Goldfrank's toxicologic emergencies. New York: McGraw-Hill.
      10. Chirica, M., Resche-Rigon, M., Pariente, B., Fieux, F., Sabatier, F., Loiseaux, F.,  &Cattan, P. (2014). Computed tomography evaluation of high-grade esophageal necrosis after corrosive ingestion to avoid unnecessary esophagectomy. Surgical Endoscopy, 29(6), 1452-1461.
      11. Anderson, K.D., Rouse, T.M., & Randolph, J.G. (1990). A controlled trial of corticosteroids in children with corrosive injury of the esophagus. New England Journal of Medicine, 323, 637-640.
      12. Usta, M et al. (2014). High Doses of Methylprednisolone in the Management of Caustic Esophageal Burns. Pediatrics, 133(6), 1518-1524.
      13. Contini, S., & Scarpignato, C. (2013). Caustic injury of the upper gastrointestinal tract: A comprehensive review. World Journal of Gastroenterology : WJG, 19(25), 3918–3930.