Intern Report 7.12

Case Presentation by Derek Kennedy, MD

CC: Unobtainable

HPI: A 79-year-old woman who is nonverbal at baseline is brought to the ED via EMS for a decrease in responsiveness and increased work of breathing These symptoms were noted to begin this morning by nursing staff.  EMS reports an oxygen saturation of 96% obtained upon their nursing home arrival,  Pt minimally responsive to painful stimuli.

ROS, social and family history: Unable to obtain.

PMHx: Dementia, OA, psychiatric disorder. Per previous echo, pulm HTN noted. Per EMS, notes Pt recently diagnosed with heart failure but no EMR documentation found

PSHx: PEG tube

Medications: Zantac, neurontin, keppra, aspirin, aricept, actonel, namenda


Physical Exam:
Gen: Laying in bed, nonresponsive to verbal cues, responds to painful stimuli. GCS
Vitals: BP 144/92, HR 118, RR 19, T 37.6 obtained rectally, O2sat 100% on 4L NC
HEENT: Normocephalic, atraumatic, PERRLA, no tracking.  Dry mucous membranes with crusting at b/l commissure noted, edentulous at upper jaw, multiple broken teeth with enamel darkening noted along lower jaw.
Neck: No JVD
CV: RRR with no noted murmur, rub, gallop
PULM: Clear to auscultation b/l with coarse breath sounds throughout and expiratory wheeze noted at bases.
ABD: Soft, nontender, nondistended abdomen w/ bowel sounds
Fecal occult blood test positive, weakened rectal tone, gross light brown feces, no gross blood
MSK: FROM to passive pressure with pulses noted in all 4 extremities. No peripheral edema
Skin: Skin breakdown noted at the anterior neck, upper chest, Right forearm, Left thigh, perirectal region

Labs / Imaging / ED course

ABG: pH 7.35
pCO2 42
pO2 68
HCO3 23
O2sat 96.6

Na 151
Cl 115
Gluc 118

WBC 11.9
Hgb 10.4
Plt 202

INR 1.12
PT 12.0

Trop 0.318
Trop 4 hrs later 0.241

UA: Negative except 1+ prot, 1+ bact, unrecognized amorphous sediment.

Head CT no acute process, some chronic ischemic changes 2/2 microvascular disease and diffuse brain atrophy noted.




 Medical Course:
Pt responded well to 250cc 0.9%NS IVF bolus, eye tracking returned, repeat vitals BP 119/74, HR 114, RR 17, satting 96% on 4L NC.



1) Which of the following has been connected with elevated BNP in the absence of elevated troponin?

a) Subarachnoid hemorrhage
b) Acute kidney injury secondary to dehydration
c) Acute pulmonary embolism
d) COPD exacerbation
e) Anemia

2) Which of the following is an absolute contraindication for heparin use?
a) Elevated INR
b) Active GI bleeding
c) Chronic alcoholism
d) Hepatic disease
e) DIC without severe thrombocytopenia

3) Is elderly abuse a concern here?
a) No, with appropriate evidence in support
b) Yes, with appropriate evidence in support
c) Likely, without sufficient evidence of support
d) Likely no, without sufficient evidence of support


Answers & Discussion:

Questions 1: E. Troponin I is a commonly ordered lab in the ED. One study examining 69,299 patients admitted through the emergency department found 48% had their troponin measured. Of these, 2,344 patients (3.3% overall, or 7.0% of those that had a troponin I measured) had an elevated concentration. Of those with a positive troponin, 42.7% did not have ACS (3). Common causes of non-ACS troponin elevation in acutely ill patients include severe hypertension or hypotension, upper gastrointestinal bleeding,and sepsis (with or without acute respiratory distress syndrome).  Many chronic conditions also cause troponin elevation, including LVH, heart failure, pulmonary HTN, and kidney diseases, even when CKD is asymptomatic.  Musculoskeletal injury including rhabdomyolisis, blunt force trauma, and recent surgical intervention also have been identified.  Dehydration and resultant AKI (choice B), PE (choice C), and COPD exacerbation  (choice D) have also been connected to elevated troponins. SAH (choice A)  is less studied in the sense of direct troponin elevation, but a study evaluating nontraumatic SAH and troponins levels impacting hospital mortality shows the strong linkage(2).  Anemia does not cause elevated troponins, but has been connected to elevated BNP in patients already with diagnosed heart failure (1).   Major takeaway from this discussion is to not disregard non-ACS troponin elevation as an elevated troponin in the absence of ACS is most often associated with a worse prognosis to overall morbidity and mortality.  A table of common causes of troponin I elevation separated by system is provided below.

System Causes of Troponin Elevation
Cardiovascular Acute aortic dissection
Medical ICU patients
Heart failure
Apical ballooning syndrome
Cardiac inflammation
• Endocarditis, myocarditis, pericarditis
Infiltrative disease
• Amyloidosis, sarcoidosis, hemochromatosis, scleroderm
Left ventricular hypertrophy
Myocardial Injury Blunt chest trauma
Cardiac surgeries
Cardiac procedures
• Ablation, cardioversion, percutaneous intervention
Hypersensitivity drug reactions
Respiratory Acute PE
Infectious/Immune Sepsis/SIRS
Viral illness
Thrombotic thrombocytopenic purpura
Gastrointestinal Severe GI bleeding
Nervous system Acute stroke
• Ischemic stroke
• Hemorrhagic stroke
Head trauma
Renal Chronic kidney disease
Endocrine Diabetes
Musculoskeletal Rhabdomyolysis
Integumentary Extensive skin burns
Inherited Neurofibromatosis
Duchenne muscular dystrophy
Klippel-feil syndrome
Others Endurance exercise
Environmental exposure
• Carbon monoxide, hydrogen sulfide


Question 2: B. Heparin exerts its anticoagulative effect by activating and accelerating the proteolytic activity of plasma cofactor antithrombin. Heparin binds to the lysine site on antithrombin, producing a conformational change at the arginine-reactive site that converts antithrombin from a slow, progressive thrombin (factor IIa) inhibitor to a rapid inhibitor of thrombin and factor Xa, thereby preventing thrombus propagation (4).  Heparin also binds to a number of different circulating plasma proteins (acute phase reactants), blood cells, and endothelial cells, which contributes to its differing anticoagulative effects in different patients. Therefore, close and frequent monitoring of the aPTT is necessary to ensure a safe therapeutic range

Heparin is commonly used in clinical practice as an early invasive strategy for most cases of confirmed NSTEMI, but AHA guidelines recommend early invasive strategy in those ACS patients with associated high-risk indicators with an ischemia-guided strategy for those patients without such factors.  These include recurrent angina or ischemia at rest or with low-level activity, despite intensive anti-ischemic therapy, elevated cardiac-specific troponin level (troponin I or T), new or presumably new ST-segment depression, recurrent angina or ischemia with symptoms of congestive heart failure, an S3 gallop, pulmonary edema, worsening rales, or new or worsening mitral regurgitation, high-risk findings on noninvasive stress testing, depressed left ventricular function (e.g., ejection fraction < 40% on noninvasive study), hemodynamic instability, sustained ventricular tachycardia, percutaneous coronary intervention within previous six months, previous coronary artery bypass grafting (5).  Elderly patients, when compared to their younger counterparts, show a greater absolute and relative benefit to early invasive therapy even despite their risk of associated bleeding.  In general, compared with standard therapy with aspirin, the use of heparin does not reduce mortality, the need for revascularization, major bleeding, thrombocytopenia, or recurrent angina. Heparin use does increase the incidence of minor bleeding.

There are contraindications to the use of heparin as it is associated with several risks including those listed above. Absolute contraindications to heparin include known hypersensitivity, past or present heparin-induced thrombocytopenia and active bleeding (choice B).  Elevated INR (choice A) is a contraindication that can be reversed via FFP (shorter) or Vit K administration. Hepatic disease (choice D) leading to coagulopathy contraindicates heparin admin as well as chronic alcoholism (choice C) leading to both chronic hematologic changes as well as hepatic disease contraindicating heparin administration.  DIC (choice E) is the only option listed that is not a contraindication, absolute or relative, to heparin administration with the noted NOT severe thrombocytopenia, which is a contraindication.

Question 3: A. Untreated skin breakdown noted on exam, minimal medical works sent with Pt favor possible abuse.  Pt with normal limits creatinine making dehydration supporting neglect less likely and call by nursing home to EMS placed on day of change in mental status favoring appropriate care, which is the more likely scenario based off of her presentation.

Elderly abuse is an underrecognized problem in our society, and with the increasing survival rate of our nation’s population, this issue warrants further investigation. A systematic review in 2008 found 6% of older people surveyed globally reported abuse with a range of 3-27% across cultures. Psychological abuse was reported by nearly ¼ of those victims. US data from 2002 indicate that 1.6 million people live in 17,000 licensed nursing homes with another 900,000 in similar facilities.  When one takes into account the suspected rates of undiagnosed dementia, recurrent AMS in the elderly due to infectious and comorbid conditions, and the 41% of community-residing Medicare beneficiaries over 65 with difficulty with ADL’s, it is likely the 6% is an underreported sampling.  Physical, psychological, and sexual are the most reported insults, but several exist, including:

  • Physical Abuse—inflicting physical pain or injury on a senior, e.g. slapping, bruising, or restraining by physical or chemical means.
  • Sexual Abuse—non-consensual sexual contact of any kind.
  • Neglect—the failure by those responsible to provide food, shelter, health care, or protection for a vulnerable elder.
  • Exploitation—the illegal taking, misuse, or concealment of funds, property, or assets of a senior for someone else’s benefit.
  • Emotional Abuse—inflicting mental pain, anguish, or distress on an elder person through verbal or nonverbal acts, e.g. humiliating, intimidating, or threatening.
  • Abandonment—desertion of a vulnerable elder by anyone who has assumed the responsibility for care or custody of that person.
  • Self-neglect—characterized as the failure of a person to perform essential, self-care tasks and that such failure threatens his/her own health or safety.

While one sign does not necessarily indicate abuse, some tell-tale signs that there could be a problem:

  • Bruises, pressure marks, broken bones, abrasions, and burns may be an indication of physical abuse, neglect, or mistreatment.
  • Unexplained withdrawal from normal activities, a sudden change in alertness, and unusual depression may be indicators of emotional abuse.
  • Bruises around the breasts or genital area can occur from sexual abuse.
  • Sudden changes in financial situations may be the result of exploitation.
  • Bedsores, unattended medical needs, poor hygiene, and unusual weight loss are indicators of possible neglect.
  • Behavior such as belittling, threats, and other uses of power and control by spouses are indicators of verbal or emotional abuse.
  • Strained or tense relationships, frequent arguments between the caregiver and elderly person are also signs.


(1) Ralli S, Horwich TB, Fonarow GC. Relationship between anemia, cardiac troponin I,  and B-type natriuretic peptide levels and mortality in patients with advanced heart failure. Am Heart J. 2005 Dec; 150 (6) : 1220-7.

(2) Gupte M, John S, Prabhakaran S, Lee VH. Troponin elevation in subarachnoid hemorrhage does not impact in-hospital mortality. Neurocrit Care. 2013 Jun; 18 (3):368-73

(3) Waxman, D.A., et al., A model for troponin I as a quantitative predictor of in-hospital mortality. J Am Coll Cardiol 2006. 48(9): p. 1755-62.

(4) Hirsh J, Warkentin TE, Shaughnessy SG, Anand SS, Halperin JL, Raschke R, et al. Heparin and low-molecular-weight heparin: mechanisms of action, pharmacokinetics, dosing, monitoring, efficacy, and safety. Chest 2001;119(1 Suppl): 64S-94S.

(5) STEPHEN D. WIVIOTT, M.D., and EUGENE BRAUNWALD, M.D., Thrombolysis in Myocardial Infarction Study Group, Brigham and Women’s Hospital, and Harvard Medical School, Boston, Massachusetts. Am Fam Physician. 2004 Aug 1;70(3):525-532.

Amit Kumar, MD and Christopher P. Cannon, MD. Acute Coronary Syndromes:Diagnosis and Management, Part 1. Mayo Clinic Proceedings 2009 October; 84(10):

Maan Jokhadar and Nanette K Wenger. Review of the treatment of acute coronary syndrome in the elderly patients. Clin Interv Aging, 2009; 4:435-444.

Uptodate: Elevated cardiac troponin concentration in the absence of an acutre coronary syndrome.


Uptodate: Elder mistreatment: Abuse, neglect, and financial exploitation.

Intern Report 7.10

Case Presentation by Dr. Lauren Holmquist, MD

Chief Complaint: “I had chest palpitations”

History of Present Illness:
Patient is a 77-year-old female who presents to the Emergency Department after feeling heart palpitations earlier that day at home. She was made a medical code secondary to bradycardia and hypotension. In the resuscitation bay, patient states that she called the ambulance because her heart was racing.  History is somewhat limited due to underlying dementia. The patient has no complaints of dizziness, shortness of breath, chest pain, or abdominal pain. She denies any current chest palpitations.

According to the patient’s daughter, she had complained of feeling lightheaded earlier that day. She said that her mother had three episodes of dizziness and had fainted once while walking to the bathroom. After her fainting episode, EMS was called. The patient’s daughter denied tongue biting or loss of bladder or bowel continence.

Review of Systems:
Constitutional: Denies fevers or chills
Eyes: Denies vision loss
Ears, Nose, Mouth, Throat: Denies earache
Cardiovascular: Positive for history of heart palpitations
Respiratory: Denies cough or shortness of breath
Gastrointestinal: Denies epigastric pain, nausea, vomiting and diarrhea
Genitourinary: Denies dysuria
Musculoskeletal: Denies joint pain
Skin: Denies new rashes
Neurological: Positive for syncopal episode

Past Medical History: Hypertension, atrial fibrillation, diabetes, dementia, kidney disease (no dialysis), and cardiac stents in 1995 status most MI

Past Surgical History: Hysterectomy, cataract surgery

Medications:  Per the patient’s daughter, she takes lopressor 50 mg daily, cardizem 60 mg daily, simvastatin 40 mg daily, procardia 20 mg daily, digoxin 0.125 mg daily, isosorbide mononitrate 30 mg daily, potassium chloride 10 mEq daily, lasix 20 mg daily, seroquel 25 mg daily, aspirin 81 mg daily, clonazepam 0.5 mg daily, ativan 1 mg daily, oxybutynin 5 mg daily, donepezil

Allergies: Penicillin, codeine, shellfish

Social History: Patient denies any alcohol, tobacco, and illicit drug use

Family History: Hypertension

Physical Exam:
General: Patient is alert and oriented x 1 (to herself only). In no apparent distress. Non-toxic appearing. No slurred speech.
Vital signs: Blood pressure 92/40, pulse 57, respirations 16, temperature 36.7, pulse ox 96% on room air
Eyes: Pupils equal, round, and reactive to light. 3mm bilaterally. Extraocular movements intact
Ears, Nose, Throat: Dry mucus membranes
Neck: Supple, no lymphadenopathy, no JVD
Cardiovascular: Bradycardic, regular rhythm, S1 and S2 heard without murmurs. No pitting edema. Palpable and equal pulses in all four extremities.
Respiratory: Lungs clear to auscultation bilaterally. No wheezing or rhonchi heard.
Gastrointestinal: Soft, nondistended, nontender to palpation. No obvious palpable masses.
Musculoskeletal: Spontaneously moving all four extremities
Skin: Warm, dry
Neurologic: Alert and oriented. Speaking coherently. No facial asymmetry, tongue protrudes midline. No dysmetria or dysdiadochokinesia noted.  Muscle strength 4/5 in all four extremities. Sensation to light touch intact throughout entire face and all four extremities.

Labs/Imaging/ED course:

Accu-check: 266

Electrolytes: Na 135, K 5.8, Cl 103, CO2 22, BUN 29, Cr 1.72; Anion gap 10; Ca 9.1, Mg 2.0

CBC: WBC 9.8, Hb 11.2, Hct 36.3, Platelets 273

UA: Negative for infection

Troponin: 0.021

Digoxin level: 2.1

NT-Pro BNP: 5.077

Holm 1

Vent. Rate 42, QRS 82 ms, QT/QTc 458/382 ms
Holm 2

The patient was given a 500 cc fluid bolus.  She was also given insulin, D50 and sodium bicarbonate for treatment of hyperkalemia. A repeat set of vitals included a blood pressure of 83/42 and a heart rate of 42. The patient was transferred back to the module for further work up.


1) For this patient, what is the recommended initial treatment?
a. Calcium
b. Digibind
c. Hemodialysis
d. Transvenous pacing

2) Above what potassium level has been associated with 100% mortality in the untreated patient?
a. >5
b. >5.5
c. >6
d. >6.5

3) There are various other toxic ingestions that can present as hypotension and bradycardia. What is one physical exam finding that would distinguish clonidine overdose from the others?
a. Hyperglycemia
b. Lethargy
c. Miotic pupils
d. Visual disturbances


Answers and Discussion:
1) B
2) B
3) C

Question 1:
The patient in this case presentation is presenting with digoxin toxicity, which is manifested by hypotension, bradycardia, and elevated potassium levels.  This patient has a history of kidney disease and presents with an elevated creatinine; therefore her digoxin toxicity is most likely secondary to dehydration and renal failure, as the kidney eliminates digoxin. The treatment for digoxin poisoning is the administration of digoxin-specific fragment antigen-binding (Fab) antibodies (DigiFab). All other interventions are considered adjunctive. Digibind treatment should be reserved for cases of severe cardiovascular toxicity. In acute toxicity, antibody treatment should be used for a potassium value greater than 5 mEq/L or unstable dysrthmias.  Treatment of digibind is indicated in this patient because her potassium is 5.8 and she has symptomatic bradycardia.

Dose of Digibind (in number of vials): [Level x weight (kg)]/100  **round to nearest vial**

Due to the patient’s hyperkalemia and history of kidney disease, you may have been tempted to give calcium. While calcium administration is indicated in the setting of hyperkalemia to stabilize the cardiac membrane, the administration of calcium in the digoxin-poisoned patient may precipitate “stone heart”, also known as cardiac standstill. The theory of “stone heart” is actually quite controversial. While there is a fear that IV calcium can precipitate life-threatening arrhythmias in the digoxin-toxic patient, the study by Levine M et al concluded that calcium did not seem to cause cardiac standstill or increase mortality. The paper notes that there have only been five case reports of deaths in patients on cardiac glycosides after they had been treated with IV calcium. Digoxin inhibits the sodium-potassium ATPase pump, increasing intracellular sodium and calcium in the myocardium. Since calcium causes myocardial contraction, it is not illogical to believe that increased intracellular levels of the cation would produce irreversible contraction.

Hemodialysis is insufficient in digoxin toxicity because the drug has a large volume of distribution and is mostly protein bound, therefore, will not be removed with HD.

Pacing may be needed temporarily while waiting for Digibind to take effect. There have been reports of successful transcutaneous pacing, however it is generally recommended that transvenous pacing be withheld unless external pacing fails. Digoxin already irritates the myocardium, which may be worsened with the catheter in transvenous pacing.

Question 2:
Hyperkalemia develops in digoxin toxicity due to inhibition of the Na/K ATPase pump, and it is the most important predictor of outcome in the setting of acute digoxin toxicity. The serum potassium level is in fact a better predictor of mortality than the initial digoxin concentration. This was first shown in a classic study by Bismuth, C. before the advent of antidotal therapy using digoxin-specific antibody fragments. In this study of 91 patients primarily with acute digoxin toxicity rather than intentional overdose, nearly 50% of untreated patients with a potassium level between 5-5.5 died. No patients with a potassium level less than 5 died. 100% of patients (all 10 in the study) with potassium exceeding 5.5 died.

Even with Digibind, treatment of severe hyperkalemia with IV glucose, insulin, and sodium bicarbonate should be still done. All of these treatments were given in this particular patient.

Question 3:
Clonidine is a commonly used central alpha-2-adrenergic agonist, used in the management of hypertension. Stimulation of these receptors inhibits the release of peripheral catecholamines, which results in a decrease of heart rate, contractility, and peripheral vascular resistance. While a paradoxical hypertension may occur right after ingestion of clonidine, it ultimately manifest as hypotension and bradycardia, similar to digoxin toxicity. However, unlike digoxin, clonidine also stimulates the same mu receptor as opioids, leading to miotic pupils. This is not seen in digoxin overdose.

Both digoxin and clonidine overdose can cause lethargy. One of the characteristic features of digoxin toxicity is its visual disturbances, including yellow-green chromatopsia (also red, brown, and blue).  Beta-blocker and calcium channel blocker overdoses can also cause hypotension and bradycardia. Beta blocker overdose usually causes hypoglycemia while calcium channel blocker overdose can cause hyperglycemia.

Key Points:

  • Digoxin works by inhibiting the sodium/potassium ATPase pump on the cardiac cell membrane, which leads to increased intracellular calcium and extracellular potassium.
  • Hyperkalemia is biggest predictor of mortality in the acutely digoxin-toxic patient.
  • Digibind is sufficient for treatment of digoxin-induced hyperkalemia. For an exam, never give calcium to these patients, but note the theory of “stone heart” is controversial.
  • Common EKG findings: PVCs, Atrial fibrillation with AV dissociation, Atrial tachycardia with block, Nonparoxysmal junctional tachycardia, Bidirectional ventricular tachycardia
  • Treatment of choice is Digibind FAB. Atropine can be used for bradycardia with high AV block.
  • Chronic digoxin toxicity is often more difficult to diagnose, as symptom onset is more insidious. GI symptoms are less pronounced, whereas neurological manifestations may be more prominent. In chronic digoxin toxicity, hypokalemia is of greater concern.


  1. The Effects of Intravenous Calcium in Patients with Digoxin Toxicity. Levine, M et al. J Emergency Medicine 2011. Jan;40:41-6.
  2. Digitalis (cardiac glycoside) poisoning. Levine, M et al. UpToDate.
  3. Cardiac arrhythmias due to digoxin toxicity. Goldberger, A. UpToDate.
  4. Rosen’s Emergency Medicine, Concepts and Clinical Practice. 8th Edition.

Intern Report 7.9

Case Presentation by Dr. David Viau, MD

CC: Motor Vehicle Crash

A 27 y.o. hispanic female is brought into Marquette, MI ED (a rural emergency department) by EMS as a trauma code on a backboard with a c-collar. The patient was driving on US41 (a small two lane highway) during a blizzard at 60mph when she all of a sudden she lost control of her car. The vehicle was found in the ditch with the front end smashed in by a large tree. Airbags were deployed. The patient was found by EMS standing next to the SUV, leaning on it for support, barely able to hold herself up. She does not remember what happened or if she was wearing a seat belt. She is currently complaining of feeling cold, neck pain and interscapular pain.

Constitutional: Denies fevers
ENT: Denies epistaxis
Cardiovascular: Denies palpitation
Respiratory: Denies shortness of breath
Gastrointestional: Denies vomiting
Genitourinary: Denies hematuria
Musculoskeletal: Denies joint swelling
Integumentary: Denies rash
Neurological: Denies seizures
Psychiatric: Denies auditory or visual hallucinations

PMH: Histoplasmosis (from harvesting bat guano in Mexican caves), typhoid fever
PSH: 1 caesarian section for placenta previa
Social Hx: Patient denies smoking cigarettes and illicit drug use. She admits to EtOH consumption. Denies drink today. Last menstrual cycle 5 weeks ago.
Family HX: Hypertension, dyslipidemia, type 2 diabetes and obesity
Meds: prenatal vitamins
Allergies: Seasonal, Sulfa

Physical Exam:
Temperature: 34, HR 90s, BP 160/90, RR16, Sat 98% on RA
Constitutional: non-obese female immobilized on backboard w/c-collar.
Head and Neck: diffuse tenderness to palpation of the cervical spine.  There are no step-offs or deformities.  There are no raccoon eyes or battle signs present.
Eyes: Pupils are 3 mm round reactive to light bilaterally.  There is a good consensual reaction to light.  No sign of trauma to the eyes.
ENT: There is no hemotympanum present.  No rhinorrhea or bleeding from the naris.  The tongue is not swollen. Patient has a hoarse/raspy voice.
Cardiovascular: There is a normal S1 and S2 without murmur present.  The patient has 2+ pulses in the radial arteries bilaterally. There are 1+ pulses in the femoral arteries bilaterally.
Respiratory: Lung sounds are present bilaterally with appropriate air movement.  There is no wheezing appreciated.
Gastrointestional: Abdomen is soft, nondistended and nontender to palpation.  There is no guarding or rigidity.
Genitourinary: There is no signs of vaginal bleeding.
Musculoskeletal: No obvious deformity is noted in the extremities. Patient has 5/5 muscle strength to in arm flexion and extension, leg flexion and extenstion, dorsiflexion and plantar flexion bilaterally. She can touch thumb to each ringer and is able to resist separation of thumb from fingers appropriately .
Integument: Patient has a small haemostatic laceration on her left cheek. There is a seatbelt sign across the patient’s chest.
Neurological: GCS of 15, Patient is able to stick out tongue and move to both sides.  Uvula is not deviated. Smile and forehead wrinkling is symmetric.  Patient is able to shrug shoulders against resistance.  Patient has sensation in the V1, V2 and V3 distribution of the trigeminal nerve.  Extraocular eye movements are intact.  Patient has normal finger to nose test and normal heel-to-shin test.  There is a negative Babinski bilaterally.

Fast Exam: Did not reveal any intraperitoneal fluid or cardiac tamponade.

CXR: Did not show any acute cardiopulmonary process as per radiology intern.



1.  What is the most sensitive diagnostic modality currently available given this patient’s scenario?
a) CT  Abdomen scan w/contrast
b) Chest x-ray
c) ED thoracotomy
d) Transesophageal echocardiogram
e) CT Chest w/contrast
f) CT head w/without contrast

2.  What is the best management for the patient with their suspected injury?
a) Nitroglycerin
b) Esmolol
c) Amlodipine
d) Dyazide

3. The patient complains of diffuse cervical spine tenderness to palpation. What is the most sensitive modality to detecting an injury?
a) Obtain a complete cervical spine x-ray series plus obliques.
b) CT c-spine
c) Able to use nexus criteria to clear c-spine without imaging.
d) Cervical spine sonography

Answers & Discussion:

1) e
2) b
3) b

1. The patient has an aortic tear secondary to a deceleration injury. Clues to this include the intrascapular pain, hoarse voice (compression of laryngeal nerve and slight compression of trachea, sometimes tracheal deviation will be observed) and decreased femoral pulses. Often the patients are hypertensive secondary to stretching the afferent sympathetic fibers at the isthmus of the aorta that may cause reflex hypertension(Rosen’s p. 452).

Initial diagnostic testing is as simple as a (b) chest x-ray. The big clue is widening of the superior mediastinum (50-90% sensitivity, 10% specificity). However mediastinum widening is not present in everyone with a blunt aortic injury, 7-44% of patients have no mediastinal widening. This implies mediastinal widening should increase our worry of a possible deceleration injury, but can neither confirm or rule out it’s existence. (a) CT scan w/contrast have nearly 100% sensitivity and specificity and are often thought of as better than historical gold standards of Aortogram. It is recommended that all patients with significant mechanism of injury under go a CT scan regardless of findings in the CXR. (d)Transesophageal echocardiogram (TEE) also provides great diagnostic power with a sensitivity of 87-100% (variability secondary to operator skill) and specificity of 98-100%.  Often surgical intervention will be started with TEE results alone.  (c) ED thoracotomy is not indicated here.

CORRECT ANSWER is (e), CT scanner is the most sensitive way to evaluate patients for aortic deceleration injuries..  

2. Management of the aortic rupture includes basic ABCs in the ED. Not all tears lead to immediate exsanguination. Other injuries such as intracranial injury or intra-abdominal hemorrhage may take priority. Strict blood pressure control should be maintained at all time with goal systolic blood pressures ranging from 100-120 mmHg. The goal with the decreased blood pressure is to decrease shearing forces exerted on the aorta. This is done by decreasing the number of pulsatile loads (heart rate) and managing the blood pressure.  (b) Beta blockers are the drugs of choice. Often a short acting titratable Esmolol is used, but lebatolol can be is used too.

Definitive management is surgical intervention either by open technique or utilizing endovascular technique. Patients should have prompt repair of the tear to decrease risk of rupture. However repair can often be delayed if more life threatening circumstances are present.

CORRECT ANSWER is (b) esmolol. (a,c,d) do not decrease heart rate, hence the shear force is not decreased. Rosen’s p.454


(google image)

flow across the vessel wall creates a Force perpendicular to the direction of flow. If the aorta intima has a tear it is liable to rupture through the adventitial layers and hemorrhage. Each pulsatile cycle increases risk.

3. (c)Complete cervical spine x-ray series plus oblique views are able to recognize spinal injuries with high accuracy as long as all seven cervical vertebrae are adequately visualized. They fail to recognize injury in 0.07% of patients with injuries and 0.008% of patients with unstable spinal injury. (Rosen’s p.403). That being said adequate visualization of all 7 cervical vertebrae is not obtainable on up to 25% of patients. Obesity is a risk factor for inadequate visualization of all 7 vertebrae.  The question needs rework.  I would get cross table lateral and transfer.

Often EM physicians lean on the (b) CT cervical scan too much to clear a c-spine, especially if the patients body habitus lends to easy x-ray visualization of all cervical vertebrae. That being said CT scans are superior to x-rays in the 25% of patients that we are unable to get adequate visualization of all cervical vertebrae. The sensitivity for CT to detect fractures varies according to studies, but generally has a sensitivity around 99.3-100%.

Other considerations are cost CT $4386 verses x-rays $513 and radiation exposure CT 26 mSv verses 4 mSv.

(c) Not accurate. The patient has cervical tenderness. Nexus criteria can be employed only if patient is non-tender. (d) this answer makes no sense, ultrasound is not used to detect injuries to the cervical spine.

Correct answer is (b). CT scan is the most sensitive way to detect c-spine injuries. That being said complete cervical spine X-ray series are appropriate and sufficient in many patients. X-rays have the advantage of being cheaper, less radiation and readily available. That being said there is 25% of the patient population who do not have adequate visualization of the cervical spine. These patients often being obese

Rosen’s Emergency Medicine 8th edition.
Google image search for blood vessel image

Intern Report 7.8

Case Presentation by Dr. Jessie Swan, MD

History of Present Illness:
A 62-year-old African American male  was brought to the Emergency Department by EMS after being found lying on the ground inside an abandoned house.  His friends had called EMS because he had been lying in the same spot for the past three days.  Per EMS there were no pill bottles or alcohol bottles around the patient.  The outdoor temperature  was in the 20s and EMS states that the house was not heated;  actually it felt colder inside the building than outdoors.  You  were unable to obtain any other history from the patient as he is only able to mumble incoherently.

Past Medical History (per EMR):

Social history (per EMR):
-Denied tobacco, alcohol or other drugs

Medication (per EMR):
-Norvasc 5mg daily

Physical Exam:
Vitals: BP 94/64, P 67, RR 14, T 28.4 °Celsius rectal, oxygen  saturation unable to obtain.
GENERAL:  He is lying in bed and  appeared  disheveled.  Dressed in only one layer of long underwear under jeans and a jacket.  He mumbled incoherently in response to stimuli.

HEAD:  Without evidence of trauma.

EYES:  Pupils are 3 mm, round and nonreactive to light bilaterally.

EARS, NOSE, MOUTH, AND THROAT:  Throat was clear.  Mucous membranes appear to be dry.

NECK:  Trachea midline.

RESPIRATORY:  Lungs revealed clear breath sounds bilaterally.

CARDIOVASCULAR:  The patient had a heart rate of 67 beats/minute and rhythm was regular.  He had faint palpable pulses in his wrist and feet bilaterally.

GASTROINTESTINAL:  Abdomen is soft, nondistended, nontender to palpation.  No palpable masses.

EXTREMITIES:  No edema.  He had cyanosis of his feet bilaterally.

SKIN:  Extremely cold to the touch without evidence of skin rash.  He had some previous signs of skin grafting and scarring in his right upper chest wall.

NEUROLOGIC:  He had spontaneous eye opening.  He did appear to follow some simple commands, He could not provide any further information.  Patient was not flaccid however was weak in the upper and lower extremities.  Localized to painful stimuli.

Labs / Imaging / ED course:
Na 132, K 3.8, Cl 86, Bicarb 5, BUN 58, Cr 3.09, Glucose 74, Anion gap 41
WBC 7.3, Hgb 13.5, Platelet 186, MCV 96.3
CPK 3932, Lactic Acid 10.9, Trop 0.247, EtOH 283

ABG: pH 6.84PCO2 19.0PO2 6.9HCO3 2.0

U/A neg

CXR: Patchy multifocal airspace opacities noted bilaterally concerning for multifocal pneumonia and/or aspiration pneumonia.

EKG: Difficult to interpret due to wavy baseline with pt shivering.  QTc was 599.
ECG 7.8

The patient was covered with warm blankets and fluid resuscitated with a total of warmed 3L 0.9% NS. A femoral central line was placed using a Zoll triple-lumen central line femoral vein catheter and central rewarming was initiated.  Patient was also started on Azithromycin and Ceftriaxone, given 2 Amps NaHCO3, and given a rectal aspirin.  He was admitted to the MICU.

1.  What is the acid/base disturbance?
a.  Primary: non anion gap metabolic acidosis. Secondary: respiratory alkalosis
b.  Primary: anion gap metabolic acidosis. Secondary: respiratory acidosis
c.  Primary: anion gap metabolic acidosis. Secondary: respiratory alkalosis
d.  Primary: non anion gap metabolic acidosis. Secondary: respiratory acidosis.

2.  All of the following are common physiologic EKG findings associated with hypothermia EXCEPT?
a.  Bradycardia
b.  Atrial fibrillation
c.  J waves
d.  Ventricular fibrillation

3.  Under what circumstance is further intervention generally considered futile?
a.  A potassium level >12mmol/L
b.  After 2 hours of CPR
c.  When the patient presents initially without signs of life and absent vital signs.
d.  When, after rescue and initial intervention, the patient’s core temperature continues to drop.

Answers & Discussion:
1. B
Primary metabolic acidosis, with increased anion gap, mixed with a metabolic alkalosis, with superimposed respiratory acidosis

First: pH is 6.84 which is an acidosis

Second: pCO2 is low at 19, Bicarb is low at 2.0 so this is a primary metabolic acidosis

Third: Winters Formula PCO2=1.5(HCO3)+8±2; PCO2=9to13; actual CO2 is higher at 19 so there is a secondary respiratory acidosis

Fourth: Anion Gap=Na-(Cl+HCO3); Anion Gap=41; the anion gap is >12 so this is an anion gap metabolic acidosis

EXTRA: Fifth: Delta Gap=(AG-12)-(24-HCO3); Delta Gap=10; the delta gap is >6 so this represents an anion gap metabolic acidosis with a mixed metabolic alkalosis.

2. D
A. At a core temperature of 28 degrees Celsius oxygen consumption and the pulse rate are usually decreased by 50%.

B. Atrial fibrillation is common when the core temperature is less than 32 degrees Celsius and is generally not worrisome in the absence of other signs of cardiac instability.  It rarely leads to a ventricular response.

C. J waves (Osborne waves) appear secondary to an exaggerated outward potassium current leading to a repolarization abnormality. These waves are detectable in 80% of the patients with a core body temperature lower than 30°C. J waves are seen in lead II and precordial leads V2-V6.

D. Ventricular findings are serious when seen in hypothermic patients.  Ventricular arrhythmias are very difficult to correct in these patients and often result in asystole.

3.  A
A.  A severely elevated serum potassium level is associated with nonsurvival.  It is an indication of hypoxia before cooling.  If the serum potassium level is higher than 12mmol/L termination of CPR should be considered.  The highest recorded levels of serum potassium in patients with hypothermia who were successfully resuscitated are 11.8 in children and 7.9 in adults.  At a level between 10 and 12 it is recommended that consideration of ECMO or CPB should be made. A level below 10 should prompt continued CPR until the patient is rewarmed as survival without neurologic impairment may be possible

B.  The longest reported duration of CPR in a hypothermic patient who subsequently achieved full neurologic recovery is 190 minutes in a patient receiving extracorporeal rewarming.

C.  Stage HT IV of the Swiss staging system is characterized by a core temperature of <24ºC with no vital signs.  In these patients appropriate treatment includes active external and minimally invasive rewarming techniques, airway management as required, ECMO or CPB if cardiac instability is refractory to medical management, plus CPR with up to three doses of epinephrine and defibrillation with further dosing guided by clinical response.

D.  A drop in temperature, indicating continued core cooling after rescue, is a documented phenomena.  This may also be the result of discrepancies between different methods of temperature measurement.

Intern Report 7.6

Case Presentation by Dr. Megan Wolf, MD

An 86-year-old female presents with 3 weeks of gradually worsening diffuse dull constant abdominal pain.  Her abdominal pain is exacerbated by movement and is not relieved by any particular factors.  It does not radiate anywhere. She has also had decreased appetite and multiple episodes of nonbloody emesis. She has not had a bowel movement in 3 days.

Constitutional: Denies fevers or chills. Reports weight loss.
Cardiovascular: Denies chest pain.
Respiratory: Reports shortness of breath.
Gastrointestinal: Denies diarrhea or blood in the stool.

PAST MEDICAL HISTORY: hypertension, diabetes, cholelithiasis

PAST SURGICAL HISTORY: cholecystectomy


ALLERGIES: No known drug allergies

SOCIAL HISTORY: Denies alcohol, tobacco, and drug use.

Vitals: BP 94/53, HR 87, RR 24, T 36.2, SpO2 100% on room air
General: Overweight elderly female who appears uncomfortable.
Head:  Atraumatic, normocephalic.
Eyes:  No conjunctival pallor. No scleral icterus.  Pupils equal, round and reactive to light.  Extraocular movements intact.
Nose, Mouth, Throat: Moist mucous membranes.  Uvula midline.
Neck:  Trachea midline.  No jugular venous distension.
Respiratory: Tachypneic. Clear breath sounds bilaterally.  No rales, wheezing, or rhonchi.
Cardiovascular:  Regular rate and rhythm with no murmurs, rubs, or gallops.
Gastrointestinal:  Abdomen is markedly distended and tense. Significant dullness to percussion.  A fluid wave is noted. Tenderness to palpation diffusely throughout the entire abdomen.  Bowel sounds are present.  No organomegaly.
Extremities: 2+ pulses in all extremities.  No lower extremity edema.
Skin: Warm and well perfused. No rashes. No jaundice. No spider angiomata or palmar erythema.
Neurologic: Alert and appropriate.  Answers questions and follows commands.  No asterixis.

Na 129, K 3.9, Cl 93, CO2 27, BUN 14, Cr 0.96, Glu 106, Ca 8.6

ALT 15, AST 23, Alk Phos 131, Total bilirubin 0.5, Direct bilirubin 0.1

Amylase 41, Lipase 145, Albumin 2.3

WBC 6.8, Hb 9.2, Hct 28.9, Plt 583, MCV 72.6

APTT 30.4, PT 11.4, INR 1.06

Bedside ultrasound of the abdomen reveals significant free fluid in Morrison’s pouch.  A diagnostic and therapeutic paracentesis is performed, resulting in immediate return of cloudy yellow fluid. Four liters of peritoneal fluid are removed.  The patient’s discomfort is significantly relieved and her respiratory rate returns to normal. The peritoneal fluid is sent for analysis.


#1 Which of the following is a contraindication to performing paracentesis?
a) pregnancy
b) disseminated intravascular coagulation
c) prolonged prothrombin time
d) thrombocytopenia

#2 Which of the following tests of the peritoneal fluid would be most helpful in determining the cause of the ascites?
a) pH
b) lactate
c) cholesterol
d) albumin

#3 The peritoneal fluid is analyzed and is positive for malignant cells. You suspect ovarian carcinoma. Which of the following serum tumor markers is associated with ovarian carcinoma?
a) CA-125
b) S-100
c) alpha fetoprotein
d) CEA

Answers & Discussion:

#1 Answer: b. disseminated intravascular coagulation
Many patients undergoing paracentesis have a prolonged prothrombin time or thrombocytopenia as a result of hepatic disease. These are not considered contraindications to performing paracentesis as the incidence of clinically significant bleeding complications in these patients is low.  In a retrospective study of over 4500 paracenteses, severe hemorrhage occurred in <0.2% of cases.  Although paracentesis should be performed with caution in pregnant patients, pregnancy is not a contraindication to paracentesis.

The indications for abdominal paracentesis include the evaluation of new onset ascites, the evaluation of a patient with existing ascites who is being admitted to the hospital for any reason, and the evaluation of a patient with ascites who has signs of clinical deterioration (fever, abdominal pain, hepatic encephalopathy, peripheral leukocytosis, decline in renal function, or metabolic acidosis).

The following are relative contraindications to paracentesis: disseminated intravascular coagulation, primary fibrinolysis, and massive ileus with bowel distension (unless the paracentesis is performed under ultrasound guidance).  If there are surgical scars present on the abdomen, then the needle should be inserted several centimeters away from the scars because the bowel may be adherent to the peritoneal wall at the site of the scar.

#2 Answer: d. albumin
The serum-ascites albumin gradient (SAAG) is equal to the serum albumin level minus the ascitic fluid albumin level.  In this case, the ascitic fluid albumin level is 2.6, so the SAAG is 2.3 – 2.6 = -0.3.  Etiologies of ascites that are related to portal hypertension will have a SAAG >1.1 and these include presinusoidal causes (splenic or portal vein thrombosis, schistosomiasis), sinusoidal causes (cirrhosis), and postsinusoidal causes (right heart failure, constrictive pericarditis, Budd-Chiari syndrome).   Etiologies of ascites that are not related to portal hypertension will have a SAAG <1.1 and these include nephrotic syndrome, tuberculosis, and malignancy with peritoneal carcinomatosis such as ovarian carcinoma. In this patient, the SAAG is <1.1, indicating that the ascites is not related to portal hypertension.

#3 Answer: a. CA-125
The presence of malignant cells in the peritoneal fluid suggests peritoneal carcinomatosis, which is typically caused by secondary peritoneal surface malignancies (ovarian, colorectal, pancreatic, uterine) or extra-abdominal tumors (lymphoma, lung, breast). Malignant ascites is a poor prognostic sign.  Tumor markers are not used as a primary means of diagnosing malignancy, but in a patient with evidence of malignancy, such as malignant cells present in ascites, tumor markers can help in identifying the site of the primary. Currently CA-125 is approved by the FDA only for monitoring response to therapy in women with known epithelial ovarian carcinoma. With regard to diagnosing ovarian carcinoma in postmenopausal women, elevated serum CA-125 has a sensitivity for ovarian cancer of 69-87% and has a specificity for ovarian cancer of 81-93%.  In this patient, the CT thorax/abdomen/pelvis revealed nodular changes of the pleura and peritoneum that possibly related to a metastatic process, but did not reveal a primary tumor.  We did obtain a CA-125 level for this patient which was markedly elevated, and although it is not specific for ovarian carcinoma, it did provide guidance for what type of further imaging to pursue.  In this case we obtained a pelvic ultrasound to attempt to better visualize the ovaries.

When a patient presents to the ED with new onset ascites, two of the main questions you need to answer are whether the fluid is infected and whether the ascites is related to portal hypertension.  Routine tests that should be ordered on all ascitic fluid include cell count and differential, albumin, and total protein.

The results of the cell count and differential will indicate whether the fluid is infected. While a fluid culture may take hours to days to return, a cell count should be available much earlier, allowing for early detection of infection and initiation of antibiotic therapy. You should consider starting antibiotics in any patient whose ascitic fluid corrected neutrophil count is greater than or equal to 250/mm3. One WBC should be subtracted from the WBC count for every 750 RBCs to reveal to corrected WBC count.  One neutrophil should be subtracted from the absolute neutrophil count for every 250 RBCs to reveal the corrected neutrophil count.

It is crucial not to miss spontaneous bacterial peritonitis in a patient with ascites who presents to the ED since shock and multi-system organ failure may occur rapidly if antibiotics are not promptly initiated. Patients with spontaneous bacterial peritonitis often present with fever, altered mental status, and diffuse abdominal pain. They may have lab findings including leukocytosis, metabolic acidosis, and azotemia.

As discussed above, the albumin level in the ascitic fluid, along with the serum albumin level, will allow you to calculate the serum-ascites albumin gradient and determine whether the fluid is related to portal hypertension or not.

If the total protein level in the ascitic fluid is greater than or equal to 2.5 g/dL, it is classified as an exudate. If it is less than 2.5, then it is a transudate.

Other tests that you should consider ordering for ascitic fluid include culture, glucose, lactate dehydrogenase, gram stain, and amylase.

Key Points:

  • Consider paracentesis in any patient with new onset ascites or in any patient with existing ascites who is being admitted or exhibits signs of clinical deterioration.
  • When you send ascitic fluid for analysis, always order cell count and differential, albumin, and total protein.
  • Start antibiotics early if the corrected neutrophil count suggests spontaneous bacterial peritonitis.
  • Calculate the serum-ascites albumin gradient to determine whether the ascites is related to portal hypertension or not

Runyon BA et al. Ascitic fluid pH and lactate: insensitive and nonspecific tests in detecting ascitic fluid infection. 1991. Hepatology 13(5):929.

Runyon BA. Malignancy-related ascites and ascitic fluid ‘humoral tests of malignancy.’ 1994 J Clin Gastroenterol. 18(2):94.

Runyon BA. Evaluation of adults with ascites. UptoDate. 2013.

Sangisetty SL et al. Malignant ascites: a review of prognostic factors, pathophysiology, and therapeutic measures.  2012. World Journal of Gastrointestinal Surgery. 4(4): 87-95.

Thomsen TW et al. Paracentesis. 2006. New England Journal of Medicine 355:e21.

Intern Report 7.5

Case Presentation by Dr. Sean Teshima McCormick, MD

The patient is a 74 year old male with a history of HTN, HLD who reports to the emergency department complaining of vision loss in his right eye 2 hours prior to presentation. The patient reports that he was sitting on his couch watching TV when it looked like someone was “turning down a dimmer switch” on the vision in his right eye. After a few seconds, it went completely black. He denies any pain at the time or currently. He denies any trauma. He denies seeing flashing lights, floating specs or cobwebs in his vision. He denies seeing anything that looked like a curtain coming over his vision. He reports no changes in his left eye. He denies any headaches, dizziness, focal numbness or weakness.

Reports changes in his vision as described above
Denies fever, headache, chest pain, shortness of breath, N/V, diarrhea, constipation, dysuria, bleeding problems, new rashes

PSH: Left knee
Medications: HCTZ, simvastatin
Allergies: NKDA
SH: reports 1 pack per day tobacco use, reports occ alcohol use, denies any illegal drugs

Physical exam:
BP: 170/ 110 HR: 64 RR: 18 T: 37.0  Spo2: 99%
General: well-appearing thin man in no acute distress
Eyes: right pupil is round, shows afferent pupillary defect, left pupil is round and reactive, EOM intact bilaterally, painless, visual acuity is hand motion only right side, 20/40 on left, loss of confrontation fields on right eye, no conjuctival hemorrhage bilaterally, no signs of trauma
Cardiovascular: RRR, normal s1, s2
Respiratory: CTAB, no wheezes, crackles
Gastrointestinal:  abdomen soft, non-tender, non-distended, no organomegaly
Neurological: APD noted on right pupil, other CN intact, strength 5/5 bilaterally in upper and lower extremities, no sensory deficits
Musculoskeletal: no lower extremity edema
Skin: no rashes seen


1) Based on the history and physical examination, what is the most likely diagnosis?
a) Retinal Detachment
b) Vitreous Hemorrhage
c) Amaurosis Fugax
d) Central Retinal Artery Occlusion
e) Pituitary tumor

2) What would you expect to see on fundoscopic exam?



3) Which diagnostic test should be ordered immediately?
a) Ocular Ultrasound
b) MRI Head and Brain
c) Carotid Duplex
d) Fluorescein Stain
e) Optical Coherence Tomography


Answers and Discussion:

1) D. Central Retinal Artery Occlusion.
CRAO causes sudden painless monocular vision loss. Patients often describe the vison loss as someone slowly dimming their vision until it is completely black. These patients will only be able to see hand motions out of the affected eye and will have an afferent pupillary defect. The most common risk factors for CRAO are HTN, HLD and smoking. Patients with a retinal detachment can also experience a sudden painless monocular vision loss. However, these patients will often describe flashing lights and floating specs, thought to be caused by nonspecific stimulation of the retina as it detatches. They will describe their visual field as obscured by a moving curtain. They should still have parts of their visual field intact. Patients with vitreous hemorrhage will decribe their vison as seeing “cobwebs.” This is usually a progression of diabetic disease or the result of trauma. Amaurosis fugax is by definition a transient phenomenon and often is resolved by the time the patient presents to a healthcare professional. Pituitary tumor will cause a bitemporal hemianopsia, not a monocular vision loss.

2) B.
CRAO is caused by the occulsion of  the central retinal artery, which supplies the portion of the retina responsible for central vision. In this image, since the artery is occluded, the central retina is pale. A “cherry red spot”  is seen at the macula. This occurs because the retina is thinner at the macula and the retinal pigment and choroid vessels can be seen. Additionaly, some people have addional blood supply to the macula that may result in a small area of preserved vision known as macular sparing. Image A is a branch retinal artery occlusion. Here you can see the area of pallor is confined to smaller distribution in the inferior portion of the retina instead of the entire central vision. Image C is a retinal detachment. Image D is a vitreous hemorhage. Image E is a normal retina. In contrast to image B, here you can see good blood supply to the central retina.

3) C. Carotid Duplex
The most common cause of CRAO is ipsilateral carotid artery athlerosclerosis. Since these patients are at risk of stroke, carotid duplex must be ordered emergently. Cardiogenic embolism is the second most common cause so an EKG should also be ordered. An echocardiogram should be considered if there are significant risk factrors. Risk factors for cardiogenic source include atrial fibrillation, endocarditis, valvular disease, MI, IVDA. An ocular ultrasound would aid in the diagnosis of retinal detachment. An MRI would aid in the diagnosis of intracranial mass. A fluorescein stain would aid in the diagnosis of corneal abrasion. OCT would aid in the diagnosis of macular degneration, macular edema and epiretinal membrane.

CRAO will present as sudden painless monocular vision loss that patients describe as “dimming” of their vision. This is an emergency due to the risk of stroke. Patients with HTN, HLD and smoking are at greater risk. On physical exam, patients will have an APD in the affected eye and will often only be able to make out hand movements. Diagnosis is made by fundoscopic examination which reveals a pale central retina often with macular sparing which appears as a “cherry red spot.” Since carotid artery atherosclerosis and cardiogenic emboli are the most common etiologies, there is concern for cerebral vascular accident. A work up should include carodtid duplex and EKG, and possibly an echocardiogram. 10-15% of CRAO are associated with giant cell arteritits so a CRP and ESR should also be ordered. Vasculitis, sickle cell disease and hypercoagulable states are less common causes. Therefore, hematologic and coagulation studies should also be considered. Currently there is no standard treatment, however several therapies have been associated with better outcomes. Ocular massage and anti-platelet therapy may be initiated to help restore blood flow. Hyperbaric oxygen therapy has also been shown to improve outcomes in CRAO and Detroit Receiving Hospital is a hyperbaric referral center. Other experimental therapies include thrombolytics, mannitol to decrease intraocular pressure and nitroglycerin to increase bloodflow.

Intern Report 7.3

Case Presentation by Dr. Jeffrey Van Laere, MD

HPI: 5 year-old girl with who presents to the emergency department as a transfer from an outside hospital with abdominal pain and diarrhea for 2 days. The patient reports worsening abdominal pain, which she describes as 6/10, diffuse, but worse in the right lower quadrant. She also reports “nearly constant” diarrhea that is non-bloody and watery. Patient states that she feels nauseous, but has had no vomiting.

Negative for fever, vomiting, chest pain, shortness of breath, hematochezia.
Positive for diarrhea, abdominal pain, nausea.

PMH: None
PSH: Tonsillectomy and Adenoidectomy
Medications: None
Social History: Immunizations up to date. Grandmother with recent illness, lives in nursing home.

Physical Exam
Vitals: P 126  BP 112/64  RR 18  T 37.4  O2 98%
General: Well developed, well nourished female, lying still, appears uncomfortable.
HEENT: Dry mucosal membranes, no mucosal lesions, EOMI, PEERL
Resp: CTAB
CV: Tachycardic, RRR, no M/G/R
GI: Soft, Mild diffuse tenderness. Negative Murphy’s sign and pain at McBurny’s point. No hepatosplenomegaly.
MS: Full range of motion in extremities, no clubbing, cyanosis or edema.
Neuro: AAOx4, normal reflexes in biceps, triceps and Achilles tendons. Light touch sensation intact.

Na: 137
K:  4.7
Cl: 103
CO2:  25
BUN: 32.4
Cr: 2.6
Gluc: 87

WBC: 37.2
Hgb: 9.2
Hct: 27.6
Plt: 23

LDH: 1286

7.4 pic

Question #1: After reviewing the patient’s laboratory values, you return to discuss the results with the family. What do you think is the most likely diagnosis?
A) Thrombotic Thrombocytopenic Purpura
B) Hemolytic Uremic Syndrome
C) Clostridium difficile Infection
D) Appendicitis

Question #2: After discussing the diagnosis with the family, they are concerned and ask what the next step is in treating this?
A)  Platelet transfusion
B) Start IV fluids and IV antibiotics
C) Supportive care
D) Consult General Surgery

Question #3: After discussion of the treatment plan with the family, they are comforted by knowledge of this disease.  You discuss the concerns you have for this patient. What is the most serious complication of this disease?
A) Renal Failure
B) Dehydration
C) Arthritis
D) Bleeding

Answers & Discussion

1) Answer:  B – Hemolytic Uremic Syndrome
Hemolytic Uremic Syndrome is a multi-system disorder resulting in acute renal failure, thrombocytopenia, and microangiopathic hemolytic anemia.  The differential diagnosis for HUS includes TTP, DIC, appendicitis, gastroenteritis, and SLE. HUS and TTP share microangiopathic hemolysis, renal failure, and thrombocytopenia, however TTP will include a history of being febrile and neurologic changes in 40% of cases. While the patient may have symptoms of an infectious diarrhea, c difficile is an extremely rare cause of HUS. Appendicitis is a common cause of abdominal pain and leukocytosis, however this does not account for the patient’s thrombocytopenia, presence of schistocytes on peripheral smear, and elevated LDH.

2) Answer: C – Supportive care
While HUS is often associated with an infectious diarrhea, use of antibiotics for treatment is contraindicated, as it will increase the risk of development of HUS. Transfusion of platelets is contraindicated, as the thrombocytopenia is seen secondary to a consumptive process. Platelet transfusion will only exacerbate the underlying condition. As this is an infective process, there are no surgical indications, thus no need for a surgical consult.

3) Answer: A – Renal Failure
The pathogenesis of HUS includes the development of microthrombi that will migrate to the kidneys and deposit in the parenchema of the kidney. This will cause acute renal failure. These patients may develop hypertension, peripheral edema, oliguria or anuria. It is recommended to follow the patient’s renal function closely, as dialysis may be necessary. Dehydration is common in any diarrheal illness, but the majority of patients will survive the acute phase of the illness. Long term, up to one third of patients will have mild chronic kidney dysfunction. Many patients will develop purpura secondary to thrombocytopenia, however bleeding is not known to be a common cause of mortality in HUS. Arthritis is not associated with HUS.


Hemolytic-Uremic Syndrome is one of the most common causes of acute renal failure in children. It commonly presents early in life, with a mean age of presentation being 3 years old, but it may present later into childhood. The most common cause of HUS is E. coli O157:H7, however it may also be caused by Shigella, S. pneumonia, Pseudomonas, HIV, or as a result of medications.

Patients will often present early with watery diarrhea, abdominal pain, and possibly fever. As the disease develops, approximately day 2-5, the patients may develop bloody diarrhea. After the initial course of gastroenteritis, the patients will later develop the triad of thrombocytopenia, hemolytic anemia, and acute renal insufficiency.

The pathophysiology of HUS stems from injury to the renal vascular endothelium. There is an initial injury to the endothelium, followed by deposition of complement, platelets, and fibrin. This deposition will cause narrowed renal vessels that will cause injury to RBCs and the microangiopathic hemolytic anemia. The result of this hemolysis will be seen through elevated LDH, as well as schistocytes, tear drop cells, and burr cells on peripheral smear.

As previously discussed, the most important aspects of treatment are supportive therapy and early peritoneal dialysis. Given the patient’s acute renal insufficiency and diarrhea, you should rehydrate the patient, but be cautious to avoid fluid overloading.  It is also important to follow the patient’s hyperkalemia and treat appropriately. Although these patients are often anemic, pRBCs are usually held until hemoglobin falls below 6 g/dL, and platelets are avoided unless life-threatening bleeding or procedures are necessary. Although there have been no studies, it is currently recommended that antibiotics be avoided due to concern for verotoxin release and worsening symptoms with administration.  An important distinction in treatment between TTP and HUS is that plasmapheresis is used with TTP, and may be used with suspected HUS that exhibits neurologic involvement.

Recommended Reading
Rosen, P., Marx, J. A. (2014). Chapter 122. Disorders of Hemostasis. p. 1609-1612 Rosen’s emergency medicine: Concepts and clinical practice

Rosen, P., Marx, J. A. (2014). Chapter 174. Genitourinary and Renal Tract Disorders. p. 2222-2223 Rosen’s emergency medicine: Concepts and clinical practice.

Fauci, A. S., & Harrison, T. R. (2012). Harrison’s online: Featuring the complete contents of Harrison’s Principles of internal medicine, 18th edition. Chapter 115. Disorders of Platelets and Vessel Wall. New York: McGraw-Hill, Medical Pub. Division.

Intern Report 7.2

Case Presentation by Dr. Hannah Ferenchick, MD

Chief complaint: “My lip is swollen”

A 34-year-old man presents to the ED for lip swelling that has been present for several hours. The patient states that at work earlier today he was removing a car bumper. It came loose and popped up and hit the patient in the lip. At the time, the patient had no bleeding or pain in the area. However, 1-2 hours after this, the patient stated that his lip became irritated and then swollen. Patient states that for the last few hours his lip has stayed swollen. Patient denies pain in this area, trouble swallowing or trouble breathing. The patient states that for the last few months he has had periodic issues with swelling. He states he has swelling randomly occur on his side and under his arms. In addition, he has occasional scrotal swelling. These areas of swelling are self resolving. He has a history of hypertension, for which he previously was on lisinopril. However, his PCP switched him to amlodipine since these swelling episodes began. Patient denies any recent fevers, chills, chest pain, shortness of breath, abdominal pain, diarrhea, constipation, dysuria, penile discharge, headache, increased urination or thirst, hives or urticaria.

ROS: negative except as noted per HPI

PMH: Hx of hypertension
PSH: negative
Meds: Amlodipine 5 mg BID
Allergies: No known medication allergies
FH: Hypertension
SH: Drinks alcohol socially, denies cigarette smoking and illicit drug use

PE: vitals: T 98.7, HR 78, BP 156/89, RR 18, pulse ox 100% RA, weight 241, 5’ 9’’
General: Well-appearing, overweight male, appropriate for stated age, resting in bed comfortably, no acute distress
HEENT: Normocephalic, atraumatic. PERRLA. No erythema or exudates in posterior oropharynx. Patient’s upper lip is swollen and edematous, no erythema noted. No abrasions, lesions or urticaria noted. Tongue is non edematous, Mallampati grade II. No tracheal deviation or neck masses.
Cardio: RRR, S1 and S2 heard, no murmurs
Respiratory: Lungs clear to auscultation bilaterally
Abdomen: Soft, non tender, non distended. Positive bowel sounds
Musculoskeletal: +2 radial and DP pulses bilaterally. No pitting edema in lower extremities.
Skin: No rashes, hives or lesions noted
Neuro: Alert and orientated X3



1. Which of the following is the most likely diagnosis?
A. Allergic angioedema
B. Drug-induced angioedema
C. Hereditary angioedema
D. Idiopathic angioedema

2. Which of the following is considered an indication for screening for c1 inhibitor disorders?
A. Recurrent angioedema with urticaria
B. Recurrent unexplained episodes of colicky abdominal pain
C. History of angioedema with ACE-inhibitor use
D. History of refractory anaphylaxis

3. First line treatment of acute attacks of angioedema in adults with known c1-inhibitor deficiency includes which of the following?
A. 0.5 mg epipinephrine IM
B.  Ranitidine 50 mg IV
C. C1-esterase inhibitor (Berinert®) 20 units/ kg
D. 2 units fresh frozen plasma

Answers and Discussion

1)  The answer is C. The patient is having angioedema without related symptoms of a hypersensitivity reaction. Therefore, the most likely cause is a C1 inhibitor deficiency disorder, either hereditary angioedema or acquired C1 inhibitor deficiency (which is very rare and most commonly associated with lymphoproliferative disorders).

The patient has no signs of hypersensitivity reaction such as urticaria, wheezing or hypotension. Therefore, this is not likely due to an allergic-type reaction. The patient was taking lisinopril, which is known to cause angioedema due to the inhibition of ACE, and subsequent increased production of bradykinin. However, the patient stopped his ACE-I and continued to have symptoms which makes this diagnosis less likely. Finally, idiopathic angioedema is a diagnosis of exclusion.

2) The answer is B. GI attacks in hereditary angioedema (HAE) present as intermittent episodes of GI colic, nausea, vomiting and diarrhea. These symptoms result from bowel wall edema. GI attacks are experienced by most patients with HAE and may be the only presenting symptoms in up to ¼th of these patients. The presence of urticaria is associated with allergic angioedema, which is caused by hypersensitivity reactions. These are triggered by common allergens and rarely physical stimuli such as trauma or temperature changes. The inhibition of angiotensin-converting enzyme by ACE-inhibitors results in decreased metabolism of substance P and bradykinin, which contributes to tissue inflammation and can lead to angioedema. These patients often tolerate ARBs well. Refractory anaphylactic shock may require a continuous infusion of epipinephrine in the treatment if intramuscular epipinephine and volume expansion with normal saline have not succeeded in normalizing vital signs. However, it is not an indication for HAE screening.

 3) The answer is C. Cinryze and berinert are C1 inhibitor concentrates derived from plasma. They are among first line therapies for C1 inhibitor deficiency angioedema. Other medications that are also considered first line include icatibant, which is a synthetic bradykinin receptor antagonist and ecallantide, a recombinant plasma kallikrein inhibitor that blocks the production of bradykinin by inhibiting plasma kallikrein. It is approved in US for treatment of acute attacks of HAE in patients 16 yrs and older. Cinreyze is technically not FDA approved for acute angioedema attacks, but is being has been used in Europe with success. IM epinephrine is typically not thought to be helpful in C1-inhibitor deficiency cases. It does not address the known pathophysiologic mechanism of underlying C1ID, although it may help decrease mucosal edema. It is considered first line in the treatment of allergic angioedema. H2 antihistamines are indicated in the treatment of allergic angioedema. Finally, FFP has c1 inhibitor and has been reported to be effective in acute attacks. It is considered 2nd line in treatment of HAE, to be used when first line medications are not available.

The differential diagnosis for this patient includes allergic reaction/anaphylaxis, drug-induced angioedema, allergic contact dermatitis, hereditary angioedema, acquired C1-esterase deficiency angioedema and idiopathic angioedema. Allergic reactions and anaphylaxis often present with systemic symptoms involving multiple organ systems simultaneously, such as wheezing, urticaria, and hypotension. The patient does not exhibit any of these, which makes this diagnosis unlikely. Drug induced angioedema is associated with ACE-inhibitors and NSAIDs. However, the patient had stopped his ACE-inhibitor without resolution of his angioedema. Allergic contact dermatitis often presents as erythematous, scaly plaques and occurs in association with cosmetic and topical pharmaceuticals. Idiopathic angioedema is a diagnosis of exclusion and therefore not appropriate in this case. The most likely cause of this patient’s presentation is a bradykinin-induced angioedema, either hereditary angioedema or acquired C1-esterase deficiency.

Angioedema results from vasodilation and edema of the deeper dermal and subcutaneous layers of the skin. The skin may appear normal color or pink due to the swelling being located in deeper layers of the skin. Angioedema may cause pain and is not necessarily associated with pruritus. The majority of angioedema is caused by hypersensitivity reactions commonly triggered by allergens, referred to as allergic angioedema (or mast cell mediated angioedema). Mast-cell mediated angioedema often presents with other systemic signs of mast cell mediator release: urticaria, pruritus, bronchospasm, and hypotension. The patient had none of these symptoms; therefore the most likely cause of this patient’s presentation is a bradykinin-induced angioedema. These are nonallergic types of angioedema and are caused by bradykinin excess. The distinction between mast-cell mediated angioedema and bradykinin induced angioedema is crucial for treatment and management of the disease. The causes of bradykinin-induced angioedema include hereditary angioedema (HAE), acquired C1 inhibitor deficiency and ACE inhibitors. In the case of HAE and ACID, the deficiency of C1 inhibitor results in increased bradykinin levels. These types of angioedema do not respond to the typical treatments for allergic hypersensitivity reactions such as steroids, antihistamines and IM epipinephrine. As always, early airway stabilization is key in management.

Although this patient was not currently demonstrating any signs of airway compromise, ENT was consulted in the emergency department.  They did a bedside bronchoscopy, which showed some signs of edema at the base of the tongue. Therefore, they recommended that the patient be observed in the ICU for 24 hours, with a low threshold for intubation and cricothyroidotomy tray at bedside. Patient was given methylprednisone 125 mg IV, zantac 25 mg IV and Benadryl 25 mg IV push in the emergency department and was admitted to the ICU. Patient was given Decadron 10 mg q8hr, zantac 50 mg Q8 hours and Benadryl 50 mg IV Q8 hours. Patient did well overnight, with no signs of airway compromise. Repeat bronchoscopy was done the following day which showed significant improvement in edema. Therefore, patient was cleared by ENT and discharged home with a 5-7 day course of Zantac and Benadryl, as well as a prescription for Medrol dose pack and close follow-up with allergy/immunology for evaluation of possible genetic or environmental causes of his angioedema.

Atkinson, JP., Cicardi, M,  Zuraw, B. Hereditary angioedema: Treatment of acute attacks. In: UpToDate, Saini S (Ed), UpToDate, Waltham, MA, 2013.

Atkinson, JP., Cicardi, M,  Zuraw, B. Hereditary angioedema: Epidemiology, clinical manifestations, exacerbating factors, and prognosis. In: UpToDate, Saini S (Ed), UpToDate, Waltham, MA, 2013.

Cicardi, M. Acquired C1 inhibitor deficiency: Clinical manifestations, epidemiology, pathogenesis, and diagnosis. In: UpToDate, Saini S (Ed), UpToDate, Waltham, MA, 2013.

Tran, Paul T. and Muelleman, Robert. “Allergy, hypersensitivity, angioedema and anaphylaxis.” In. Rosen’s Emergency Medicine: Concepts and Clinical Practice 8th ed. Ed. Marx. 2014.

Intern Report 7.1

Case Presentation by Dr. Henry White

Chief Complaint: Headache and fever

History of Present Illness: 13 year old male presents complaining of a headache for the last 2 days and a fever 4 days. The headache gradually started it is global in distribution, constant ache, 6-8/10 over the last 24 hours, currently at a 7/10.  It improves with ibuprofen or acetaminophen, it is not aggravated by sight or sound, and he denies any vision or hearing changes. The fever has been ranged between 99-101 for the past 4 days.

The parents state he is currently being evaluated for a constellation of symptoms, but no diagnosis has been made.  These include microscopic hematuria and occasionally pink tinged urine for the last 3 weeks.  Sporadic bilateral conjunctivitis without uveitis per ophthalmology with no vision changes or pain.  He has had polymigratory arthralgias over the past month, mostly located in his elbows and knees, but also in the small joints of his hands, feet and ankles bilaterally, sparing hips and shoulders.  This pain improves with the ibuprofen.  He has also had a blotchy rash over legs, ankles and elbows, with lower extremities affected more than the upper.  Parents also deny any sick contacts, and say the patient was previously healthy before these symptoms started one month ago.

General: Positive for fever and for 5 pound weight loss over last month with overall decreased activity level. Negative chills/sweats
HEENT: occasional epistaxis, no sore throat or congestion
Pulmonary: Intermittent cough, no dyspnea/wheezing
Cardiovascular: No chest pain
Gastrointestinal: Positive anorexia, no nausea/vomiting/diarrhea/constipation/blood in stool/melena, no abdominal pain
Musculoskeletal: no weakness or myalgias
Integumentary: no increased bruising or bleeding

Past Medical History: none – currently being worked up for above
Surgical History: none
Medications: ibuprofen, last dose 2 hours prior to arrival, acetaminophen, unknown eye drops
Allergies: none
Family History: hypertension
Social History: no alcohol/tobacco/other drugs, patient denies any sexual history

Physical Exam

Vitals: BP 125/76,HR 100,RR 14,T 100.1, 98% on RA, 5’2” weighing 122 lbs
General: Patient is lying on exam bed in obvious discomfort, holding his head with both hands

HEENT: normocephalic, scalp nontender to palpation, bilateral  conjunctivitis (represented below), EOMI without pain through visual range of motion, 20/20 vision b/l , MMM with no posterior oropharynx erythema or ulcerations

Neck: no lymphadenopathy noted, neck supple with no meningeal signs.

Pulmonary: Slight crackles over bilateral lower lung fields, no wheezes, good air exchange, no accessory muscle use or peripheral cyanosis

Cardiovascular: RRR with no r/g/m/c, 2+ D.P/Radial pulses b/l, brisk capillary refill

Abdomen: soft, nontender, nondistended

Genitourinary: normal, no inguinal adenopathy

Musculoskeletal: Musculoskeletal: Pain with active motion of elbows R>L, and ankles equal bilaterally, no pain with passive motion.  Able to ambulate normally but with significant amounts of pain.  5/5 strength in all extremities, good muscle tone in all limbs.  Joints nontender to palpation, no warmth, swelling or redness over any joint

Integumentary: Nonblanching, flat purpura over b/l lower extremities with concentrated over the anterior shin/ankles with some extension into soles of feet, as well as some over b/l elbows.  Not painful to palpation, some petechia noted over elbows/forearms.  No ecchymosis/abrasions/blisters noted, no involvement of torso or facial areas.

Neurological: AOx3, CN 2-7, 9-12 intact, speech fluid, heel to shin and finger to nose normal b/l, sensation intact to light touch over all extremities

case 7.1j

Question 1

This patient was admitted to Observation overnight, during which he developed some hemoptysis and epistaxis.  Bleeding stopped spontaneously, but patient was sent for chest CT that showed multiple cavitary lesions.  What is the most likely diagnosis in this patient?
a)  Kawasaki’s Disease
b)  Polymyalgia Rheumatica
c)  Wegner’s Granulomatosis
d)  Lyme Disease

Question 2

What is the gold standard for diagnosis of this disease?
a)  Biopsy
b)  ANCA
c)  Clinical diagnosis, no single lab test diagnostic
d)  Western Blot and ELISA serology

Question 3.

What is the mainstay of treatment for this disease?
a)  Doxycycline
b)  Long term corticosteroids
c)  Long term corticosteroids and cyclophosphamide
d)  IVIG and aspirin

Answers: 1. C, 2. A, 3. C

Answer Discussion

  1. The above vignette is a description of pediatric Wegner’s patient.  Definitely a challenging disease process with a lot of overlap with other conditions  It is a small vessel vasculitis classically taught to affect kidneys and lungs, but also can present with many other symptoms.   This patient presents with renal, pulmonary, cutaneous, and musculoskeletal symptoms.  Kawasaki’s disease is a large vessel vasculitis which classically presents as a high fever for more than 5 days with a predominance of conjunctivitis, mucous membrane involvement, and lymphadenopathy and potentially many other symptoms.  And while there are overlaps between kawasaki’s and Wegner’s, the low grade fever is more in line with Wegner’s.  Polymyalgia Rheumatica can also present with a large range of symptoms, with the arthralgias focused on the neck, shoulders and hips.  Lyme disease is a tick borne infection that can present during a spectrum of the disease process.  Early manifestations include a target rash and flu-like symptoms with later symptoms predominately affecting neurological and cardiac systems.
  2. While there are numerous tests to help rule in or out Wegner’s as the possible disease state, only a tissue sample can give the definitive diagnosis.  A sample taken from an active site of inflammation is diagnostic, and necessary due to the potential severe side effects of medical treatment.  ANCA testing is the laboratory test of choice, but only 82-94% sensitive.  Serology is the testing of choice for Lyme disease, and Kawasaki’s and Polymyalgia are clinically diagnosed and no single test is diagnostic.
  3. The mainstay of treatment for Wegner’s is steroids and immunosuppression with cyclophosphamide/methotrexate/rituximab.  This is important to know because Wegner’s patients undergoing treatment will be functionally immunosuppressed and at risk for overwhelming infections, even PCP.  Patients are also at risk for DVTs secondary to the disease progress, and untreated, the disease can be fatal by as little as 5 months.  Doxycycline is the first line treatment for Lyme disease.  Long term steroids are the treatment for Polymyalgia Rheumatica, but immunosuppressants are required for Wegner’s.  IVIG and aspirin are the treatment for Kawasaki’s.


This is a pediatric case of Granulomatosis with Polyangiitis (Wegner’s), a predominately small vessel vasculitis.  Though the two most common vasculitidies of childhood are Henoch-Schonlein purpura and Kawasaki disease, Wegner’s is a potentially lethal disease process if not treated appropriately.

The clinical presentation can be misleading as well, early symptoms are non-specific including fever, malaise, anorexia and weight loss as well as migratory arthralgias and can persist for months before other organ involvement.

Ocular symptoms can include conjunctivitis, scleritis, proptosis or uveitis

Wegner’s also can present with numerous ENT symptoms, including epistaxis, sinusitis, persistent rhinorrhea or even saddle nose deformity or laryngotracheobronchial stenosis.  Pulmonary manifestations can involve anything from intermittent coughing or wheezing to hemoptysis, dyspnea pulmonary fibrosis or pulmonary arterial hypertension with chest x-rays variably showing nodules, opacities and possibly infiltrates.  CT scan can show nodules, cavitary lesions or infiltrates

Cardiac and gastrointestinal symptoms are much less common, ex. pericarditis

Renal disease is one of the most common manifestations.  Glomerulonephritis develops in up to 80% of patients within the first 2 years, and is common at time of diagnosis.  ANCA positive patients are at greater risk for progression to end stage renal disease.  Other common signs are usually nephritic range proteinuria, hematuria, and AKI with cellular casts

Musculoskeletal disease usually presents as migratory arthralgias and myalgias

Cutaneous disease is present in up to half of cases and the most common lesion is leukocytoclastic angiitis – shown in example picture, but may also have focal necrosis/ulceration, hives, livida reticularis or tender nodules.

Nervous system involvement can present with cranial nerve abnormalities, CNS lesions or external ophthalmoplegia

There are multiple diagnostic criteria including the American College of Rheumatology (ACR) and Chapel Hill Consensus Conference Criteria (CHCC), both criteria are limited in distinguishing Wegner’s from Microscopic Polyangiitis, and recommend a definitive diagnosis with tissue biopsy from a site of active inflammation (lung/kidney).  Confirmation with biopsy is also indicated before starting a patient on immunosuppressant therapy with steroids and cyclophosphamide/methotrexate/rituximab etc.  ANCA is positive in 82-94% of cases.  Other lab values include an elevated ESR, elevated CRP, leukocytosis, normochromic normocytic anemia, thrombocytosis or thrombocytopenia and evidence of AKI.

CHCC guidelines might permit the diagnosis of Wegners in the absence of biopsy with:

  1. Radiographic evidence of pulmonary involvement for more than 1 month
  2. Upper airway symptoms for more than 1 month as listed above
  3. Glomerulonephritis
  4. ANCA positive

After remission induction, patients remain at risk for flare-ups, usually following an infection, and are also at increased risk for PCP or disseminated VZV.  Patients are also at increased risk for DVTs and long term side effects of the immunosuppressing medications.

Vasculitides Overview

Large Vessel Vasculitides

Temporal Arteritis: Commonly women in their 60’s/70’s.  Multiple systemic symptoms, as well as ischemic symptoms to branches of internal and external carotid.  30-40% also have Polymyalgia Rheumatica.  Lab assessment can include ESR, CRP, and anemia.  Treatment is corticosteroids, most effective within 24hrs of symptom onset.

Takayasu’s Arteritis (Pulseless disease): Chronic recurring disease affecting aorta and it’s branches. Primarily seen in young women.  Early diagnosis extremely difficult, symptoms are minor and nonspecific.  Later symptoms include uneven to absent pulses, claudication, retinopathy, strokes, and other ischemic type symptoms.  Treatment is prednisone, and further treatment may require immunosuppressants.

Medium Vessel Vasculitides

Polyarteritis Nodosa: Predominately in males in their 50’s/60’s, but can present at any age. Early symptoms include fevers, myalgias, arthralgias, and cutaneous manifestations (usually palpable purpura possibly with ulcerations), later manifestations include peripheral neuropathy and bowel ischemia.  Treatment is corticosteroids and add immunosuppressants if there is organ involvement.

Buerger’s Disease: Vaso-occlusive disease of young male smokers typically in lower extremities.  Symptoms can start as mild paresthesia’s/pain and progress to severe pain with claudication and possibly ulceration.  Treatment is abstinence from tobacco, and possibly calcium channel blockers.  Half of all patients who continue using tobacco need amputation.

Small Vessel Vasculitides

Behcet’s Disease: A chronic relapsing vasculitis that can affect large vessels, presents with oral/genital ulcers, skin lesions and possibly ophthalmologic/ neurologic/ gastrointestinal manifestations, and typically men between 25-35.  Oral ulcers are an early sign and required for diagnosis.  Kidney and cardiac involvement is rare, and diagnosis is by tissue biopsy. Treatment is focused on presenting symptoms.

Wegner’s Granulomatosis: discussed above

Churg-Strauss: It is a granulomatis vasculitis of multiple organs presenting as asthma and allergic rhinitis with eosinophilia.  Associated with allergy/atopic disorders.  Asthma usually presents during adulthood.  Pulmonary, ENT, and cutaneous symptoms predominate along with nonspecific symptoms of fever and weight loss.  Neurological and cardiac symptoms are also common.  Labs may show eosinophilia >1500/mm3, possibly p-ANCA, and chest x-ray may show Loffler’s syndrome/consolidation/cavitation.  Diagnosis is by tissue biopsy, and treatment is corticosteroids and possibly cyclophosphamide.

Microscopic Polyangiitis: Another ANCA positive vasculitis with a high degree of overlap with Wegner’s, with common symptoms of alveolar hemorrhage and glomerulonephritis, with the other most common symptoms including weight loss, mononeuritis multiplex, fever and cutaneous findings.  Diagnosis is by tissue biopsy, and treatment is corticosteroids and immunosuppressants.

Goodpasture’s Syndrome (Anti-GBM syndrome): Caused by the build-up of anti-glomerular basement membrane antibodies in the alveolar and glomerular basement membrane.   The disease has bimodal peak incidence during the 20’s and 50’s/60’s.

Like Wegner’s, initial symptoms include fever, malaise and arthralgia.  Hemoptysis occurs in 70% of cases, and glomerulonephritis is another frequent complication of the disease.  Notable tests include elevated ESR, UA with RBC casts, and Anti-GBM Ab positive.  Diagnosis is made with kidney biopsy, and treatment is corticosteroids and possibly immunosuppressants, and patients may end up requiring renal transplant if able to get anti-GBM antibodies to undetectable levels.

Henoch-Schonlein Purpura: Another small vessel vasculitis with a large degree of overlap with Wegner’s disease.  It typically involves the skin, gastrointestinal tract, and kidneys.  The disease predominately affects the pediatric population, and male to female ratio of 2:1.  Up to 2/3 of patients have a history of a respiratory infection 10 days before developing symptoms.  Classically, these symptoms include abdominal pain, fever, palpable purpura, hematuria and arthralgias. Gastrointestinal complaints in 70% with renal involvement in up to 50%.  Neurological involvement is rare.  Treatment is aimed at the underlying cause, if applicable, and multiple possible treatment regimens are currently being researched.  However, this disease is usually self limited, over the course of 6-8 weeks, and prolonged treatment may not be needed.

Key Points:

Wegner’s is a complex disease process potentially involving many different organ systems.  In medical school it was taught as the vasculitis that involves the kidneys and lungs, but it’s important to be aware that it can involve much more than those systems.

Missing the diagnosis can potentially have severe consequences in terms of morbidity and mortality.  Important lab/imaging work-up includes Urinalysis with microscopic analysis for urinary sediment and presence of blood, BMP (they know what these tests are for, CBC .  ANCA, ESR, CRP, LFTs, hepatits panel, HIV screen, and blood cultures as indicated to rule out other disease processes.  A baseline chest x-ray or possibly CT to assess pulmonary involvement.

Wegner’s Diagnosis is based on tissue biopsy.  Patients with suspected Wegner’s are an indication for admission and further work-up for diagnosis as well as medical treatment induction.

Patients being treated for Wegner’s are immunosuppressed and at risk for infections including disseminated VZV and PCP.  They are also at risk for DVT’s as well as numerous medication side effects.


  1. American Academy of Ophthamology -
  2. John’s Hopkins Vasculitis Center -
  3. Bosch et al, Treatment of Antineutorphil Cytoplasmic Antibody Associated Vasculitis -, JAMA 2007
  4. Lehrmann, Jill and Sercombe, Clare, Systemic Lupus Erythematosus and the Vasculitides, Rosen’s Emergency Medicine 7th edition
  5. Cabral et al, Classification and incidence of childhood vasculitis, updated June 5th 20013
  6. Falk et al, Clinical manifestations and diagnosis of granulomatosis with polyangiitis and microscopic polyangiitis, updated September 25th 2012
  7. Gnann Jr., John, Antiviral therapy of Varicella Zoster virus infections Chapter 65 of Human Herpesviruses: Biology, Therapy and Immunoprophylaxis 2007

Intern Report 6.13

Case Presentation by Dr. Sarah Michael

CC: I can’t breathe!

A 21-year-old female is transported to the emergency department after an apparent domestic dispute. On arrival, it is apparent that she has multiple stab wounds to her chest and abdomen. She is alert and oriented but in acute distress. Her blood pressure is 98/64, pulse 112, respirations 32 and oxygen saturation 94% on nonrebreather mask. There is no jugular venous distension. You can appreciate a small degree of tracheal deviation. An eFAST is performed which includes the following findings.




1. The most appropriate next step in the management of this patient is:

A: Needle decompression of the right hemithorax

B: Left-sided chest tube

C: CT of the chest, abdomen and pelvis

D: Emergent transport to OR

2. The patient’s clinical status remains unchanged.  A repeat U/S shows the following:


Now the most appropriate next step is:

A: Chest tube placement

B: Intubation

C: Finger thoracostomy

D: Chest x-ray

3. Which of the following is true regarding the patient’s belongings?

A: They should be placed in a plastic bag and remain with her.

B: They should be placed in paper bags and offered to the police.

C: If ED staff handles them they lose their forensic value.

D: Blood-soaked items should be placed in biohazard waste.

Answers & Discussion:

1. The answer is A, needle decompression.

The patient in the vignette is in shock and her physical exam is concerning for a  tension pneumothorax with respiratory distress and hypotension. Notably, JVD may be absent in the hypotensive patient. In order to correctly answer the question, you need to be able to interpret the eFAST findings.

An eFAST (extended FAST) exam includes the normal FAST structures as well as the lung at the 3-4 intercostal space on the anterior chest wall. This is the most superior aspect of the chest in a supine patient and the location where you would expect air to accumulate.  You’re given 3 images to interpret.

The first image is of Morrison’s pouch, the most sensitive FAST view for intraperitoneal free fluid. This patient has a renal fat pad that could be mistaken for free fluid. You should be able to appreciate that the structure is lenticular with internal echoes and bounded by the hyperechoic line of the renal capsule.  This is known as the double line sign and is a frequent cause of a false positive FAST examination. Therefore, it is not a reason to rush the patient to the OR. If it’s helpful, think about it as a renal corollary of the pericardial fat pad that can sometimes mimic pericardial effusion.

6.13 ans -1j

The second image shows you a normal M-mode ultrasound of the right lung. You can see the “seashore sign” with an abrupt transition between the chest wall and lung parenchyma at the pleura. It would be imprudent to place a chest tube on the unaffected side.  

6.13 ans-2

The third image shows you the lung point of the left lung, indicating the presence of a pneumothorax. This is the place on the chest wall where the lung transitions from pneumothorax to being against the chest wall. In M-mode, you’d be able to see both the “seashore” and “barcode” signs vary with respiration.  In a setting concerning for tension, needle decompression is the way to go.  Intubating the patient before decompression risks further destabilization.   Fixing a tension pneumothorax may also prevent the need for intubation.

6.13 ans-4

2: The correct answer is A, chest tube placement.

In the trauma patient with persistent respiratory distress and decreased breath sounds after needle decompression, you should consider chest tube placement for presumptive hemothorax per ATLS guidelines. Chest tube placement is certainly indicated given the ultrasound image, which demonstrates a massive hemothorax. There is near complete consolidation of the lung as it floats in a sea of fluid. The M-mode graphic shows the movement of the lung edge with respiratory variation.

6.13-ans 3

The patient may need intubation for respiratory failure (and definitely for her trip to the OR). But intubation before tension is resolved would likely worsen the tension and could be disastrous.  Similarly, tension pneumo- or hemo-thorax is a clinical diagnosis and treatment should not be delayed by imaging.

Thoracotomy in the OR is indicated for patients who have a chest tube output of 1500 cc or greater of blood during the first hour. Given the appearance on ultrasound, more than 1500 cc would be expected. However, the tension should be relieved at once and not delayed by transportation to the OR.

Finger thoracotomy should be considered and is an option if you are uncertain of the diagnosis of hemothorax. In this case the diagnosis is not in doubt and chest tube is required.  A chest tube is also indicated once a decompressive needle thoracostomy is performed.  Furthermore, a hemothorax this large will likely re-accumulate very quickly.

3. The correct answer is B.

The patient is a victim of a violent crime and her clothing, through which she was stabbed, likely contains valuable forensic evidence. Caring for the patient obviously takes priority over the preservation of such evidence, but steps can be taken to maintain evidence integrity so long as they do not delay care. When removing a patient’s clothing, try to avoid cutting through stab or bullet holes and always wear gloves. In some cases, the frequent changing of gloves can help to keep from cross-contaminating evidence.  Even if evidence is collected or handled suboptimally in the provision of care for the patient, it is not worthless and should still be made available to investigators.

After being removed from the patient, clothing should be placed in separate paper bags and given to law enforcement. The paper bags will allow the blood to dry in a way that does not promote the formation of mildew, which can destroy the evidence. Blood soaked items should be placed in separate plastic bags followed by separate paper bags. Law enforcement should be informed that the items are soaked so they can be dried appropriately.

If law enforcement declines the evidence, it should be returned to the patient.

Riviello, edited by Ralph J. (2010). Manual of forensic emergency medicine : a guide for clinicians. Sudbury, Mass.: Jones and Bartlett Publishers. ISBN 978-0-7637-4462-5.


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