Senior Report 6.27

Case Presentation by Dr. Jeff Cloyd

CHIEF COMPLAINT: “My right eye hurts”


53-year-old female presents to the ARC complaining of pain in her right eye over last 24 hours.  She began to notice some redness in the right eye during the day yesterday, but as the evening wore on last night she noticed a sharp pain in her right eye and worsening redness.  She has not noticed any clear or purulent discharge from the eye.  She states she has always had some sinus congestion providing a sensation of pressure behind both eyes, but this feels no worse today.  She states the pain seems to be worse when she looks into bright lights, and gets better when she goes into dark places.  She is not noticing pain when moving her eyes.  She does report that she has had some decreased vision in the right eye when compared with the left.  She never had anything like this before and denies trauma to this eye.  She has not had any medications for her eye pain.


Constitutional: No fevers, chills, sweating, or hot flashes

Eyes: Eye pain with decreased vision

ENT: No rhinorrhea, sore throat

CV: No palpitations

Respiratory: No cough

GI: No nausea, vomiting, diarrhea



PMH: Negative for glaucoma, rheumatoid arthritis, or sarcoidosis

PSH: None

Medications: None

Allergies: None

FH: Negative for glaucoma, rheumatoid arthritis, or sarcoidosis

SH: Pt lives at home. Pt denies tobacco and illicit drug use. Pt denies alcohol use.


VS: Heart rate 84, blood pressure 140/78, respiratory rate 18, temperature 36.3 orally

Constitutional: Well-developed, well-nourished, patient is alert and oriented x3.  She is seen moving her head comfortably in all directions, cooperative and interactive on exam.

Eyes: Extra-ocular movements are intact in all directions without pain. Pupils are equal at 3 mm, and reactive to light.  Bilateral pupils are symmetric.  Patient has erythema of the conjunctiva of the right eye worse immediately adjacent to the iris and improving distally.  When light is shined in the right eye the patient experiences pain in the same; when light is shined in the left eye, she reports pain in the right eye.  She has no pain relief with proparacaine instillation.  Pressures in the bilateral eyes averaged 14 mmHg.  No fluorescein uptake is appreciated in bilateral corneas.  Slit-lamp examination reveals no cell or flare in the anterior chamber of the bilateral eyes.  Visual acuity is 20/50 in the affected eye and 20/25 in the unaffected eye. No swelling of the soft tissues appreciated peri-orbitally bilaterally.

Nose: No rhinorrhea, mucous membranes are pink and moist. No mucosal edema

Mouth: No erythema or exudates in the posterior pharynx, tonsillar lymph nodes are not enlarged.

Neck: Supple, no meningismus, no anterior cervical lymphadenopathy.

Skin: No rash, no diaphoresis.

Neurological: No facial asymmetry/droop. Patient is able to shake hands with expected strength and is moving all of her extremities spontaneously. Sensation is appreciated as normal in all extremities. No aphasia or dysarthria, tongue protrudes midline. Normal gait.

Question #1: What is the most appropriate treatment for this patient’s diagnosis?

a) Oral Cefalexin

b) Timolol drops

c) Warm compresses

d) Intravenous Ampicillin-sulbactam

e) Homatropine drops

f) Bacitracin ophthalmic ointment

g) Prednisolone acetate ophthalmic suspension

Question #2:  Iritis, unlike acute angle-closure glaucoma, is not an immediately vision-threatening disease.  However, these patients do require rapid Ophthalmology follow-up (ideally within 24 hours).  This patient was seen late in the evening in the ARC, but an appointment was made for the patient the following morning at the Ophthalmology clinic.  Which investigative study might be considered prior to this patient’s discharge?

a) CBC

b) Electrolytes

c) HLA-B27

d) RPR

e) Chest xray

Question #3:  During your next shift in the ARC one week later this patient presents with a chief complaint of “foreign body in left eye”.  She reports that her right eye symptoms have almost completely resolved.  However, she reports that she has been keeping her eye drops in her desk drawer…. the same drawer in which she also keeps her super glue.  One hour prior to arrival she placed three or four drops of what she thought was Pred-forte into her left eye but immediately noticed that her eyelids were sticking together.  After realizing her mistake she attempted to flush her eyes with water but presents now for evaluation.

On exam you remove some pieces of hardened glue from the conjunctiva.  The palpebral conjunctiva appears to be adhered to the sclera in the upper, outer quadrant and fluoroscein staining reveals a generalized uptake over the entire surface of the cornea.  In addition to removing any large pieces and flushing the patient’s eye with water, which medication will you provide this patient?

a) Homatropine

b) Erythromycin ophthalmic

c) Glucagon

d) Normal saline ophthalmic

e) Reading glasses


Answers & Discussion

1)  Answer: E

This patient is presenting to the ARC with a classic non-traumatic iritis (aka anterior uveitis).  Classic physical examination findings in iritis include

Erythema of the eye secondary to dilated ciliary vessels (shown below)

Blurred vision

Photophobia, worsening eye pain with pupillary constriction

Cell and flare in the anterior chamber

Irregular or asymmetric pupil (shown below)

Keratic precipitates on the posterior surface of the cornea.



Iritis can be classically differentiated from conjunctivitis with erythema immediately adjacent to the iris which improves distally, while conjunctivitis classically shows distal erythema with perilimbic sparing (shown below).


Patients with acute angle-closure glaucoma experience worsening pain with pupillary dilation secondary to blockage of the trabecular network draining into the canal of Schlemm – this is the cause for worsened pain when walking into a dark room.  Inflammation of the ciliary muscles causes pain with constriction and worsened pain with light exposure.  The consensual light reflex causes pain in the affected eye even when light is shined in the opposite pupil (as was noted in this patient).  More severe inflammation can result in a “frozen” pupil that does not constrict with light (causing photophobia), or an asymmetrical pupillary constriction (see below).


Also noted in this image is an hypopion, a late finding appreciated in patients with iritis.

The most appropriate medication for treatment of this patient’s iritis is homatropine.  Homatropine is a muscarinic antagonist used as a cycloplegic to temporarily paralyze accommodation and thereby eliminating pain.  Patients are encouraged to instill one drop in the affected eye four times daily.  However, note that homatropine is used for symptomatic treatment.  Iritis is also typically treated with Pred-forte (Prednisolone eye drops) to limit inflammation, but patients should typically be evaluated by an Ophthalmologist prior to initiation of this treatment and delay 12 – 24 hours has not been shown to affect the outcome of the disease.  This patient has no evidence of pre-septal or orbital cellulitis and there is no utility in initiating oral or intravenous antibiotic therapy.  Beta-blocker medications are used in the treatment of glaucoma, and will likely worsen a patient with iritis.  Compresses and topical antibiotics are the mainstay of conjunctivitis but have not shown utility in the treatment of iritis.

2) Answer:  D

Although most cases of iritis are idiopathic and presumed to be secondary to a viral infection, there are a number of less common causes that should at least be considered in patients presenting to the Emergency Department with iritis.  These include all of the auto-immune diseases (ankylosing spondylitis, multiple sclerosis, inflammatory bowel disease, sarcoidosis).  HLA-B27 is associated with ankylosing spondylitis and a chest x-ray may be used to evaluate for sarcoidosis, but neither of these studies must be performed in the ED.  There is no utility in a CBC or electrolytes in this case.  However, iritis may be an early manifestation of secondary syphilis or a reactive arthritis such as Reiter’s syndrome.  As these diseases pose significant risks to patients and the population at large, the patient’s physical examination and social history may prompt a physician to obtain an RPR (and DNA probes for Gonorrhea and Chlamydia).

3) Answer :  B

Patient’s very commonly present to the ED with foreign bodies in the eye.  Following a thorough history and physical examination, effort should be made to remove the foreign body and fluoroscein staining should be performed to ensure no corneal damage (in this case, the fluoroscein uptake across the entire cornea is likely secondary to a fine coating of super glue, rather than corneal injury).  Symptomatic treatment and follow-up with an Ophthalmologist is typically appropriate.  However, there is some anecdotal evidence that erythromycin ointment (not drops) facilitate rapid degradation of super glue and should be provided to these patients at discharge.

Patients should also be encouraged to keep their super glue in a separate location.

Senior Report 6.26

Case Presentation by Dr. Justin Kessler

CC:”I tried to kill myself”

HPI:Patient is a 26-year-old male history of depression and recently diagnosed bipolar disorder.  The patient states he tried to kill himself with “300 unknown pills.” The patient states he took 30 in each mouthful until they were all gone. The patient is having nausea and has vomited.  The patient is highly agitated he states he is feeling warm and dehydrated. Patient states his heart is beating real fast.  His mother is en route behind EMS and she states she found 6 empty bottles of No doze 200mg maximum strength caffeine pills behind the patient’s house. The bottles contents included 50 Tabs each.

ROS: Constitutional Positive fever

Cardio: Positive palpitations, Positive CP

Respiratory: Positive SOB

Gastrointestinal: Positive N+V Denies BPR

Musculoskeletal: Positive Weakness

Neuro: Positive Headache

Immune: Denies immune deficiency

Psych : Positive previous suicide attempt, Positive Bipolar

PMH: Previous hernia, recently diagnosed bipolar disorder and depression

PSH: Hernia repair

Medications: Atarax Klonopin Trileptal Zoloft Requip

Allergies: No Known

FH: unknown to patient

SH: Patient lives with his grandparents he denies alcohol or illicit drug use


VS:Vitals: BP 162/65 heart rate 129 respiratory rate 36 temperature 36.0 pulse ox 100% room air, Weight 168kG

Consitutional/Psychiatric:The patient was awake, sitting upright actively vomiting.  He was highly agitated and vomiting. Patient was morbidly obese BMI 51.7.

Head,Eyes, Ears, Nose, Mouth and Throat:

HEAD: Normocephalic, atraumatic

EYES: The pupils are equal, round, 6mm reactive to light, no scleral icterus, no conjunctival pallor

Mouth: Mucous membranes were dry

Respiratory and Lungs: chest rise symmetrical, clear to auscultation, bilaterally, no wheezes, no rales, no ronchi,

Cardiovascular and Heart: S1-S2 present the patient was tachycardic he did have a palpable heave as well as systolic murmurs the patient had a slight gallop

Chest: Symmetrical,  heart can be seen bounding through chest wall.

Gastrointestinal and Abdomen: Abdomen was non-distended, non-tender to palpation. There was normal active bowel sounds to auscultation patient does have a surgical scar from previous hernia repair normal bowel sounds

Musculoskeletal and Extremities: Hands, fingers and nails were free of deformity, or lesions. There was no tenderness and no edema.  Strength 5/5 upper ext to bicept &tricept activation against resistance Lower Extremity 5/5 to hip and knee flexion against resistance.

Skin: patient was diaphoretic


Patient is awake alert and oriented to person, place, and time, normal speech and hearing, face symmetrical, sensation is equal and intact throughout, patient is highly agitated he does have intermittent twitching of his right lower extremity. Reflexes were hyper-reflexive in brachioradialis and patellar bilaterally equal.

Medical Decision Making:

Cardiac Monitor, EKG, IV, 0.9% NaCl 1L Bolus, BMP,CBC, TROP,AST,ALT, CPK, UDS, SDS

EKG: 136BPM, PR112, QRS120ms, QTc 532ms






1.) What is the reported weight based lethal dose of oral caffeine?



c. 240-300mg/kg

d. weight based doesn’t apply with oral ingestion

2.) Given the lab/ekg and rate at which potassium can be replaced on an IV -(see Dr. Levy recent lecture,) what is the most appropriate antiemetic to use in this patient to prevent further GI K+ loss?

a. timethobenzamide (Tigan)

b. prochlorperazine (Compazine)

c.ondansetron  (Zofran)

d. metoclopramide (Reglan)

e. droperidol  (Insapine)


3.) What is the correct initial combined medical and decontamination therapy for this patient?

a. benzos, K+,whole bowel irrigation

b.phenobarb, mg++, whole bowel irrigation

c.benzos, K+,mg++, activated charcoal

d.bezos, K+,Ca++, activated charcoal

e. Phenytoin,K+,mg++, hemodialysis


4.) If this patient should become immediately hypotensive, what is the preferred initial vasoactive agent?

a. propanolol

b.dopamine low dose

c. dopamine high dose

d. epinepherine

e. phenylepherine


Answers & Discussion:

1) b 150-200mg/kg.

The reported lethal oral dose is 10 g (150–200 mg/kg), although one case report documents survival after a 24-g ingestion. In children, ingestion of 35 mg/kg may lead to moderate toxicity. Coffee contains 50–200 mg (tea, 40–100 mg) of caffeine per cup depending on how it is brewed. No-Doz and other sleep suppressants usually contain about 200 mg per tablet. “Thermogenic” dietary supplements, which are sold as energy beverages (eg, Red Bull), bars, capsules, tablets, or liquid drops, contain the equivalent of 40–200 mg of caffeine per serving as either concentrated plant extracts or synthetic caffeine.  Given this patients body weight and stated dose =60,000 mg of caffeine patient estimated level is 357mg/kg! Way over the highest reported case report of survival!


2) d. metoclopramide  (reglan)

Caffeine is a is a trimethylxanthine that is closely related to theophylline. It acts primarily through nonselective inhibition of adenosine receptors. Given the shifting of K+ that can occur because of this inhibition as well as the stimulated GI losses patients who present with toxic ingestion almost always have a severe hypokalemia.  The problem is that the patient is actively vomiting and can not take oral K+ and IV 20mEq would take 2 Hrs to safely replace.  In this case we were instructed to stay away from the 5HT3 agents as the patient EKG QTc was 532 likely from his chronic use of  oxcabazepine.  Alkinalization with bicarb to is an option but given the hypokalemia it may potentiate torsades. Tigan action is unknown if it causes QTc prolongation and can not be used IV form and is only usually in oral formulary.  Recommendation was for use of reglan at 0.2mg/kg for initial dose and increase if necessary to 0.5mg/kg max.  Metoclopramide blocks dopamine receptors in CNS and increases upper GI motility through sensitization of acetylcholine.  After 33mg of metoclopramide the patient stopped vomiting in order for us to push K+ down his NGT!

Major Adverse Effects of Antiemetic Agents:


Antiemetic class

Adverse effects

Antihistamines and anticholinergics Sedation, urinary retention, blurred vision, exacerbation of narrow-angle glaucoma
Dopamine antagonists Sedation, extrapyramidal effects, QT prolongation, severe hypotension; rarely, seizures, agranulocytosis, neuroleptic malignant syndrome, blood dyscrasias
Serotonin antagonists QT prolongation, QRS widening; rarely, hypersensitivity reactions


3) c.

Replacement of K+ with concomitant mg++ replacement is key to the hypokalemia with a methylxanthine overdose.  Benzodiazepines are utilized for seizure prevention and for catecholemine surge.  People with caffeine overdose have a high mortality with seizures and Phenytoin has been found to increase mortality with cases of methylxanthine induced status epilepticus. Charcoal is the accepted method of decontamination.  In this patient inital charcoal was carefully given via NGT only after the risk of vomiting and aspiration subsided.  100g initial followed by 25-50g every 2hrs for up to 8 hrs.


4) a propanolol.

In Caffeine with overdose there is considerable beta1– and beta2-adrenergic stimulation secondary to release of endogenous catecholamines. This is not seen with chronic caffeine use toxicity.  Although it seems counterintuitive, Beta blockers effectively reverse cardiotoxic and hypotensive effects mediated by excessive beta-adrenergic stimulation. Treat tachyarrhythmias and hypotension with IV propranolol, 0.01–0.02 mg/kg  or esmolol, 0.025–0.1 mg/kg/min  beginning with low doses and titrating to effect. If vasopressor drugs are required,  or phenylephrine  is recommended to avoid the potassium-lowering effects of catecholamines.

There were many pitfalls to this case and there was a good outcome. The patient was discharged in 5 days after psych clearance.  The patient lived and did not have seizure or life threatening arrhythmia I believe due to the swift plan of the poison control center and the communication with everyone involved nurses, techs, ICU, psych on the strict adherence to the goals of care with close observation as any one of the medical treatments could have lead to a bad outcome if calculated wrong or given at the wrong time in the clinical course. 

-Special thanks to Dr Aaron for making this case a teaching pearl and for a thorough consultation as I was by myself for the first time and happened to get this patient.

Questions? Email me



-Flake, Z., et al  Practical guide to antiemetics Am Fam Physician. 2004 Mar

-Benowitz NL. Chapter 39. Caffeine. In: Olson KR, ed. Poisoning & Drug Overdose. 6th ed. New York: McGraw-Hill; 2012

-Gresham C, Brooks DE. Chapter 186. Methylxanthines and Nicotine. In: Tintinalli JE, Stapczynski JS, Cline DM, Ma OJ, Cydulka RK, Meckler GD, eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York:

-O’Brien CP. Chapter 24. Drug Addiction. In: Brunton LL, Chabner BA, Knollmann BC, eds. Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 12th ed. New York: McGraw-Hill; 2011

Senior Report 6.25

Case Presentation by Dr. John Wilburn

CC: Chest pain


24 year-old male presents to the emergency with complaints of chest pain, he points to the left upper sternal border and left upper chest. He reports it began about a month ago.  He describes it as a constant, dull pressure. He reports the intensity of the pain has significantly increased over the past 5 days and is now radiating to the right side of his chest.  Patient has not tried anything to alleviate this pain.  He reports taking a deep breath exacerbates his pain. He denies any fevers. He reports a dry cough that is non productive, which he attributes to smoking. He denies any trauma or dyspnea.


Constitutional: Denies night sweats, fatigue or weight loss.

Cardiovascular: Denies syncope

Respiratory: Denies hemoptysis

Gastrointestinal: Denies Abdominal pain

Genitourinary: Denies scrotal masses

Musculoskeletal: Denies extremity pain or swelling

PMH: Denies hypertension, pneumothorax, or diabetes

PSH: None

Allergies: None

Medications: None

FHx: Reports Hypertension denies CAD

Social Hx: Patient smokes cigarettes daily, and marijuana occasionally. Denies IVDU or Cocaine. Reports to socially drinking less than 3 times per month.

Physical Examination:

General/Psychiatric: WNWD non-toxic appearing male sitting upright in the stretcher in no acute respiratory distress, speaking in full sentences. A&Ox3.

Vital signs: 122/65 HR: 58 RR 14 Temperature 37 C Pulse oximetry 96% RA

HEENT: NC/AT PERRL EOMI. No nasal discharge, or nasal flaring.. Mucous membranes of the mouth are moist. No tonsil enlargement no erythema.

Neck: Supple, No JVD Trachea Midline. Full Range of Motion, No lymphadenopathy.

Back: No Tenderness to palpation

Chest: Left sided chest wall tenderness to palpation – front back level?.

Respiratory: CTAB no wheezes rhonchi or rales.

Cardiovascular: S1S2 present no M/R/G.

Abdomen: Thin Soft ND/NT no rigidity or rebound tenderness.

Musculoskeletal: Strength 5/5 in the upper and lower ext. Palpable and symmetric radial and dorsalis pedis pulses. No edema or asymmetry. No tenderness to palpation.

Neuro: Normal speech and gait..

Medical Decision Making/Course in the ED:

Patient Received Motrin and Maalox, ECG and CXR obtained







1) Where is the abnormality located in this patients chest radiograph?

a) Anterior Mediastinum

b) Ascending Aorta

c) Carina

d) Right Atrium

e) Posterior Mediastinum

2) Which of the following statements is correct?

a) The anterior mediastinum extends from the sternum anteriorly to the esophagus posteriorly.

b) The anterior mediastinum contains the thymus gland.

c) The anterior mediastinum contains the transverse arches of the aorta.

d) The middle mediastinum contains the esophagus.

e) All of the above are correct.

3) Which is the most appropriate next step in this patient’s management?

a) Obtain blood cultures, start antibiotics and consult cardiothoracic surgery.

b) Obtain a CT-Thorax with contrast.

c) Obtain a Transthoracic Echocardiogram.

d) Perform a Color Doppler Ultrasound Guided Thoracentesis.

e) Start the patient on Heparin and admit to the hospital.

4) Which of the following is the most common tumor of the anterior mediastinum?

a) Bronchogenic Cysts

b) Germ Cell Tumors

c) Lymphoma Hodgkin’s disease

d) Non-Hodgkin Lymphoma

e) Thymoma

5) What is the initial diagnostic study of choice?

6) Bonus Question: What was this patient’s final diagnosis?

a) Empyema

b) Germ Cell Tumor

c) Lymphoma Hodgkin’s Disease

d) Thymoma


Answers & Discussion:

1) Answer: a. Anterior Mediastinum

Brief review of radiographic anatomy eliminates b, c, d.


Patient’s Radiograph:  The radiograph does demonstrate two findings helpful in identifying the location of the mass. See below.


3 3b


The Hilum overlay sign is a useful tool to help identify probable location of a mediastinal mass

Another way to evaluate for mass in either the middle or posterior mediastinum is look for the azygoesophageal recess reflection. (below)


2)Answer: b. the thymus is located in the anterior mediastinum

The mediastinum is divided into 4 compartments

  1. The Anterior Mediastinum– extends from the sternum anteriorly to the pericardium and brachiocephalic vessels posteriorly


  • Thymus and residue of thymus
  • Fat
  • Lymph glands

The Middle Mediastinum– lies between the anterior and posterior mediastina.


  • Heart
  • Pericardium
  • Ascending aorta
  • Trachea
  • Main bronchi
  • Lymph nodes
  • Pulmonary artery
  • Pulmonary veins
  • Phrenic nerve

Posterior Mediastinum– bounded by the pericardium/trachea anteriorly and the vertebral column posteriorly.


  • Descending aorta
  • Esophagus
  • Azygous vein
  • Hemiazygous veins
  • Lymph glands
  • Thoracic duct
  • Autonomic nerves
  • Vagus nerve

Superior Mediastinum– bounded superiorly by the thoracic inlet and inferiorly by and arbitrary plane passing horizontally and posteriorly from the manubriosternal joint to the junction of T4/T5 vertebra.  Anteriorly bounded by the sternum and posteriorly by the upper thoracic vertebra.


  • Trachea
  • Esophagus
  • Great vessels
  1. Arch of aorta
  2. Thoracic portions of left common carotid and left subclavian arteries
  • Veins
  1. Innominate veins
  2.  Upper ½ superior vena cava
  • Thymus
  • Phrenic and vagus nerves
  • Thoracic duct
  • Lymph glands


3) Answer: b. CT Thorax w/ contrast should be ordered next. (Explanation below).




 4) Answer: e. Thymoma

The most common causes of anterior mediastinal masses: Thymoma (20%) Germ Cell Tumors (seminoma, teratoma, etc(15%)); thyroid disease (15%); and lymphoma HD and non-HD (10%). Masses of the middle mediastinum are typically congenital cysts. Neurogenic tumors are the most common cause of posterior mediastinal masses.  Overall, two thirds of mediastinal tumors are benign, however masses in the anterior compartment are more likely to be malignant.



The clinical sequelae can range from asymptomatic to symptoms of cough, chest pain, dyspnea, and fevers/chills. The likelihood of malignancy is influenced by mass location, patient age, and the degree of symptoms. Age is a strong predictor of malignancy, lymphomas and germ cell tumors (GCTs) occur mostly during the second and fourth decades. Symptomatic patients are more likely to have a malignancy. Symptoms may be delineated between localizing symptoms (mass effect) and systemic symptoms (hormonal/antibody effect). In Davis et al,7 85% of patients with a malignancy were symptomatic at presentation, compared to 46% of patients with benign neoplasms.

The initial workup of a suspected mediastinal mass involves obtaining posteroanterior and lateral chest radiographs. CT scanning is used to further characterize mediastinal masses (cystic, vascular, and soft-tissue structures) and their relationship to surrounding structures.

Other more rare imaging modalities include, fluoroscopy, and barium swallow. MRI may be used in evaluating a neurogenic tumor, and identifies vascular invasion and cardiac involvement.

Tissue diagnosis is almost always required. Biopsy may be obtained via, transthoracic or transbronchial needle aspiration, mediastinoscopy, anterior mediastinotomy, or video-assisted thoracic surgery. Modality of choice is sometimes case dependent.  Fluoroscopic or CT guided transthoracic needle biopsy, has been shown to be faster, cheaper, and better tolerated by patients. It has been shown to have good diagnostic accuracy, although sometimes specimens are inconclusive requiring further investigation.

5) Answer: CT Guided Transthoracic Needle Biopsy, however some evidence suggests Thoracoscopic biopsy is just as safe and slightly more accurate.

 6) Answer: b. Germ Cell Tumor (Seminoma)



A Diagnostic Approach to Mediastinal Abnormalities

Camilla R. Whitten, MRCS, FRCR, Sameer Khan, MRCP, FRCR, Graham J. Munneke, MRCP, FRCR and Sisa Grubnic, MRCP, FRCR

2)Tumors of the Mediastinum

Beau V. Duwe, MD; Daniel H. Sterman, MD. FCCP; Ali I. Musani, MD, FCCP

Chest. 2005; 128(4):2893-2909.


4)Harrison’s Principles of Internal Medicine 16th edition

5) Anterior mediastinal masses: utility of transthoracic needle biopsy.

S J HermanR V HolubG L Weisbrod and D W Chamberlain

Department of Radiology, Toronto General Hospital, Ont, Canada.


Thoracoscopic diagnosis and treatment of mediastinal masses

Ann Thorac Surg 1993;56;92-96

7)Davis, RD, Jr, Newland Oldham, H, Jr, Sabiston, DC, Jr Primary cysts and neoplasms of the mediastinum: recent changes in clinical presentation, methods of diagnosis, management and results. Ann Thorac Surg 1987; 44, 229-237 [CrossRef] [PubMed]


Percutaneous Transthoracic Needle Biopsy

Jack L. Westcott, MD

Department of Radiology, Hospital of Saint Raphael, New Haven, CT.

Senior Report 6.24

Case Presentation by Dr. Stefanie Wise

53-year-old man presents to the ED complaining of dizziness. His symptoms started approximately 30 minutes prior to arrival. He had some mild abdominal pain initially, which felt like “one of my gallbladder attacks”, although it was located in the epigastric and left upper abdominal regions. The pain has improved, but his dizziness persists. He describes it as feeling lightheaded and like he is going to pass out. The room is not spinning. He has no headache, no vision loss and no hearing loss or tinnitus. He denies any focal weakness or numbness. Upon arrival his triage blood pressure is 68/34 with a heart rate of 60 and he is triaged as a medical code. Review of systems is otherwise negative.

PMH: Bicuspid aortic valve, Factor V Leiden, no previous surgeries

Medications: Warfarin, aspirin 81mg, vitamin B12

Allergies: NKDA

FH: No heart disease, no diabetes

SH: No tobacco, illicit drugs or alcohol

Physical Exam:

Vitals: Resuscitation BP 112/66, HR 86, RR 16, temp 37.6 rectal, pulse ox 100% on room air

General: Well-developed slender Caucasian man laying on stretcher, appears pale and mildly diaphoretic, calm and cooperative

Eyes: Sclera anicteric, PERRL at 3mm, EOMI

HENT: Mucous membranes moist, no intraoral lesions; trachea midline, no thyromegaly, no lymphadenopathy

CV:  Regular rhythm, intermittently bradycardic; S1 and S2 heard, no significant murmur appreciated; no JVD; pulses 2+ in all four extremities, no significant delay in capillary refill

Respiratory: Breath sounds equal and clear to auscultation bilaterally, no wheezes or crackles, no tachypnea

Abdomen: Soft, non-tender, non-distended, normally active bowel sounds; no rebound or guarding, no Murphy’s sign

Rectal: Guaiac negative brown stool

Skin: Pallor improved with Trendelenberg positioning; warm, mildly diaphoretic on arrival, no rashes, no petechiae

MSK: Normal tone, full range of motion in all extremities

Neuro: AOx3; speech is clear, face symmetrical, gait steady; strength 5/5 in all four extremities, sensation intact to light touch throughout extremities and face

Medical Course:

The patient is immediately placed on cardiac and pulse oximetry monitoring. IV is established and labs are drawn by nursing staff. IV fluid boluses are initiated.

A 12-lead ECG is performed:

6.24-1 ecg

Orthostatic vitals signs are then obtained. This is not tolerated well due to extreme positivity (50/30 standing). Bedside abdominal ultrasound is performed. There is no free fluid identified. Aorta is normal in caliber. There is no pericardial effusion. The patient is moved to the module pending laboratory studies.




In the medical module, the patient experiences intermittent episodes of dizziness despite Trendelenberg positioning. During these episodes, his heart rate drops to the 40s, blood pressure approximately 60/40. Atropine 0.5mg is given , increasing his heart rate to the 50s. The decision is made to place a central line and repeat the CBC. MICU is consulted.

During the placement of the central line, the patient experiences tenesmus and passes loose, dark brown stool. Hemoccult is repeated and is again negative.

The patient begins to experience increasing generalized abdominal pain. Bedside ultrasound is repeated, demonstrating blood in Morrison’s pouch and behind the bladder. The patient has developed generalized abdominal guarding and rebound tenderness.

Repeat CBC (2 hours later):


Blood products are ordered by massive transfusion protocol. General surgery is consulted. The patient is moved to resuscitation as RBCs and plasma are manually pumped. He is taken to the CT scan accompanied by the surgery senior resident and then immediately to the operating room.



1) Which is true of non-traumatic splenic rupture?

a. Most cases occur in the absence of identifiable hematologic, vascular or splenic pathology

b. Malaria is the most common infectious etiology in the United States

c. Associated radiation of pain to the left shoulder is known as Kehr’s sign

d. Chronically enlarged spleens are most susceptible to rupture versus acute splenomegaly

2) Which is true of infectious etiologies of splenomegaly?

a. The majority of splenic ruptures associated with malaria occur during the acute infection with the primary attack

b. 15% of mononucleosis infection cases will have associated splenomegaly

c. Significant trauma, such as that experienced in contact sports, is required to incite spontaneous rupture

d. Surgical intervention is mandatory in cases of splenic hematoma or small tears when associated with an infectious etiology

3) Splenic artery aneurysms:

a. Are most commonly seen in middle-aged males

b. Are mostly associated with symptoms of left upper quadrant or epigastric pain

c. Carry a 70% mortality rate if rupture occurs during pregnancy

d. Are typically larger than 2 cm in diameter



1. C

Non-traumatic splenic rupture is rare but life-threatening. The majority of cases occur in the presence of identifiable pathology, such as hematologic malignancy, infection, infiltration (amyloidosis) or connective tissue diseases. Worldwide, malaria is the most common cause. In the US, mononucleosis is most common. Chronically enlarged spleens are less likely to rupture than acute cases. In the event of rupture, symptoms may include vague LUQ or epigastric abdominal pain, pain radiating to the left shoulder (Kehr’s sign), tachycardia, abdominal pain with peritonitis, lightheadedness, hypotension and potentially other signs of hemorrhagic shock.

 2. A

Malaria-related splenic rupture is most common in the acute and primary infection. In mononucleosis, 50% of patients will have splenomegaly. In either infection, small inciting events such as coughing or vomiting can cause significant rupture. Although cases of large rupture with hemodynamic instability must be surgically managed, smaller tears and hematomas may be managed conservatively with observation.

3. C

Splenic artery aneurysms are most commonly associated with pregnancy, due to the increased AV shunting to the splenic vasculature. Most cases are asymptomatic, and symptoms (LUQ or epigastric abdominal pain) indicate need for intervention. The majority of splenic aneurysms are less than 2 cm in size, making diagnosis by physical exam difficult. Diagnosis is most often incidental by ultrasound or CT, with confirmation by angiogram. While only 2% of splenic artery aneurysms lead to life-threatening rupture, 95% of the ruptures occur in young pregnant women, carrying a 70% mortality rate if they do rupture during the pregnancy.

Case conclusion: The patient was taken to the operating room for splenectomy. Pathology revealed wall rupture of an intra-splenic artery and associated hematoma without any other identifiable abnormality. The patient required no further post-surgical transfusion of blood products. He improved quickly and on post-operative day #3 was transferred to his primary health care team’s hospital for evaluation and further management of possible acute versus chronic endocarditis of his aortic valve.


– Becker, J. et al. (2006) Essentials of Surgery. Philadelphia: Saunders Elsevier.

– Gedik, E. et al.  Non-traumatic splenic rupture: Report of seven cases and review of the literature. World J Gastroenterol (2008) 14(43): 6711-6716)

– Marx, J. et al. (2010) Rosen’s Emergency Medicine 7th edition, Volume 1. Philadelphia:   Mosby Elsevier.

Senior Report 6.23

Case Presentation by Dr. Deshon Moore

A 40 year old man, smoker with no past co-morbids presented to DRH with left facial swelling, sudden loss of vision, HA, and nausea. Symptoms started 10 days prior with mild headache and otalgia. There was no history of trauma. He was treated with analgesics but symptoms worsened. No prior history of otitis media or sinusitis could be elicited. You see him in mod 2 and notice a well built man with obvious swelling of left face, severe proptosis and chemosis of left eye, left mastoid swelling and left complete ophthalmoplegia. He also had a low-grade fever. Visual Acuity was diminished. The pt had little perception of light with relative afferent pupillary defect.


1) What is the best imaging modality to confirm this diagnosis?

a) CT scan w/o contrast

b) X-ray orbit

c) CT scan w contrast

d) MRI

e) Cerebral angiography

2) Which cranial nerve deficit would be the first expected with this condition?

a) CN VIII & X

b) CN VI only


d) CN, III,IV, V & VI

e) All of the above

3) What antibiotic regimen would you use for coverage?

a) Erythromycin ophthalmic

b) Clindamycin and vancomycin

c) Vancomycin, Cefotaxime & Flagyl

d) Gentamycin Ophthalmic

e) Ceftriaxone & Flagyl

f) No abx needed

Answers & Discussion:

Cavernous sinus thrombosis (CST) is life threatening but thankfully rare disorder that can affect a person at any age.

This condition happens when a blot clot blocks a vein that runs through a hollow space located underneath the brain and behind the eye sockets. The cavernous sinuses are the most centrally located of the dural sinuses and lie on either side of the sella turcica. These sinuses are just lateral and superior to the sphenoid sinus and are immediately posterior to the optic chiasm.  There is a picture below to depict this. This venous system carries blood from the face and head back to the heart. CST is usually caused by an infection that spreads from the face, teeth or sinuses. It can happen from ear or eye infections but less commonly. Studies show that 25% of the time CST was a result of a furuncle that was either removed surgically or squeezed by a patient and it’s contents spread intracranial. The body creates a blood clot to close off the infection, which creates the CST.

When it happens there is a high mortality rate of about 30-50%. Prompt recognition and treatment is essential.


There are many symptoms of CST.  Some include severe headache, proptosis, periorbital edema, APD, fever, vision loss, seizures, and chemosis among others. There are mimics of this condition including acute angle glaucoma, subdural hematoma, spinal epidural abscess and others but history and physical should guide you in your diagnosis of CST.


1) D

In current practice, computed tomography (CT) scan or magnetic resonance imaging (MRI) with contrast is the modality of choice to confirm the diagnosis of CST and to differentiate it from alternatives such as orbital cellulitis, which may have a similar clinical presentation.

MRI with MR venogram (MRV) is the preferred imaging choice as the MRV will show the absence of venous flow in the affected cavernous sinus.

With non-contrast CT, thrombosis of the cavernous sinus can be appreciated as increased density. The introduction of intravenous contrast can reveal filling defects within the cavernous sinus as well as thickening of the superior ophthalmic vein. Nevertheless, CT scan findings may be subtle, and a negative CT scan cannot rule out CST reliably when the clinical suspicion is high.

Carotid angiography can demonstrate narrowing or obstruction of the inter-cavernous segment of the carotid artery. MRI and CT scan can also show this narrowing and/or obstruction of the carotid artery. Carotid angiography is not ideal in the emergency department as it takes about the same amount of time to get an MRI if not longer and the sensitivity of an MRI is better.

Lab analysis is generally nonspecific but the best supporting labs would be CBC w diff showing leukocytosis w left shift, blood cultures likely showing causative organism and maybe LP which would show inflammatory cells. Fungal cultures would reveal fungal source, which is less likely than bacterial except in diabetics or those with chronic sinusitis. PE and imaging are the primary diagnostic tools of this disease.

2) B

Lateral gaze palsy (isolated cranial nerve VI) is usually seen first since CN VI lies freely within the sinus in contrast to CN III and IV, which lie within the lateral walls of the sinus. Eventually the disease can spread if not treated and one can get contralateral findings. Eventually CN III and IV deficits can happen including mydriasis, ptosis, eye muscle weakness and superior oblique muscle paralysis.

3) C

Staphylococcus aureus accounts for approximately 70% of all infections. Streptococcus pneumoniae, gram-negative bacilli, and anaerobes can also be seen. Fungi are a less common pathogen and may include Aspergillus and Rhizopus species.

Empiric antibiotic therapy should include a penicillinase-resistant penicillin plus a third- or fourth-generation cephalosporin. If dental infection or other anaerobic infection is suspected, an anaerobic coverage should also be added. Recommended treatment is with IV antibiotics for at least 3-4 weeks.

Anticoagulation for cavernous sinus thrombosis is recommended at DRH according to our Neuro Intensivist. There has been controversy over anti-coagulation for this disorder. There are no prospective trials looking at the use of anticoagulation for CST.  This is likely because the condition is so rare. Some retrospective studies have shown a decrease in mortality and clot further clot formation by anticoagulation. A Cochrane review found 2 small trials involving 79 patients who were treated with anticoagulants. Limited evidence suggests anticoagulant drugs are probably safe and may be beneficial for people with sinus thrombosis. Accordingly, we should consider anticoagulation (especially since our Neuro Intensivist recommend it) with heparin since the goal is to prevent further thrombosis and reduce the incidence of septic emboli. Before starting heparin just make sure the patient does not have an intracerebral hemorrhage or other bleeding diathesis.

Corticosteroids may help reduce inflammation and edema and should be considered as an adjunctive therapy.



-Duong DK, Leo MM, Mitchell EL. Neuro-ophthalmology. Emerg Med Clin North Am. Feb 2008; 26(1):137-80, vii.

-Karlin RJ, Robinson WA. Septic cavernous sinus thrombosis. Ann Emerg Med. Jun 1984;13(6):449-55

-Rosen’s, Emergency Medicine, 7th edition Volume 2

Senior Report 6.22

Case Presentation by Dr. Dan Paling

HPI: 3 year-old female presents to the emergency department accompanied by her parents with complaints of worsening rash. The mother states that her child developed the rash 2 days ago. She states that it acutely worsened overnight. The patient reportedly developed a fever overnight of 102.6. She states that she is currently being treated for acute bilateral otitis media. The patient was taken to her pediatrician when the rash was first noticed on the patient’s legs and feet. The pediatrician told the patient’s mother to discontinue using amoxicillin and to start trimethoprim-sulfamethoxazole. The pediatrician stated that the rash should go away after stopping the amoxicillin. The mother states that she gave the first dose of the new antibiotic the evening before the rash worsened. The mother denies any coughing or difficulty in breathing. She denies nausea, vomiting, and diarrhea. The mother states that the patient has not had this type of rash in the past.

The mother attempted Benadryl without any improvement of the rash.

PMH: none

Allergies: NKDA

Immunizations: UTD

Physical Exam:

Constitutional: no acute distress

Vitals: Temp 39.2, BP 107/67, HR 130, RR 14, O2 Sat 99%

HEENT: PERRL, no conjunctival or scleral injection, few intraoral lesions

Respiratory: CTAB, no wheezing, no retractions

Cardiovascular: tachycardic with regular rhythm, normal S1 S2

Skin: Diffuse blanching papular rash not involving palms and soles. Mucous membrane involvement. Majority of lesions in acral distribution however scattered lesions on face, chest, abdomen, and back. Less than 10% BSA skin desquamation.

6.21-1 copy


1) What is the diagnosis?

a) Urticaria

b) Erythema Nodosum

c) Erythema Multiforme Minor

d) Erythema Multiforme Major

2) What is the probable etiology for this child’s condition?

a) Virus

b) Post-Group A Strep infection

c) Amoxicillin

d) Food Allergy

3) What is the most common cause of Erythema Multiforme?

a) Penicillins

b) Sulfonamides

c) Herpes Simplex Virus

d) Group-A Streptococcal infection


Discussion & Answers:

1)  Correct answer D

Erythema Multiforme Major constitutes painless blanching target-like papular rash that is usually first noticed on the extremities. This rash spares the palms and soles. Rashes involving the mucous membranes are considered Erythema Multiforme (EM) Major with total BSA desquamation less than 10%. Desquamation rash involving mucous membranes that involves more than 10% but less than 30% total BSA is considered SJS. More than 30% BSA is considered TEN.

(A)  This rash is not an annular urticarial rash because urticaria usually resolves within 24 hours of its onset. Urticaria will not form target-type lesions. Urticaria most often resolves with antihistamines.

(B)  Erythema Nodosum lesions are painful erythematous nodules most often occurring on patient’s lower extremities that do not exhibit central clearing.

(C)  This rash involves at least one mucous membrane therefore is considered EM Major. EM Minor primarily exhibits acral distribution. EM Minor typically will not involve the face, trunk, chest, or back

2) Correct answer C

In this case, it is probable that Amoxicillin was the cause of this EM Major rash. HSV is most often the cause EM however the child does not have any vesicular lesions suggesting HSV infection. Common pharmacologic causes of EM are penicillins, sulfonamides, phenytoin, barbiturates, and aspirin. EM does not occur as a result of a Group-A Streptococcal infection. Erythema Nodosum is noted to be a post-streptococcal complication. Urticaria can be a result of an allergic reaction to food however EM has not been linked.

3) Correct answer C

Herpes Simplex Virus-1 and Mycoplasma are the most common predisposing factors that lead to the development of EM. Penicillins and sulfonamides result in fewer total cases of EM however the majority of the most severe cases are medication induced. Group-A Steptococcal infections have not been linked to the development of EM.

Erythema Multiforme is considered a Type IV delayed hypersensitivity reaction.

Senior Report 6.21

Case Presentation by Dr. Deepa Japra


1.) A 19 year old female presents with decreased hearing from her right ear since going diving earlier today. Otoscopic exam reveals the findings in the picture, which of the following is an acceptable treatment?


a) oral ciprofloxacin

b) topical neomycin

c) hydrogen peroxide

d) ciprofloxacin otic solution

2.) Your next patient arrives with a chief complaint of ear pain and with 45 minutes left in your shift, you know it’s bad form to push it off for the next resident to see. You are dreading having to see yet another cerumen impaction, and are startled to observe the following findings on physical exam. Which of the following is central to management of this condition?


a) admission for IV antibiotics

b) emergent bedside incision and drainage

c) ENT consult for emergency mastoidectomy

d) outpatient antibiotics with urgent ENT follow up

3) Your next patient presents with a foreign body in the ear. You grab your alligator forceps with 10 minutes left in your shift, but which of the following findings should prompt an ENT evaluation instead of attempted removal by the ED physician?

a) disk-shaped battery

b) live insect

c) cotton ball

d) object present more than 8 hours

Answers & Discussion

1) d

2) a

3) b

Question 1 –  d

The picture above is of a perforated tympanic membrane. This can occur through various mechanisms, including a direct blow to the ear, blast injury, scuba diving, air travel while having an upper respiratory infection, and more commonly from the traumatic usage of cotton swabs to clean the ear. In the case of this patient, TM perforation occurred during a diving injury. Topical antibiotics, such as d) ciprofloxacin otic solution, can be safely prescribed, especially in this case since the perforation likely occurred in a contaminated setting while the patient was in water. It is important to note, however, that usage of topical anitbiotics in TM perforation is not proven by evidence, but can also be given in cases of external puncture or canals occluded with blood or drainage.  Most cases of tympanic membrane perforation heal spontaneously. Larger, more central lesions such as those greater than 25% of the total drum surface area may require operative repair, especially in patients that do not heal spontaneously in 4 weeks. Lesions in elderly patients are also less likely to heal on their own. Topical ototoxic agents should be avoided in perforated TM and includes aminoglycosides like, b) neomycin, and antiseptics and compounds with low pH including c) hydrogen peroxide and acetic acid. Alcohol is also ototoxic and should not be applied.  If the clinician cannot fully visualize the tympanic membrane and is unsure of whether it is disrupted and there is an index of suspicion for perforation, it is best to avoid these ototoxic agents. After the diagnosis is made, patients with small isolated tympanic membrane perforation with minimal hearing loss can be managed with avoidance of water exposure for 4 to 6 weeks, possible topical antibiotics in contaminated settings as described above, the recommendation for audiometry within 24 hours, and follow up with ENT within 4 weeks to ensure the perforation is closed and the hearing deficit has resolved. There is no indication for oral antibiotics, a), in a perforated TM with no signs of infection.  Patients with more marked hearing loss, vestibular signs such as nystagmus, vomiting, and ataxia, or those with findings consistent with facial nerve injury should have emergent ENT evaluation if possible or within 48 hours of injury.

If the mechanism for perforation is secondary to barotrauma, such as air travel with a URI, diving, or blast injury, making the diagnosis of perforated TM can give insight to other injuries. The tympanic membrane is sensitive to changes in pressure and more likely to be injured at lower pressures than any other organ. Some studies suggest that it can be used as a triage tool in blasts with multiple victims, especially with patients that are initially healthy appearing, in order to identify patients that have a higher risk of delayed sequelae including pulmonary or gastrointestinal injury.

Question 2 – a

The picture represents acute mastoiditis, which occurs most likely as a complication of acute otitis media. Acute mastoiditis is more common in children than adults, and the incidence has declined with the use of antibiotics for the treatment of otitis media, and is now relatively rare. The mastoid air cells are connected to the distal end of the middle ear through the antrum. While most episodes of acute otitis media are associated with some inflammation of the mastoid, mastoiditis occurs when the mucous lining of the middle ear lining the mastoid becomes persistently inflamed and purulent material accumulates in the mastoid air cells.

The clinical presentation of mastoiditis can include fever, posterior ear pain, local erythema and tenderness over the mastoid bone, edema of the pinna, and posterior and downward displacement of the auricle. If mastoiditis is suspected, the patient should be a) admitted for IV antibiotics and a CT scan of the temporal bone should be performed.  CT scan can demonstrate air-fluid levels and identifies the extent of the disease, but it is important to note that the isolated or incidental finding of mastoid air-fluid levels on CT should not prompt a change in treatment in a well appearing patient without other clinical signs of mastoiditis. IV antibiotics should be directed against streptococcus pneumoniae, the most common pathogen, with consideration for broader coverage against pseudomonas, staphylococcus aureus, and enteric gram negative rods when mastoiditis presents as a complication of a more chronic disease. A third-generation cephalosporin is acceptable as an initial antibiotic choice, and other recommendations include vancomycin, clindamycin, or imipenem. Answer d) outpatient antibiotics with ENT follow up is inappropriate as acute mastoiditis can lead to further intracranial spread and neurological sequelae if not appropriately diagnosed and treated. Choice b) emergency bedside incision and drainage is not an appropriate treatment option for acute mastoiditis. Though an emergency ENT consult is warranted, choice c), an emergency mastoidectomy for debridement of necrotic bone, is not an initial intervention performed and is sometimes indicated if the patient does not respond to conservative therapy with IV antibiotics. A myringotomy by ENT for aspirate and fluid cultures is an appropriate initial treatment choice in order to guide antibiotic therapy and may include placement of a tympanostomy tube for drainage.

Question 3 – a

When removing a foreign body in the ear in the emergency department, the clinician should remember that smaller instruments are more likely to cause damage to the canal so one should use the largest, bluntest instrument that has the capacity to grasp the object or pass a hook behind it.  Choice b) live insect, can be safely removed by the ED physician, and the insect should be killed first with solutions such as lidocaine (2% gel or liquid) or mineral oil prior to removal. Though some studies suggest that ethanol causes the most rapid killing of insects, this should not be routinely used because alcohol is ototoxic and contraindicated unless the TM is intact, which is difficult to assess with an insect blocking visualization.

Choice a) disk-shaped battery should prompt an ENT evaluation because of its ability to cause burns or liquefactive necrosis of the external auditory canal. The battery’s electrical potential is damaging and does not need to leak or rupture in order to cause damage. Choice c) cotton ball, can be safely removed as long as the object is easily visualized and accessible. Choice d) object present more than 8 hours, is not a definite ENT referral. Some studies suggest that primary ENT referral should be performed for any sharp-edged or spherical object, any vegetable matter or disk-shaped battery, location adjacent o the TM, age less than 4 years, previous unsuccessful removal attempts, and time in ear exceeding 24 hours, all of which were associated with increased complications. Other studies suggest that there is no increase in complication rates related to patient age or the time object is present in the ear.

After removal of any foreign body, the physician should perform appropriate inspection of the ear canal for signs of damage to the external canal, TM perforation, or infection, and treat these conditions appropriately.