Senior Report 7.10

Case Presentation by Dr. Jessica Ruffino, MD

CC: Headache

HPI: Patient is 14y/o female who presents to the emergency department with her mother with the above complaint.   Patient states that she has been having headaches intermittently for the past 3 weeks, however her headache has been getting much worse over the past 3 days. She states that the pain is located on the left side of her forehead and behind her left eye. Describes the pain as throbbing and constant. Associated with photophobia, as well as nausea but no vomiting. Does note some neck pain. She thinks she may have a fever but has not checked her temperature. She noticed left eye swelling over past day, but today she can’t open her left eye. Denies any blurry vision or double vision, no discharge from eye. She states that she has been to several other emergency departments over past few weeks regarding her headache and was told she has migraines. She has tried taking ibuprofen with little relief. She states she has had a cold recently with nasal congestion. She denies any trauma, does not wear contacts and usually does not have headaches.

Constitutional: Subjective fever
Eyes: Left eye swelling
Ears, Nose, Mouth, Throat: Nasal congestion
Musculoskeletal: Denies joint pain
Skin: Denies rash
Neurological: Headache

PMH: Asthma, no history of migraines

PSH: None

Immunizations: Up-to-date

Allergies: None

Medications: Albuterol

Social History: Denies alcohol, tobacco, or drug use. 8th grade student.

Physical Exam:
General: Patient is alert and oriented x 3. Laying on stretcher with lights off in room. Uncomfortable but she is cooperative.
Vital signs: Blood pressure 95/40, pulse 115, respiratory rate 16, temperature 39.2, pulse ox 99% on room air
Eyes: There is erythema, edema of left eyelid and periorbital edema of the left eye. Left eye proptosis present. Chemosis of left sclera. Pupils equal, round, and reactive to light.   Extraocular movements appear to be intact, however exam somewhat limited secondary to edema of left eye. There is pain with movement of left eye. Vision 20/20 bilaterally. Photophobia noted bilaterally.
Ears, Nose, Throat: Tympanic membranes are not red or bulging. No rhinorrhea. No erythema or exudates, no sinus tenderness, oral exam wnl
Neck: Supple, nontender, no meningismus
Cardiovascular: Tachycardic. Regular rhythm, S1 and S2 with no murmurs, gallops or rubs
Neurologic: Alert and oriented times 3. Cranial nerves II-XII appear to be intact, again with some limitation of assessing extraocular movements of left eye secondary to edema. Strength 5/5 bilateral upper and lower extremities.   Sensation to light touch intact throughout. No dysmetria or dysdiadochokinesia.









  1. Which of the following physical exam findings are indicative of orbital cellulitis, compared to preseptal cellulitis
    b) Proptosis
    d) All of the above
  2. Which of the following is seen in preseptal cellulitis?
    a) Subperiosteal abscess
    b) Vision loss
    c) Cavernous sinus thrombosis
    d) Periorbital edema and erythema
  3. What is the best choice for initial antibiotic regimen in treating orbital cellulitis?
    a) Vancomycin and Ampicillin-sulbactam
    b) Vancomycin and metronidazole
    c) Ceftriaxone
    d) Augmentin

    Answers & Discussion:

    1) D
    2) D
    3) A

    Orbital Cellulitis
    Orbital cellulitis is an infection involving the contents of the orbit including fat and ocular muscles. Preseptal cellulitis or periorbital cellulitis is infection of the anterior portion of the eyelid. Neither involves the globe itself.

    Sometimes preseptal and orbital cellulitis are difficult to distinguish clinically because both can cause ocular pain and eyelid swelling and erythema. It is important to distinguish the two as they have very different clinical implications. Preseptal cellulitis rarely leads to serious complications, whereas orbital cellulitis may cause vision loss and even death. Distinguishing clinical features of orbital cellulitis include ophthalmoplegia, pain with eye movements, and proptosis. Also diagnosed by imaging studies (CT and possibly MRI). If unsure if a patient has orbital versus preseptal cellulitis, treat the patient as if they have orbital cellulitis.   This would mean that this patient would need to be admitted for IV antibiotics. It is extremely important to carefully examine the patient for pain with eye movement. CT scan with contrast is used to make diagnosis. Axial views should include low, narrow cuts of the frontal lobes to rule out peridural and parenchymal brain abscess formation. Coronal views are helpful in determining the presence and extent of any subperiorbital abscesses. MRI may be helpful in defining orbital abscesses and in evaluating the possibility of cavernous sinus disease.

    Preseptal cellulitis is much more common than orbital cellulits. Both conditions are more common in children than in adults.

    Most common cause of orbital cellulitis is rhinosinusitis, with ethmoid and pansinusitis being most common locations. Ethmoid sinuses are separated from the orbit by the lamina papyracea, a thin structure with many fenestrations. Computed tomography (CT) scanning often shows the predominant site of inflammation to be the medial aspect of the orbit, adjacent to the ethmoid sinuses, and subperiosteal abscesses most often occur in the same. Other potential causes include ophthalmic surgery, orbital trauma with fracture or foreign body, dacryocystitis, infection of the teeth, middle ear, or face, infected mucocele that erodes into the orbit.

    1. D—all of the above

    Both orbital cellulitis and preseptal cellulitis cause ocular pain and eyelid swelling with erythema. In some cases of orbital cellulitis, eyelid erythema is absent. Only orbital cellulitis causes swelling and inflammation of the extraocular muscles and fatty tissues within the orbit, leading to pain with eye movements, proptosis, and ophthalmoplegia with diplopia. Chemosis may occasionally occur in severe cases of preseptal cellulitis, but is more common with orbital cellulitis.

    Clinical features of preseptal and orbital cellulitis

    Clinical Feature Preseptal Cellulitis Orbital Cellulitis
    Eyelid swelling with or without erythema Yes Yes
    Eye pain/tenderness May be present Yes; may cause deep eye pain
    Pain with eye movements No Yes
    Proptosis No Usually, but may be subtle
    Ophthalmoplegia +/- diplopia No Yes
    Vision impairment No May be present
    Chemosis Rarely present May be present
    Fever May be present Usually present
    Leukocytosis May be present May be present


    1. D— Periorbital edema and erythema

    Preseptal cellulits and orbital cellulitis can both have periorbital edema and erythema but the other items mentioned are complications seen with orbital cellulitis and not preseptal cellulitis.

    The most common complications of orbital cellulitis are subperiosteal abscess and orbital abscess. Subperiosteal abscess occurs in 15 to 59 percent of cases in various retrospective series. Marked displacement of globe is suggestive of abscess. CT scan of orbits and sinuses, or surgery are necessary to make the diagnosis. Orbital abscesses have been reported in up to 24% of cases of orbital cellulitis. More severe proptosis, opthalmoplegia and pain with eye movements are seen with orbital abscess.

    Vision loss occurs in 3-11% of patients with orbital cellulitis. Vision loss thought to occur from several processes including optic neuritis (resulting from inflammation from nearby infection), ischemia (resulting from thrombophlebitis along orbital veins), pressure resulting in central retinal artery occlusion.

    Cavernous sinus thrombosis can occur but is a rare complication. Severe headache, intractable vomiting, mental status changes, cranial nerve palsies may be seen. Bilateral cranial nerve palsies can be a sign of bilateral cavernous sinus thrombosis.

    1. A—Vancomycin and ampicillin-sulbactam

    Most commonly identified pathogens in orbital cellulitis are streptococci followed by staph aureus. Less common causes of orbital cellulitis include Haemophilus influenzae and nonspore-forming anaerobes, Aeromonas hydrophila, Pseudomonas aeruginosa and Eikenella corrodens . Some cases are polymicrobial with combination of aerobic and anaerobic bacteria. Less common causes include fungi, especially Mucorales (mucormycosis) and Aspergillus. Consider in immunocompromised patients—mucormycosis in diabetics, aspergillus with severe neutropenia or HIV, including HIV infection.

    Antibiotic treatment includes parenterally administered broad-spectrum regimen targeted at S. aureus (including MRSA), S. pneumoniae and other streptococci, and gram-negative bacilli. When intracranial extension is suspected, the regimen should also include coverage for anaerobes. Regimens include combination of:

    Vancomycin plus one of the following:

    • Ceftriaxone or
    • Cefotaxime or
    • Ampicillin-sulbactam or
    • Piperacillin-tazobactam

    If concerned for intracranial extension, add metronidazole to cover anaerobes if using ceftriaxone or cefotaxime.

    Consult ophthalmology and ENT early—these patient require frequent and repeat physical examination with ophthalmologic and/or otolaryngologic expertise and surgery is sometimes required.



    Distinguishing clinical features of orbital cellulitis include ophthalmoplegia, pain with eye movements, and proptosis.

    When diagnosis between preseptal and orbital cellulitis uncertain, obtain CT scan with contrast to make diagnosis.



    Gappy, et al. Orbital Cellulitis. Feb 4 2014. Up to Date.

    Rosen’s Emergency Medicine, 7th Edition.

Senior Report 7.9

Case Presentation by Dr. Adam Bartsoff, MD

CHIEF COMPLAINT: “My eye fell out”

HISTORY OF PRESENT ILLNESS: This is a 25 year old African American female who presents to the emergency department stating that her right eye “fell out.” The patient states that she woke up in the early morning with a sensation that there was something in her right eye. When she attempted to wipe her eye she noticed that it was displaced slightly anterior and inferior and required to be “popped back in” with the palm of her hand. The event was non painful. The patient had some minor visual changes that she describes as blurry vision initially secondary to a glossy eye and eye watering which has since resolved. She denies any history of regular visual disturbances or eye pain. This has happened to the patient once before when she was 19. Also when the patient sneezes she always feels as though her eye is going to fall out. She has never seen an ophthalmologist regarding this. She denies any history of remote trauma to the right eye, pain with EOM, bleeding from the right eye or chronic headache.

HEENT:  Positive for: brief blurry vision, brief watery right eye
Negative for: eye trauma, eye pain, bleeding eye, double vision, recent sinus infection
NEURO:  Negative for regular headache, gait disturbances
CARDIOVASCULAR:  Negative for tachycardia, palpitations
ENDOCRINE:  Negative for heat or cold intolerance

PMH: borderline hypertension. Not up to date on tetanus immunization.
SOCIAL HISTORY: Occasional alcohol use socially. Denies tobacco or drug use.


VITALS: TEMP: 37.9 c. HR: 85 bpm. RR: 12. BP: 120/80 mmHg. SpO2: 100% RA.
GENERAL: Sitting in chair in no acute distress.
HEENT: PERRLA, EOMI. No nystagmus. Slight right eye proptosis, no left eye proptosis. No hyphema. No eye discharge or bleeding. No lid lag. No Papilledema. Mild right eye conjunctival erythema. Fluorescein stain of the right eye reveals small corneal abrasion at the 7:00 o’clock position. Negative Seidel’s Sign. Slit lamp examination of the right eye reveals: No foreign body, No cell and flare, quiet anterior chamber, No corneal ulceration.

Visual Acuity: 20/30 bilaterally.

MSK: No pain to palpation of the orbit. No gross deformity of the facial bones.

NEURO: Non ataxic gait. No pronator drift. Negative Romberg. No dysdiadochokinesia. Symmetrical face. Tongue protrudes midline. Equal shoulder shrug. Strength in the upper and lower extremities equal and symmetrical rated 5/5. Sensation intact and symmetrical to light touch across the face and the upper and lower extremities.


More than one answer may be correct.

1.   After a complete eye exam as documented above, what is your next step?
a) Discharge the patient with close follow up with ophthalmology .
b) Patch the right eye until follow up to prevent spontaneous globe luxation.
c) Tdap, erythromycin, ophthalmic ointment, lacri-lube, close ophthalmology follow up, discharge.
d) Consult ophthalmology.

2. When should you consult ophthalmology?
a) Always
b) With bilateral globe luxation
c) With significant visual acuity differences
d) If you cannot reduce the subluxed globe

3.  What are risk factors for spontaneous globe subluxation?
a) Trauma
b) Graves Disease
c) Eye lid manipulation
d) Space occupying lesion
e) Hyperopia

4.  The majority of globe subluxation cases are:
a) Spontaneous
b) Traumatic
c) Voluntary
d) Secondary to space occupying lesion




Discussion: Globe Subluxation

The first case of spontaneous globe subluxation was reported in 1907. Fewer than 50 cases have been reported.

Globe subluxation can vary in presentation from asymptomatic to blindness. The most common cause of globe subluxation is spontaneous subluxation which usually occurs secondary to lid manipulation.

Spontaneous globe subluxation is a rare orbital complication when the equator of the globe protrudes past the retracted lid. The mechanism of spontaneous globe subluxation is simple. Manipulation of the eye lid causes pressure to increases behind the globe. When the globe advances the cornea becomes dry. This induces the blink reflex and causes contraction of the orbicularis oculi. This limits extraocular movements and prevents globe reduction. Patients who attempt to reduce the spontaneous subluxed globe may cause a corneal abrasion. Other causes of spontaneous globe subluxation include extremes of gaze and valsalva maneuvers. Case reports exist of individuals experiencing globe subluxation when attempting to insert contact lenses because this requires lid retraction and an upward gaze.

Risk Factors:
There are many common risk factors for globe subluxation. The most common risk factor is exophthalmia. Individuals with exophthalmia usually have space occupying retrobulbar lesions, shallow orbits or both. Graves disease is the most common cause of a retrobulbar space occupying lesion secondary to inflammatory cell infiltration of extraocular muscles. The volume of the intraorbital contents increase but the orbital space remains limited. This causes the globe to protrude and the lids to retract. Pathologic processes such as cerebral granulomas, orbital tumors or arteriovenous malformations can also cause proptosis. Congenital processes such as abnormally enlarged globes or brachycephaly are also potential causes for spontaneous globe subluxation.. Myopia has also been shown to be an independent risk factor for spontaneous globe subluxation

Early Reduction is Key:
Early reduction is most important with globe subluxation and is key to preventing visual loss because globe subluxation produces traction on the optic nerve and vasculature. Before reduction a brief , full eye examination should be performed and visual acuity documented. Topical ocular anesthetic agents such as 0.5% proparacaine should also be used before manipulation of the globe.

A facial nerve block can be used to relax the of orbicularis oculi muscle and has been described in the literature. Rarely conscious sedation as required but may be necessary in mentally handicapped individuals or children.

Reduction of the Subluxed Globe:
Tse DT. A Simple Maneuver to Reposit a Subluxed Globe. Arch Ophthalmol. 2000;118(3):410-411.

While the patient is maintaining a constant downward gaze posture, the upper eyelid skin is pulled upward with the fingers of one hand and the globe is simultaneously depressed with the index finger of the other hand. The importance of contacting only the scleral surface is emphasized to the patient. This maneuver permits the retracted upper eyelid to ascend the posterior scleral surface and to arch over the equator. Ask the patient then to look upward and the superior rectus action will rotate the globe under the distracted upper eyelid. This maneuver usually will reposition the globe behind the eyelids.

Bartsoff 2j

Follow up:
A patient with a subluxed global which is been reduced can safely follow up with ophthalmology in 24 hours if they have not acute visual changes associated with the subluxation. Prior to discharge, patients should be educated in the potential triggers for recurrent subluxation. They should be referred to their primary care doctor to investigate for underlying predisposing conditions such as thyroid disease or other infiltrative conditions of the orbit. The patient should also be instructed on proper repositioning techniques such as the one described. Rarely surgical interventions are indicated.



Talke. Globe Subluxation: Review and Management; 2007
Kelly EWFitch MT.

Recurrent spontaneous globe subluxation: a case report and review of manual reduction techniques; J Emerg Med. 2013 Jan;44(1):e17-20.

Senior Report 7.8

Case Presentation by Dr. Craig Sharkey, MD

HPI: 43 year old male brought in by EMS for altered mental status. History provided by EMS: Patient was at home, drinking alcohol. He was found by family at the bottom of the stoop. Family notes that although he was drinking, he did not appear intoxicated. He had been at his normal state of health prior to the incident. No further history can be obtained; family is on their way via private vehicle.

ROS: Unable to assess

PMHx: Unknown, per EMR: none
PSHx: Per EMR: none
Allergy: NKDA
Meds: unknown
Family History: Uncle died in 30s from heart attack
Social: + Alcohol

Physical Exam:
VS: T 36.5 BP 141/90 P 80 RR 18 SpO2 99% on 15 lpm via nonrebreather mask
General: Patient minimally responsive. Not warm to touch, nondiaphoretic. Gag intact, has spontaneous respirations.
Head: NCAT, no obvious external hematoma or abrasion
ENT: dried blood at nares, trachea midline, no JVD
Eyes: Pupils mid range, responsive to light, extraoccular movements unable to be assessed
CV: Regular rate and rhythm. No murmur/rub/gallop appreciated. 2+ radial and DP pulses appreciated.
Pulm: Clear to auscultation bilaterally. No wheeze/rhonchi/rales
GI: soft, nontender, nondistended. Bowel sounds appreciated.
MSK: No deformity
Neuro: Initial GCS 3. During initial exam, patient becomes arousable. He is able to say his name, but does not know the day/year/location. He would obey commands to move arms and legs, no gross focal deficit.



Chem 7: 140/3.7/102/28/13/1.3/8.7

CBC: 7/13.1/193


EtOH: 235

UDS: Neg



CT head/c-spine: Negative

On review of EMR, his last presentation was 9 years prior

ECG 2004



1) On repeat exam, he is still normotensive, no tachycardia. He has no current complaints of chest pain, dyspnea, dizziness, palpations, nausea. Given the patient’s presentation what is the most appropriate disposition:
a) Activate cardiac cath lab for suspected acute myocardial infarction, given his EKG changes.
b) Trend troponin, place in CDU for chest pain rule out and provocative testing for suspected underlying coronary artery disease.
c) Place in TCU pending sobriety and trend troponin.
d) Admit to cardiology on telemetry for sudden death prevention

2) While in the emergency department, he becomes unresponsive and the monitor is alarming. He is pulseless and the monitor is displaying a wide complex tachycardia. Your next action is:
a) defibrillation followed by 1.5 mg/kg lidocaine for V-tach prophylaxis
b) synchronized cardioversion followed by 1.5 mg/kg lidocaine for V-tach prophylaxis
c) synchronized cardioversion, admit patient for AICD placement
d) synchronized cardioversion, admit to MICU with toxicology consult

3) The pathology underlying his presentation is likely:
a) alcohol abuse, dehydration and electrolyte abnormality
b) membrane ion channel dysfunction
c) luminal defects in the coronary arterial circulation
d) undisclosed polysubstance abuse with adulterant

Answers & Discussion

1) D: This patient presented with syncope and an EKG that is typical of Brugada Syndrome.   He underwent cardiac catheterization that was normal. Electrophysiology was involved later in the course and placed an AICD in the patient. While it is common for these patients to undergo cardiac catheterization, he ultimately needs sudden cardiac death prophylaxis.

2) C: The patient requires electrical intervention for his decompensation; defibrillation or cardioversion would be effective. He should not receive any sodium channel blockade as this will possibly exacerbate the underlying brugada pathology. Lidocaine and procainamide in particular are used in the EP lab as a provocative drug challenge to assess for Brugada syndrome. Brugada syndrome can be unmasked with a variety of events such as fever, alcohol, cocaine, or other medications. The EKG can change markedly depending on these factors.

3) B: Brugada syndrome is typically thought to be due to an autosomal dominant mutation in the SCN5A sodium channel gene. This is found in 18-30% of families with Brugada syndrome. Other sodium and calcium channel genes have been implicated as the causative factor in SCN5A negative patients. This patient and his first degree relatives were tested for this genetic mutation.


Brugada syndrome: See figure 1 for diagnostic criteria.

Senior Report 7.7

Case Presentation by Dr. Adnan Sabic, MD

CC: I don’t feel well

HPI: Fifty seven year old female presents complaining of not feeling well since this morning. Patient complains of feeling dizzy, however denies feeling lightheaded. Patient denies passing out. She denies any chest pain, shortness of breath, nausea or vomiting. She does report few episodes of watery diarrhea early this morning. She does not have any other complaints.

PMH: HTN, HLD and ESRD on HD and was dialyzed 2 days ago and is due tomorrow

Vital signs: BP 70/36, HR 32, RR 13, Temp 36.7, Pulse Ox 96% on room air
General: Patient is laying in bed, eyes closed, however easily arousable and answering questions appropriately
Eyes: PERRL, no conjunctival pallor
Neck: No JVD
Cardiac: Bradycardic, no murmurs appreciated
Respiratory: LCTAB
GI: Abdomen is soft, NT/ND
Msk: Fistula present in left upper extremity. No overlying redness.
Skin: Warm and dry
Neurological: Awake and moving all extremities spontaneously. No facial droop. Pupils are equal, round and reactive to light. Strength is 5/5 in upper and lower extremities bilaterally.


Following ECG was obtained:



  1. Based on this patient’s presentation, what is the most likely to be her primary disorder?
    1. Hypocalcemia
    2. Hyperkalemia
    3. Hypemagnesemia
    4. Hypokalemia
  1. What is the best initial treatment for this patient?
    1. Calcium Gluconate 1 gm IVP
    2. NaHCO3 1 AMP IVP
    3. Atropine 0.5 mg IVP
    4. Albuterol 5 mg nebulized treatment
  1. What is the onset and duration of action of the drug that was administered in question 2?
    1. 1-5 minutes and lasts for 60 minutes
    2. 10-50 minutes and lasts for 6 hours
    3. 1 hour and lasts for 16 hours
    4. 2 hours and lasts for 24 hours


Answers & Discussion:

1)    2
2)    1
3)    1

Hyperkalemia is a very common presentation seen in the emergency departments across the country. Vast majority of the presentations are benign and most of the patients have no complications from it. However, hyperkalemia can be very serious and it can lead to death.

Hyperkalemia is defined as potassium greater than 5.5 mEq/L. Hyperkalemia is especially important in patients who are dialysis dependent. Usually ESRD patients are able to tolerate higher levels of potassium, however in patients who receive dialysis regularly, even potassium of 6.0 mEq/L can lead to severe presentations.

Most patients with hyperkalemia will be asymptomatic, however patients can present with generalized malaise, shortness of breath and in cardiac arrest. It is critical for ED physician to consider hyperkalemia in cardiac arrest in ESRD patients. In ESRD patients, it is imperative to obtain an ECG in any patient who presents with weakness, feeling short of breath, syncope or any other presentation that can be caused by hyperkalemia.

ECG changes associated with hyperkalemia have sequential progression. Patients with serum potassium levels of 5.5-6.5 mEq/L will usually have peaked tall T waves and shortened QT interval and possibly ST segment depression. Serum potassium level of 6.5-8.0 mEq/L will present with prolonged PR interval, decreased or disappearing P waves and widening of QRS. Levels higher than 8.0 mEq/L will have progressive QRS widening, bradycardia and absent P waves, which will lead to sine wave and eventuall ventricular fibrillation or asystole.

Patients who present with symptomatic hyperkalemia, should be evaluated in the resuscitation bay. IV access should be established as soon possible and patient should be placed on continuous cardiac monitoring. An ECG should be immediately obtained. If the ECG shows signs of hyperkalemia then treatment should be initiated immediately.

  • The first IV therapy should be calcium. Hyperkalemia causes irritation of cardiac membranes and this should be immediately treated with calcium gluconate or calcium chloride. Calcium gluconate can be administered thru the peripheral line. Calcium chloride should be administered thru central line. At least 1 gm of calcium gluconate or chrloride should be administered. Because of the short duration of action, definitive treatment should be initiated as soon as possible.
  • Insulin can be administered as well, which promotes intracellular movement of potassium. Five to 10 units of regular insulin should be administered.
  • Glucose should be supplemented too if the patient is euglycemic with D50.Frequent glucose checks should be ordered since insulin is metabolized by kidneys and in ESRD patients this can cause prolonged half life which can cause hypoglycemia.
  • Albuterol is an adjunctive treatment. It can be started while IV access is being established or during the process of obtaining the IV. Albuterol nebulized treatment, 5-10 mg. Albuterol shifts potassium into the cells which can last up to 2 hours.


Hemodialysis is the definitive treatment for hyperkalemia and it should be initiated as soon as possible. Kayexalate can be administered as well, however according to some of the latest nephrology research, it should be the last resort. One of the most severe side effects of Kayexalate is gastrointestinal tract ulceration and/or necrosis which can lead to perforation and further complications.

Even though hyperkalemia is benign most of the time, ED physicians should be vigilant and on the lookout for it in ESRD patients. When symptomatic, aggressive measure should be taken and nephrology should be consulted immediately.

Tox Time… Consult of the Week (COW)

Aimee Nefcy, MD
Fellow-in-training, Detroit PCC


The Bitter Truth

A 2 year old male was brought to the ER by family for decreased responsiveness. According to them, he was visiting Grandma’s house and had been seen in the back yard eating some red berries, a sample of which they have brought to the ER. He vomited once at home and then became rapidly lethargic. In the ER, he was initially unresponsive, then vomited twice and became agitated. He was bradycardic to 56 bpm and had a BP of 64/31. He was given atropine with improved vitals (117, 136/96). He was sedated, paralyzed, and intubated. Laboratory values were all within normal limits. In the ICU his BP was 90/45, HR 100. He was extubated after less than 12 hours. After extubation he had normal vital signs, but he remained drowsy yet agitated and confused. He had another episode of emesis, then improved. A photo of the plant was sent by the ER doc to the Toxicologist on call, and is shown here.



1)    Ingestion of what type of plant should you worry about with a bradycardic, hypotensive, vomiting patient?

2)    What lab test available to the ER could be potentially helpful in diagnosing this?

3)    What tests are needed to determine the need for administration of a potential antidote?

4)    What is the plant shown here?



1)    Digitalis-like plants, which commonly contain cardioactive steroids. The toxidrome for this extremely varied class of plants is identical for all: GI upset followed by bradycardia and cardiac dysrhythmias leading to cardiac arrest. Not all CAS’s are equipotent, however; eg, Convallaria majalis, Lily-of-the-valley, is relatively benign compared to Nerium oleander. Another consideration might be toxicity from organophosphate pesticides applied topically to the ingested plant, but sludge symptoms should be very prominent on exam.

2)    CAS’s in non-dig plants have some cross-reactivity with the digoxin assay, although the lab level does not correlate to the serum levels of the non-dig-CAS ingested. Children should have negative dig levels, and a detectable dig level is considered diagnostic of ingestion of a CAS.

3)    Additional labs needed to judge the severity of CAS toxicity include a potassium level (K>5 50% mortality, K>5.5 100% mortality without DSFab) and an EKG to evaluate for arrhythmias. Any of these, with or without symptomatic bradycardia, should prompt treatment with DSFab. DSFab has a limited ability to bind non-dig-CAS, therefore much larger doses are needed to treat a suspicious plant ingestion. Typically, 20-30 vials are needed depending on the severity of toxicity (compared to chronic digoxin needing 1-4 vials, and acute digoxin needing <10). Any CAS plant ingestion without GI symptoms, hyperkalemia, or EKG changes after 6hrs of observation in the ED can be cleared medically.

4)    Solanum dulcamara, known as woody or climbing nightshade, or bittersweet. This is a very common plant in Michigan, and is seen ubiquitously. The berries look and smell like little tomatoes and are seen in late summer to autumn. Solanine is the primary toxin, which has been shown in vitro to have acetylcholinesterase inhibition; there have been no reports of cholinergic toxicity, however. The primary toxicity is GI upset without CNS effects. The parts of the plant that are toxic are the leaves, fruits, stems, and shoots. This is in contrast to deadly nightshade, Atropa belladonna, which causes an antimuscarinic toxidrome.

Outcome: His symptoms were not felt to be consistent with this plant, which primarily causes GI upset. His dig level was negative. This patient’s sister had a history of being on carbamazepine, and he had detectable levels in his serum (thus depriving Aimee of her first-ever solanine-toxicity-causing-cholinergic-symptoms case report – so disappointed!). Within 24hrs of presentation he was back to baseline and was discharged with no permanent sequelae.

Recall that carbamazepine is a tricyclic anticonvulsant, and like other TCAs it tends to cause an antimuscarinic toxidrome with additional sodium-channel blockade. It is not clear why this patient was so bradycardic on presentation; possible confounders include coingestions, or maybe hypoxia from a seizure or aspiration.