Case Report

Airway obstruction in a dog afterDieffenbachia ingestionKatherine Peterson, DVM; Jessica Beymer, DVM; Elke Rudloff, DVM, DACVECC and

Mauria O’Brien, DVM, DACVECC

Abstract

Objective – To describe a case of Dieffenbachia ingestion in a dog presented for dysphagia and airwayobstruction successfully treated with a temporary tracheostomy and supportive care beyond that reported inthe veterinary literature.

Case Summary – An 8-year-old male neutered Labrador Retriever, weighing 30 kg, was presented with thecomplaint of choking and gagging. Abdominal radiographs showed that he had a distended stomach full offoreign material and a gastrotomy was performed. After receiving preanesthetic medication, the dogdeveloped inspiratory stridor and during anesthetic induction, marked oropharyngeal swelling complicatedtracheal intubation. During surgery a large amount of dog bedding and Dieffenbachia plant material wasremoved. Because of the severity of the oropharyngeal swelling, the dog required a temporary tracheostomyand treatment for an acute allergic reaction related to the Dieffenbachia ingestion. The patient was dischargedafter 6 days in the hospital and had no significant complications.

New or Unique Information Provided – To our knowledge, this is the first reported case of successfultreatment of an airway obstruction related to the toxicity of Dieffenbachia ingestion.

(J Vet Emerg Crit Care 2009; 19(6): 635–639) doi: 10.1111/j.1476-4431.2009.00486.x

Keywords: gastrointestinal tract surgery, plant toxicology, tracheostomy

Introduction

Dieffenbachia is a common household plant that causes

toxicity when ingested. Reports in humans and

dogs describe local oral mucosal irritation.1,2 With se-

rious exposure, reports from the human literature

describe respiratory failure caused by upper airwayobstruction following Dieffenbachia ingestion requiring

advanced life support measures, especially in young

children.1–3 A single report in the veterinary literature

describes the events leading to respiratory failure

and death in a dog following Dieffenbachia exposure.2

The following case report describes the successful treat-

ment of an airway obstruction in a dog following

Dieffenbachia ingestion.

Case Report

An 8-year-old male neutered Labrador Retriever,

weighing 30 kg, was presented to the emergency ser-

vice with the complaint of choking and gagging. He

was reportedly acting normally 4 hours before presen-

tation and ate a normal meal at that time. When theowner returned home 30 minutes before presentation,

the dog did not greet her at the door, was heard to be

making choking and gagging noises, and appeared le-

thargic. There was no known dietary indiscretion or

foreign body exposure at that time.

On presentation, rectal temperature was 39.11C

(102.41F), heart rate was 132/min, and respiratory rate

was 24/min. Perfusion and hydration appeared ade-quate. On initial examination, the dog was hyper-

salivating, had erythema on his upper lips, a slight dry

cracking of the skin at the lip commisure, and a slightly

audible inspiratory stridor. There was no significant

erythema or edema in the visible oropharyngeal region.

No gagging or choking was observed. The dog tensed

on abdominal palpation and a possible tubular mass

was noted in the mid-abdomen, suspected to be thespleen. The dog was admitted to the hospital for ob-

The authors declare no conflicts of interest.

Address correspondence and reprint requests toDr. Katherine Peterson, 1377 W. County Rd B, Roseville, MN 55113, USA.Email: pete1773@umn.edu

From the Animal Emergency Center, Glendale, WI 53209.

Journal of Veterinary Emergencyand Critical Care 19(6) 2009, pp 635–639

doi:10.1111/j.1476-4431.2009.00486.x

& Veterinary Emergency and Critical Care Society 2009 635

servation and radiographic evaluation of the esophagus

and stomach. The owner declined sedation to allow for

a complete oropharyngeal exam.

A lateral radiograph of the neck and thorax showed

no significant abnormalities. A lateral radiograph of the

abdomen showed a distended stomach containing ingesta

(Figure 1). After this finding, the owner agreed toadditional diagnostic evaluation, consisting of a com-

plete blood count, serum chemistry profile, electrolyte

panel, and venous blood gas. Results were within the

respective reference intervals.

Two and a half hours after admission, the owner,

upon returning home, reported that the dog’s bed and

an unidentified plant were destroyed. The owner al-

lowed us to provide supportive care but declined sur-gery at that time. A cephalic IV catheter was placed and

IV fluids were started (isotonic crystalloidsa at 10 mL/

kg/h). On repeat examination of the dog, he was found

to be unwilling to lie down, panting, and appeared

uncomfortable in the kennel, which was attributed to

foreign body ingestion. The owner was contacted and

approved endoscopic removal of the gastric contents

followed by surgery if needed. Presurgical activatedclotting time was within the reference interval.

The dog was given hydromorphoneb (0.1 mg/kg, IV)

for analgesia in preparation for anesthesia and endos-

copy. Soon after the injection, his respiratory rate in-

creased and the inspiratory stridor increased in

intensity, and was initially attributed to the hydro-

morphone injection. Acepromazinec (0.025 mg/kg, IV)

was then administered for sedative effects. There wereno improvements in respiratory rate, noise, or effort.

Following sedation, swelling of the lips, tongue, and

area under the right side of tongue was noted. The dog

was given ketamined (5 mg/kg, IV) and midazolame

(0.5 mg/kg, IV) to induce anesthesia. Marked glosso-

pharyngeal swelling prevented visualization of the la-

ryngeal folds. A polypropylene catheter was passed

into the trachea using digital manipulation, and an

endotracheal tube was fed over the polypropylenecatheter. Anesthesia was maintained with sevofluranef

in 100% oxygen. The dog was given dexamethasoneg

(0.5 mg/kg, IV) and diphenhydramineh (2.5 mg/kg, IM)

for a suspected allergic reaction causing the airway ob-

struction. Hetastarchi (1 mL/kg/h) was added to main-

tain intravascular volume during anesthesia.

Endoscopic evaluation of the esophagus was normal.

A large amount of material was present in the stomach,but could not be extracted with endoscopic retrieval

instruments. Gastrotomy was performed to remove the

gastric contents. Bedding, foam batting, and plant ma-

terial, including leaves, stems and roots, were found

within the stomach and removed. The gastric mucosa at

that time appeared normal. A nasogastric tube (NGT)

was placed for gastric decompression as well as in

preparation for postoperative nutritional support. Aprophylactic incisional gastropexy was also performed.

The plant was identified as Dieffenbachia species, and

the National Animal Poison Control Center (NAPCC)

was contacted. The recommendations of the NAPCC

veterinarian included an oral cavity milk rinse for de-

contamination, and continued corticosteroids for its anti-

inflammatory effects. They advised that the clinical signs

associated with Dieffenbachia exposure were typicallymild and resolved within 8–12 hours after exposure.

Postoperatively (Day 2) the patient could not be

extubated due to continued oropharyngeal swelling

and upper airway obstruction. The patient had spon-

taneous respirations and did not require supplemental

oxygen. Nebulization of the endotracheal tube was

performed every 4 hours and suctioned as needed for

secretions. Analgesia and sedation to permit continuedintubation was achieved with fentanylj (5 mg/kg/h, IV)

and ketamine (290 mg/kg/h, IV) infusions. In addition,

a fentanyl patchk (75mg/h) was placed in anticipation

of long-term pain management. Famotidinel (0.5 mg/kg,

IV, q 12 h) and sucralfatem,n (1 g, via NGT, q 8 h) were

started for their gastroprotectant properties, and cefa-

zolinm (22 mg/kg, IV, q 8 h) was administered for post-

operative antimicrobial coverage. Dexamethasone(0.25 mg/kg, IV, q 24 h) was continued for its anti-

inflammatory properties. The oral cavity was lavaged

using whole milk followed by suction every 4 hours.

Microenteral nutritiono (5 kcal/kg/d) as a continuous

infusion was started through the NGT to promote gas-

trointestinal tract motility and healing. Lubricant was

placed into both eyes every 6 hours and the dog wasFigure 1: Lateral radiograph of the abdomen of the dog. Note

the distended stomach filled with foreign material.

& Veterinary Emergency and Critical Care Society 2009, doi: 10.1111/j.1476-4431.2009.00486.x636

K. Peterson et al.

turned every 6 hours. Fluid therapy was continued

using hetastarch (0.8 mL/kg/h) and isotonic crystalloids

(5 mL/kg/h) to maintain hydration and intravascular

volume. Patient monitoring included blood pressure

measurement every 4 hours and a continuous ECG. The

nose and mouth were suctioned as needed after a mu-

coid discharge developed.Recheck venous blood gas, electrolytes, lactate, blood

urea nitrogen, and PCV were within reference intervals.

Total plasma protein (40 g/L [4.0 g/dL]; reference in-

terval, 54–78 g/L [5.4–7.8 g/dL]) and albumin (13 g/L

[1.3 g/dL]; reference interval, 27–38 g/L [2.7–3.8 g/dL])

were reduced. Throughout the day, superficial mucosal

sloughing developed in the oral cavity, so the milk

rinses were replaced with chlorhexidinep solutionrinses. A urinary catheter was placed to monitor urine

output and prevent urine scalding.

On Day 3 oropharyngeal swelling continued to pre-

vent extubation. A temporary tracheostomy was per-

formed to allow for reduction in the patient’s sedation,

maintain a patent airway, decrease oropharyngeal in-

jury related to orotracheal intubation, and promote re-

spiratory toilet. A jugular vein catheter was placed tofacilitate phlebotomy. The patient remained sedated

with the fentanyl and ketamine infusion and anesthesia

was administered for the procedures using propofolq

(2.5 mg/kg, IV) for induction, and sevoflurane for

maintenance. Following the tracheostomy procedure,

the continuous fentanyl and ketamine infusion was

discontinued. Airway care consisted of saline ne-

bulization of the tracheostomy tube every 4 hours fol-lowed by 5 minutes of preoxygenation then the

tracheostomy tube was suctioned until clear. Diphen-

hydramine was reinstituted at (2 mg/kg, IM, q 8 h) for

its antihistamine properties.

A mild anisocoria was noted following the procedure

and fluoresceinr stain revealed bilateral superficial cen-

tral corneal ulcers. Lubrication of the eyes was in-

creased to every 4 hours and gentamycin ophthalmicdropss (1 drop, OU, q 8 h) were started. As the dog was

recovering from anesthesia, he was agitated and trem-

bling. His mucous membranes were pink, his pulse

oximetry reading was 96%, but auscultation revealed

crackles ventrally and the dog was panting. There was

a small amount of liquid noted within the tracheostomy

tube, consistent with regurgitation, and the rectal tem-

perature increased to 40.61C (1051F). Flow-by oxygenwas provided and the fluid was suctioned from the

tube. Repeat venous blood gas, electrolytes, blood urea

nitrogen, and lactate were not significantly altered from

previous values. Midazolam (0.3 mg/kg, IV followed

by 0.2 mg/kg/h, IV) controlled the trembling and ag-

itation and was gradually reduced and discontinued

after 3 hours.

Thoracic radiographs revealed a mild alveolar pat-

tern of the left cranial and the cranial portion of the left

caudal lung lobes, suggestive of aspiration pneumonia.

A transtracheal wash was performed via the tracheos-

tomy tube to obtain samples for cytologic examination

and aerobic bacteriologic culture. Cytologic examina-

tion showed a suppurative exudate with bacterial rods,however, due to limited sample volume (0.1 mL), bac-

teriologic culture could not be performed. In addition

to airway care, coupage was started every 6 hours and

the cefazolin was continued to treat the pneumonia.

The IV lines were chilled with ice for a few hours until

the temperature decreased to 39.41C (1031F). Because of

the suspected regurgitation, cisapridet (0.5 mg/kg, via

NGT, q 8 h) was started to promote gastrointestinalmotility. Pulse oximetry was monitored every 4 hours.

By Day 4, the tongue and lip commissures had re-

turned to normal appearance; the tongue and the oral

cavity remained swollen but improved. There was no

regurgitation and minimal suction volume from the

NGT. Rectal temperature remained normal. The

tracheostomy tube was removed without incident,

and the tracheostomy site cleaned every 8 hours. Theurinary catheter was removed as he became more am-

bulatory. On Day 5 the swelling in the oral cavity con-

tinued to subside, and the dog ate voluntarily.

Cefazolin injections were discontinued and oral cepha-

lexinu was started (33.3 mg/kg, PO, q 12 h).

By Day 6 the dog was eating well, and the NGT was

removed. The swelling in the oral cavity appeared to be

completely resolved. He was breathing comfortably,however would cough and expel a mucoid discharge

through the tracheostomy site. He was discharged with

sucralfate (1 g, PO, q 8 h), cephalexin (25 mg/kg, PO, q

12 h), cisapride (0.5 mg/kg, PO, q 8 h), tramadolv

(1.6 mg/kg, PO, q 8 h), and gentamycin ophthalmic

drops (1 drop, OU, q 8 h).

Five days following hospital discharge, the staples

were removed from the abdominal incision. Thetracheostomy site had closed with healthy granulation

tissue in place. Flourescein staining of the eyes was

negative. Thoracic radiographs showed resolution of

the previous infiltrates. The cephalexin was continued

for 5 additional days and all other medications were

discontinued.

Discussion

A common household plant, approximately 30 species

of Dieffenbachia exist.4 Dieffenbachia is a member of the

Araceae family, which includes Philodendron, Caladium,

Calla lily, Elephant ear, and Jack-in-the-pulpit. Com-

mon names for Dieffenbachia include dumb cane or

mother-in-law’s tongue; folklore suggests that it was

& Veterinary Emergency and Critical Care Society 2009, doi: 10.1111/j.1476-4431.2009.00486.x 637

Airway obstruction in a dog after Dieffenbachia ingestion

used as a punishment for slaves by rubbing the juice on

their gums, which made them unable to speak due to

painful, swollen oral mucosa.1

Dieffenbachia intoxication involves several mecha-

nisms of injury. Initially, the insoluble crystalline form

of oxalic acid (calcium oxalate crystals) embeds in the

mucosa and causes local irritation.5 Following mechan-ical injury, ejector cells, called idioblasts, embed them-

selves into the mucosa and release needle-like raphides

contributing to local inflammation. Finally, trypsin-like

proteolytic enzymes that coat the raphides are released

into the tissues and stimulate a local inflammatory re-

sponse with the release of histamine and kinin.6–8

Histologically, affected tissues show marked edema,

and neutrophilic, lymphocytic, and mast cell infil-trates.5 All parts of the plant are toxic but the stem

appears to be more toxic than the petioles or the

leaves.7 Systemic effects of oxalic acid toxicity from this

plant are not reported in the veterinary literature.

The immediate local oral cavity irritation should dis-

courage further ingestion and minimize the extent of

clinical signs.5,9 Two retrospective studies of human

cases reported to poison centers showed that only18.2% and 2.1% of patients exposed to either Philoden-dron or Dieffenbachia, respectively, were symptomatic

with oral irritation but no significant oral complications

or life threatening symptoms were observed in either

study.1,9 A case report documented that an adult with

acute Dieffenbachia poisoning presented with salivation,

burning, and pain in the oral cavity with mucosal

edema and blistering that required 14 days of hospi-talization and supportive care for the corrosive injury to

the oral cavity.10 Additionally, reports from human

and veterinary literature have described corneal ulcers,

skin inflammation, and gastrointestinal erosions and

ulcerations.1,2,11

The most common clinical signs of Dieffenbachia ex-

posure anecdotally reported from NAPCC during the

initial consultation on this case include excessive sal-ivation, pain, and edema involving the oral cavity. The

dog in this case was reported by the owner to have

gagging, and showed hypersalivation and erythema of

the lips at the initial exam. Within 6 hours of presen-

tation, edema and irritation of the oral mucosa and

glossopharyngeal swelling developed. It is presumed

that the oropharyngeal swelling in this dog was asso-

ciated with the ingestion of Dieffenbachia, which wasdiscovered in the gastric contents, and not the bedding

material or other potential causes, such as insect en-

venomation or drug reaction.

Although not a proven therapy, milk is thought to

dissolve the calcium oxalate crystals lining the oral

mucosa and reduce injury. Additionally, corticosteroids

and diphenhydramine may reduce the inflammation

and pain associated with inflammatory mediator

release.7

Respiratory distress requiring advanced life support

and death due to severe upper airway obstruction have

been reported in humans suffering Dieffenbachia toxicity.3

A single case of Dieffenbachia intoxication in a dog re-sulting in death from respiratory compromise has been

described. In that case, the dog was presented to a vet-

erinarian with extensive oral ulceration and erosions af-

ter a known exposure to Dieffenbachia species. Because of

the extent of the swelling and damage to the oropha-

ryngeal area, the veterinarian was unable to intubate the

dog. The owner requested that no other measures were

taken, the patient expired, and no necropsy was per-formed.2 The oral mucosal swelling in the case reported

here was significant enough to complicate intubation

and require maintenance of an upper airway bypass in

the form of a temporary tracheostomy for 4 days.

In addition to airway compromise, superficial corneal

ulcers caused by chemical irritation have been reported

in humans exposed to Dieffenbachia.11 The dog in this

case report developed central corneal ulcers that couldhave resulted from exposure keratitis related to

Dieffenbachia, or secondary to sedation and reduced

corneal lubrication.

Surgical removal of ingested Dieffenbachia has not

been previously reported. As in other cases of irritant or

corrosive ingestion, emesis would not be recommended

because of the potential for further damage to the

esophagus and oropharynx. In this case, the gastrotomywas intended for removal of ingested bedding material,

but provided a means for discovering the etiology of

the airway obstruction, as well as removal of the toxic

plant material that could have resulted in gastrointes-

tinal irritation.

Conclusion

Although the toxic effects of Dieffenbachia are usuallylimited, this case presented here had serious morbidity

and potential mortality associated with large-volume

ingestion. Veterinarians should consider Dieffenbachiaexposure as a possible etiology in cases that present

with hypersalivation and unexplained oropharyngeal

swelling. In addition, oropharyngeal swelling can lead

to airway obstruction requiring temporary tracheos-

tomy after toxic exposure to Dieffenbachia.

Footnotesa Plasmalyte 148, Baxter Healthcare Corp, Deerfield, IL.b Hydromorphone, Baxter Healthcare Corp.c Acepromazine, Vedco Inc, St Joseph, MO.

& Veterinary Emergency and Critical Care Society 2009, doi: 10.1111/j.1476-4431.2009.00486.x638

K. Peterson et al.

d Ketamine, Ketaset, Fort Dodge Animal Health, Fort Dodge, IA.e Midazolam, Hospira Inc, Lake Forest, IL.f Sevoflurane, Halocarbon Products Corp, River Edge, NJ.g Dexamethasone sodium phosphate, American Regent Inc, Shirley, NY.h Diphenhydramine, Baxter Healthcare Corp.i Hetastarch, Hextend, Abbott Laboratories, Abbott Park, IL.j Fentanyl, Hospira Inc.k Duragesic, Janssen Pharmaceuticals, Titusville, NJ.l Famotidine, Bedford Laboratories, Bedford, OH.m Sucralfate, Teva Pharmaceuticals, Sellersville, PA.n Cefazolin, Apotex Corp, Weston, FL.o Rebound, Virbac Corp, Fort Worth, TX.p Nolvadent, Fort Dodge Animal Health.q Propofol, Propoflo, Abbott Laboratories.r Fluorescein stain, Ful-Glo, Akorn Inc, Buffalo Grove, IL.s Gentamycin ophthalmic drops, Schering-Plough Corp, Kenilworth, NJ.t Cisapride, Janssen Pharmaceuticals.u Cephalexin, Westward Pharm, Eantown, NJ.v Tramadol, Amneal Pharmaceuticals, Paterson, NJ.

References

1. Pedaci L, Krenzelok E, Jacobsen TD, Aronis J. Dieffenbachia speciesexposures: an evidence based assessment of symptom presenta-tion. Vet Human Toxicol 1999; 41:335–338.

2. Loretti A, da Silva Ilha M, Ribeiro R. Accidental fatal opisoning ofa dog by Dieffenbachia picta (dumb cane). Vet Human Toxicol 2003;45(5):233–239.

3. Cumpston K, Vogel S, Leikin J, Erickson T. Acute airway com-promise after brief exposure to Dieffenbachia plant. J Emerg Med2003; 25(4):391–397.

4. McGovern T. Botanical briefs: dumb cane – Dieffenbachia picta.Cutis 2000; 66:333–334.

5. Gardner David. Injury to the oral mucous membranes caused bythe common houseplant Dieffenbachia. Oral Surg Oral Med OralPathol 1994; 78(5):631–633.

6. Scalzo AJ. Overview of plant and herbal toxicity, In: Brent J, Wal-lace K, Burkhart K, et al. eds. Critical Care Toxicology: Diagnosisand Management of the Critically Poisoned Patient. Philadelphia:Elsevier; 2005, pp. 1303–1305.

7. Ladeira A, Andrade S, Sawaya P. Studies on Dieffenbachia pictaSchott: toxic effect in guinea pigs. Toxicol Appl Pharmacol 1975;34(3):363–373.

8. Kuballa B, Lugnier A, Anton R. Study of Dieffenbachia-inducededema in mouse and rat hindpaws: respective role of oxalate nee-dles and tripsin-like proteases. Toxicol Appl Pharmacol 1981;58(3):444–451.

9. Mvros R, Dean B, Krenzelok E. Philodendron/Dieffenbachia inges-tions: are they a problem? J Toxicol Clin Toxicol 1991; 29(4):485–491.

10. Wiese M, Kruszewska S, Kolacinski Z. Acute poisoning withDieffenbachia picta. Vet Human Toxicol 1996; 38(5):356–358.

11. Hsueh K, Lin P, Lee S, Hsieh C. Ocular injuries from plant sap ofgenera, Euphorbia and Dieffenbachia. J Chin Med Assoc 2004;67(2):93–98.

& Veterinary Emergency and Critical Care Society 2009, doi: 10.1111/j.1476-4431.2009.00486.x 639

Airway obstruction in a dog after Dieffenbachia ingestion