Dreaded Dizzy answer



The pretending wanted to admit the patient for syncope.  The attending wanted to scan the patient’s head.  The med student wasn’t sure what to do.  The chief was 5&2’ing somebody in Trauma 3 so he wasn’t involved at all.

The patient has bilateral subacute sdh.

First of all, anyone who saw the patient would agree that getting a head CT was not an obvious decision.  The guy was fine.  He had a normal neuro exam, he wasn’t in any discomfort, and he’s walking around in the ED.  When the case was presented last week at follow-up, everyone wants to get a head CT because it’s a conference case.

There are two main teaching points here.  (1) Headache + vertigo is a concerning combination.  However, patients cc this combination all the time, and the trick is to figure out who has tension HA + peripheral vertigo (or nada), and who has something more serious (see point #2).  (2) The way to decide whether to scan a patient for a headache is to look at the patient and decide whether he has a genuine headache.  I don’t go the “first, worst, different” route because it’s non-specific because 99% of ED HA patients say yes to “first, worst, different”, and you can’t scan everyone.  I get 100 patients cc HA a day, but it’s extremely rare that I ever think that the patient has a genuine HA.  Some of the things that I use to read a patient are: (a) they only cc headache and nothing else, (b) they look like the HA is bothering them, (c ) the headache does not seem like a migraine in character, (d) the patient is someone who wouldn’t come to the ED for a minor problem.

When I talked to this guy, I just could not get away from his HA cc.  However, I did not put “rule out bilateral sdh” on his ct request.

In general, bilateral chronic sdh are a disease of older patients.  They are generally very asymptomatic.  They never have focal findings.  They rarely have a headache.  The common deficit that I see is that they may not be able to walk, or they walk poorly, but it’s not an ataxic gait.

The resident was upset he missed this case.  It’s ok.  If you miss a case because you were flippant, then it’s not ok.  He had never seen a bilateral sdh before, so it’s an understandable miss.  The patient had a normal neuro exam, a generally reassuring finding.  If we sent the patient home, he would have been fine.  Nothing terrible would happen to the patient, but he would likely bounce back in a few days – weeks.
The patient was admitted.  There’s very little work-up for these chronic / acute-on-chronic bilateral subdurals.  Generally, there’s no medical reason for getting the bilateral sdh, and there’s no underlying problem (e.g. coagulopathy) to fix.  They are followed by neurosurgery and electively operated on or observed.



The patient was observed for a couple of days, then went to neurosurgery clinic.  A few weeks later, the sdhs were drained because the pt was persistently symptomatic, and the collections got a little bit bigger.  He did fine.

Which came first: the AFib or the MI?

Which came first: the atrial fibrillation or the MI?

Anna Meyendorff, MD PGY-3

(Image from: http://www.thestar.com/content/dam/thestar/life/2010/07/15/science_answers_the_question_which_came_first_the_chicken_or_the_egg/lichickenoreggjpg.jpeg.size.xxlarge.letterbox.jpeg)


Initial Presentation:

77yo AA F hx HTN, DM, CVA, former smoker presenting with chest pain. Symptoms started 24 hours prior to ED presentation while watching TV. Pain was epigastric/lower sternal, 10/10, nonradiating. Associated with SOB, but not nausea, vomiting, or diaphoresis.

Initial vitals: BP 125/61   P 114   R 21   T 98.4   95% on RA   FS 377


Initial EKG showing afib with RVR with 2mm ST elevations in III and aVF and possible small ST depressions in I, avL. Given diltiazem 20mg IVP with conversion to sinus rhythm, but not resolution of pain. Repeat EKG showing continued ST elevation in the inferior leads, so MEHEART (STEMI code) was activated by ED. Pt given aspirin, plavix, heparin IV bolus. Chest pain resolved by time of cardiology evaluation, so decision made not to proceed with transfer for immediate cardiac cath because symptoms resolved and presentation “unconvincing for STEMI” (per cardiology). In addition, lab results revealed that patient was in renal failure, further increasing the risk of dye infusion. Initial troponin was 5 (normal range <0.09). Pt was admitted to the CCU with dx: NSTEMI, plan for medical management with heparin drip.


CCU #1 course:

Overnight, patient developed worsening chest pain. Evidence of CHF/fluid overload on exam (crackles at lung bases, peripheral edema, JVD). Was given lasix 80mg IVP and started on nitro drip, without resolution of CP. She developed worsening respiratory distress requiring initiation of BIPAP. Serial troponins uptrending from initial (5) to 37 to 96. Creatinine worsened from 2.3 to 2.8. Repeat EKG revealed dynamic EKG changes with more pronounced inferior ST elevations and ST depressions in V3-V6. Pt transferred to interventional cardiology center for immediate catheterization for inferior wall STEMI.


CCU #2 course:

Cath revealed 100% circumflex occlusion and successful PCI with placement of DES. Elevated filling pressures also noted (LVEDP 35mmHg, PCWP 18mmHg), consistent with cardiogenic shock. Post-cath, pt improved and was weaned off nitro and lasix drips. Echo revealed inferolateral and inferior wall akinesis with LVEF 45%. Overnight after cath, patient noted on telemetry to be in afib with RVR (110s-140s), but was asymptomatic. She was loaded with amiodarone for rate and rhythm control. Creatinine continued to uptrend (6.7 on HD#5), urine output diminished; renal consult suspected combination of toxic AVN (contrast-induced) plus hemodynamic insults from afib, decompensated CHF, and acute MI. Discussion ongoing regarding initiation of hemodialysis at the time of this post.



So, this case got me thinking. Was the atrial fibrillation noted initially somehow related to the MI? If so, did one cause the other? Which came first?

Numerous studies have demonstrated that myocardial infarction increases risk of afib. Atrial fibrillation is common in the periinfarction period; it occurs in 6-21% of patients, usually in the first 72 hours post-MI. Development of afib in this window carries increased 30-day mortality as well as long-term mortality. Afib during acute MI can be caused by multiple factors, but is most commonly caused by atrial stretching from elevated pressure secondary to heart failure. It can also rarely be secondary to atrial ischemia or infarction, pericarditis, or atherosclerosis of the vessels supplying the SA and AV nodes. (1, 2)


New studies have been published, including several in 2015, documenting the opposite relationship: that atrial fibrillation increases risk of MI, though the mechanism is poorly understood. Soliman et al published a prospective cohort study in JAMA in January 2014. Analysis of 23,928 adult subjects without heart disease (the REGARDS cohort) over median 4.5 years demonstrated that afib conferred a nearly 2-fold increased risk of MI. Even after adjusting for smoking status, hypertension, diabetes, hyperlipidemia, BMI, aspirin use, and more risk factors, these results remained significant (Hazard Ratio 1.70 [95% CI, 1.26–2.30]). Even more interesting, the subgroup analysis also demonstrated a higher risk in women vs men (HR 2.16 vs 1.39) and in blacks vs whites (HR 2.53 vs 1.26). Recall that the patient in the case example above was both black and female. Unlike sex and race, age was not found to change the risk. Limitations of the study included lack of tracking how this risk develops over time after developing afib. It also did not evaluate asians, hispanics, or other racial groups, potentially limiting result generalizability. (3)


A second study was published by Soliman in Circulation in May 2015 with the goal of further elucidating the cause of the previously noted findings and evaluating their findings with a time variable. The study considered 14,462 participants (the ARIC cohort) over 21.6 years (median). They found that the mean time from afib diagnosis to MI was 4.82 years (median 3.35). The incidence of MI in those with afib was nearly 3-fold higher than those without afib (Incidence rate ratio 2.93), and after adjustments for cardiovascular risk factors nearly 2-fold (1.63). They replicated the findings from the previous study for women vs men (IRR 3.75 vs 2.27, P<0.001), and suggested the same in blacks vs whites (HR 2.05 vs 1.52), without statistical significance (P=0.16). In further subgroup analysis by type of MI, they found afib to be associated with increased risk of NSTEMI (HR 1.80), but not STEMI. NSTEMI is usually caused by a nonocclusive thrombus, while STEMI is usually caused by a complete arterial occlusion. According to the authors, the association with only NSTEMI suggests that direct coronary thromboembolization (the mechanism by which afib leads to stroke) is not the primary mechanism by which afib leads to MI. One proposed mechanism suggests the afib-induced prothrombotic risk (from platelet activation, inflammation, and endothelial dysfunction). An alternative mechanism proposes a rapid ventricular rate (afib with RVR) leading to demand ischemia (NSTEMI). (4)


An editorial in the same issue of Circulation includes the following figure as a graphic for understanding the interaction between these two entities. (5)

pasted image 0

Patients found with new onset atrial fibrillation in the emergency department are often admitted for initiation of anticoagulation therapy with the primary goal of preventing stroke. Atrial fibrillation increases stroke risk by 4-5 fold. Based on the newly emerging evidence, it bears noting that these patients also carry a ~2 fold increased risk for MI. More studies must be performed to evaluate whether this risk should alter the standard management of newly diagnosed atrial fibrillation. What medication regimen is optimal for both MI and CVA prevention?



(1)Angeli FF. Atrial fibrillation and mortality in patients with acute myocardial infarction: a systematic overview and meta-analysis. Current cardiology reports. 2012-10;14:601-610.


(2)Schmitt JJ. Atrial fibrillation in acute myocardial infarction: a systematic review of the incidence, clinical features and prognostic implications.. European Heart Journal. 2009-05;30:1038-1045.


(3)Soliman EE. Atrial fibrillation and the risk of myocardial infarction. JAMA internal medicine. 2014-01;174:107.


(4)Soliman EE. Atrial Fibrillation and Risk of ST-Segment-Elevation Versus Non-ST-Segment-Elevation Myocardial Infarction: The Atherosclerosis Risk in Communities (ARIC) Study. Circulation (New York, N.Y.). 2015-05;131:1843-1850.


(5)Vermond RR. Does myocardial infarction beget atrial fibrillation and atrial fibrillation beget myocardial infarction?. Circulation (New York, N.Y.). 2015-05;131:1824-1826.

Dreaded Dizzy

A 40s M presents with headache and dizziness.  The symptoms have been going on for 2-3 days.  The headache started first.  It is mild, diffuse, and slow onset (non-thunder clap) in nature.  He gets headaches now and then, but not frequently.  There is no nausea or vomiting.  The dizziness sounds more like vertigo than lightheadedness /near-syncope.  He describes a feeling of unsteadiness, not necessarily spinning, and it is somewhat positional, though the description appears to be orthostatic at times.  There are no ear / ent complaints.  He states he may have blacked out last night when he had an episode of dizziness that was very brief.  There is no recent illness, chest pain, sob, or abd pain.  He has no pmh / psh or meds.

On exam, he has normal VS.  He was examined by a med student, the chief, the pretending, and an attending.  During one of the H&Ps, someone thought he may have had mild truncal ataxia.  When everyone returned as a group to examine him, his gait is normal, and it should be noted that he was walking around in the ED while he was waiting for his labs / ekg, which are all normal.

What do we do now?

Fever, abd pain in a patient on pred, mtx – pt2

A patient on immunosuppressive drugs for any reason needs serious pan-culturing and pan work-up.  Most infections can be diagnosed easily in a normal patient because the patient will localize the infection, and you will see signs of the infection on your work-up (infiltrate on cxr, e.g.).  In a patient with wbc-altering drugs, you may not see signs of infection on your work-up – even if the patient isn’t neutropenic.  Pneumonia may show up as a normal cxr.  In a patient with intestinal perforation, they may have a normal-ish exam and a normal-ish abd ct because there may not be signs of inflammation.

I scan EVERY pt with cc of abd pain when they’re on immunosuppressives, in addition to BCx x 2-3, ua / u cx, and cxr.  In addition, I ask for a surgical consult on every pt, even if the abd ct is negative.  A good consult will understand why they’re being called.  A bad consult will wonder why they’re being called for a pt with a negative ct.  I have had a handful of pts like this ending up in the OR, even with an initial ct that was negative (most had + ct despite a benign-ish exam).

In addition to the infection work-up, the patient requires a cbc, chem, and lactate.  Lactate is needed because it’s regarded as an indication of quality of medical care in patients with sepsis criteria.  Just like BCx were once regarded as an indication of quality in patients with pneumonia, lactate is a waste of time and money.  Despite my hatred of lactate, I almost always draw it so that the patient don’t have to be stuck a second time.

Perhaps without exception, patients with a high fever on immunosuppressives should be started on iv abx and admitted, regardless of their wbc count.

The patient’s wbc was 21; chem was normal.  The fever of 103 an wbc of 21 got the attention of the surgeons; they actually came to see the pt quickly.  Cxr and ua dip were negative, abd ct was negative.  The ua micro showed bacteria without wbc or rbc.  The patient was admitted for iv abx (and serial abd exams).  This turned out to be a pan-sensitive enterococcus pyelo.  There were no signs of pyelo on the ct (done with iv and po contrast).  The pt spent a week in the hospital and did well.


Stephanie Haimowitz, PGY3


AS is a 43 yo F, on OCPs for menorrhagia, h/o recent left ACL tear and as a result decreased ambulation x3 weeks, p/w SOB, worse on exertion x2 weeks but acutely worsening on the day of presentation. On the day of presentation, the patient complained of an episode of acutely worsening dyspnea, now occurring at rest and associated with lightheadedness, chest pressure, and diaphoresis.

On Exam, the patient was mildly tachycardic with an O2 sat of 98% on RA at rest. She appeared to be breathing comfortably, although at times noted to take shallow breaths, and the remainder of her exam was unremarkable.

Labs were notable for an elevated troponin of 0.302. EKG showed sinus tach with a ventricular rate of 106 and an incomplete RBBB. CT w/PE protocol showed large bilateral pulmonary emboli in both the right and left main pulmonary arteries with extension into segmental and subsegmental branches, as well as flattening of the interventricular septum with dilatation of the right ventricle.



The patient was started on a heparin drip and admitted to the CCU for hemodynamic monitoring and catheter directed thrombolysis via EKOS, which uses ultrasound to enhance the effects of catheter directed thrombolysis. The patient underwent the endovascular intervention with improvement in her symptoms and repeat echo showed improved RV function. She was switched to Lovenox and discharged home on xarelto.

There are many factors to consider when choosing the appropriate treatment modality for a patient with a PE. In a well-appearing hemodynamically stable patient with evidence of a peripheral or subsegmental PE, anticoagulation with either heparin, a low molecular weight heparin such as lovenox, or one of the newer factor Xa inhibitor oral agents is the most common treatment modality. Factors to consider when deciding whether to escalate treatment include hemodynamic instability, evidence of right heart strain, a large central thrombus on CT, and overall clinical appearance.

While this patient was hemodynamically stable, she had clear evidence of right heart strain (e.g. troponemia, dilated right ventricle, flattening of interventricular septum, and McConnell’s sign- diminished RV systolic function with sparing of the apical wall seen here), and large bilateral pulmonary emboli on CT scan. The RV dysfunction seen on echo is often considered to be predictive of a poor short-term prognosis, thus warranting more aggressive therapeutic measures.[1]

The decision was made to use ultrasound enhanced catheter directed fibrinolysis.

The SEATTLE II Study, published in August of this year, investigated the efficacy of this technique. The use of full dose systemic thrombolysis has fallen out of favor over the past few years due to the risks of severe bleeding and intracranial hemorrhage. By using the ultrasound guided catheter directed approach, a lower dose of thrombolytic can be used because it is injected adjacent to the PE. The study was a single-arm, multicenter design with the inclusion criteria of a proximal PE, age >18, PE symptom duration <14 days, and RV/LV diameter ratio >0.9 on CT. A total of 150 patients were enrolled at 22 sites across the US, at urban, non-urban, teaching, and non-teaching hospitals. The primary outcome was a change in RV/LV diameter ratio pre and post procedure. The primary safety outcome was major bleeding within 72 hours of initiation of therapy. Major bleeding was defined as either intracranial hemorrhage or bleeding causing hemodynamic compromise and requiring intervention such as blood transfusion. Patients enrolled in the study had a mean difference RV/LV diameter of 0.42. There were 16 major bleeding events, however none of these were intracranial hemorrhage.[2]

The most glaring limitation of the study was the lack of a comparator group, such as full dose systemic fibrinolysis, half dose systemic fibrinolysis, or a/c alone. Thus, while the results of the study appear promising, additional comparative clinical studies are necessary to help define the role of ultrasound facilitated catheter directed fibrinolysis in the treatment of acute PE.




[1] 14.Grifoni S, Olivotto I, Cecchini P, et al. Short-term clinical outcome of patients with acute pulmonary embolism, normal blood pressure, and echocardiographic right ventricular dysfunction. Circulation 2000; 101:2817.

[2] Piazza, Gregory, Benjamin Hohlfelder, Michael R. Jaff, Kenneth Ouriel, Tod C. Engelhardt, Keith M. Sterling, Noah J. Jones, John C. Gurley, Rohit Bhatheja, Robert J. Kennedy, Nilesh Goswami, Kannan Natarajan, John Rundback, Immad R. Sadiq, Stephen K. Liu, Narinder Bhalla, M. Laiq Raja, Barry S. Weinstock, Jacob Cynamon, Fakhir F. Elmasri, Mark J. Garcia, Mark Kumar, Juan Ayerdi, Peter Soukas, William Kuo, Ping-Yu Liu, and Samuel Z. Goldhaber. “A Prospective, Single-Arm, Multicenter Trial of Ultrasound-Facilitated, Catheter-Directed, Low-Dose Fibrinolysis for Acute Massive and Submassive Pulmonary Embolism.”JACC: Cardiovascular Interventions 8.10 (2015): 1382-392. Web.

Goodbye MONA? Oxygen in AMI

Goodbye MONA?

From: Best Mona Lisa Parodies @ http://beforeitsnews.com/fun-news/2011/09/the-best-mona-lisa-parodies-1167194.html

Dr. Mayuri Patel PGY3

CC: Chest pain and Shortness of breath

HPI: 72F w/ PMHx of Rheumatic fever (s/p AVR repair 9 years prior), pHTN, hFrEF (EF 30%), HLD, DVT (on coumadin) s/p IVC filter BIBEMS for progressive DOE over 1 month. Prior to arrival to ED, pt developed substernal chest pain radiating to jaw associated with diaphoresis and nausea. EMS placed patient on NRB.

Triage VS afebrile BP 129/85 HR 74 RR 24 02 96%RA

General: awake, mild distress, oriented to person, place and time


Pulm: CTA – b/l

Abd: +bs, soft, nt/nd

Ext: 2+ pulses, no cyanosis or edema

EKG – Sinus rhythm, HR 74, STE II, III, aVF with reciprocal changes

Troponin – 12; CPK – 377


MEHEART was activated, patient transferred to Weiler for cardiac catheterization.

Patient given Heparin 5000 Units, NTG Sl, Plavix 600mg, ASA 162mg. En route to Weiler hospital, pt placed on 2L NC.

Hospital course:

Cardiac cath showed mild coronary artery disease for the left ventricle. The 1st acute marginal artery to the right ventricle occluded (possibly culprit). Intervention – medical management.

Patient was admitted to telemetry s/p cardiac cath. ECHO showed dilated left ventricle, EF 20-25%. Patient was elevated by heart failure team for ICD placement, because patient met NYS Class IIa criteria. Patient opted for medical management instead of ICD placement. Patient was evaluated for LifeVest and discharged after medical management.


Traditionally, we are taught that administration of high flow oxygen is the standard of care for patients presenting with cardiac emergencies. However, where does this dogma come from? The earliest evidence comes from 1900, when Steele observed that oxygen relieved pain during episodes of angina pectoris(1). The evidence for this observation came in 1928, when the cause of angina was attributed to hypoxia of the myocardium (2).

It is indeed a strange phenomena that our current day practices are based on studies in early 1900s. There have been multiple subsequent studies showing the harmful effects of oxygen. In 1950, Russek et al. showed that administration of 100% oxygen prolonged EKG changes during exercise tolerance testing and had no effect on anginal pain (3). A 1964 study reported that breathing high concentrations of oxygen (85% to 90%) for at least 30 minutes in the first 24 hours after MI resulted in decreased heart rate, reduced cardiac output, and increased systemic vascular resistance (4). In the following year, a study by Thomas et al. showed that giving 40% oxygen for 20 minutes to patients following MI resulted in a 17% decrease in cardiac output and a 5% rise in arterial blood pressure (5). Certainly not an ideal situation after an AMI. In 1969, a study by Neill showed that in “normal subjects” the availability of oxygen for myocardial metabolism was not affected until arterial oxygen saturation falls as low as 50% (6). However, in patients with CAD, myocardial ischemia was observed in some patients when oxygen saturation fell below 85%. In a subset of patients with triple-vessel disease, 6 minutes of high-flow oxygen reduced coronary blood flow sufficiently to induce myocardial ischemia (7).


The first randomized, double blinded controlled trial of oxygen therapy was conducted in 1976. The study randomized 200 consecutive patients thought to have MI to treatment with oxygen (given via medium concentration mask at 6L/min) or air for the first 24 hours. Patients with CHF, chronic pulmonary disease, or breathlessness from any cause other than AMI were excluded. The group receiving oxygen therapy had a higher level of serum aspartate aminotransferase level than the group receiving room air, indicating greater myocardial damage. Forty-three patients were excluded post-hoc when the diagnosis of MI was revoked. There was a mortality rate of 11% (9/80) in the oxygen group vs. 4% (3/77) in the air group, but this did not achieve statistical significance. The relative risk of mortality in oxygen group 2.9 (95% CI 0.81-10.3; P=0.08). The authors concluded that the results are suggestive of “deleterious effect” of oxygen and that administration of it in patients with uncomplicated MI is not beneficial (8).


What causes the deleterious effects of oxygen therapy? It is theorized that reactive oxygen species are responsible for vasoconstriction. This was shown by McNulty et al. in 2007 in patients with AMI. The study showed that breathing 100% oxygen for 10 minutes increased vascular resistance in the LAD by 23% (9). Interestingly, this increase could be prevented by co-administration of the antioxidant ascorbic acid. The diameter of the large conduit coronary arteries was not appreciably affected, suggesting that vasoconstriction occurs at the level of the myocardial microcirculation.

A Cochrane review in 2013 meta-analyzed available studies on oxygen therapy in patients with AMI. Combing the 4 randomized controlled trials (430 patients with 17 deaths) generated a relative risk of mortality of 2.11 (95% CI 0.78 to 5.68) in participants with confirmed AMI. The authors concluded that due to the small number of deaths, it could be a chance occurrence (10).

The AVOID trial from Australia might be the last straw in the age-old dogma of oxygen for AMI. It is a prospective, multicenter trial with both pre-hospital and in-hospital treatment comparing oxygen (8L/min) with air. It included patients that met STEMI criteria, had symptoms for less than 12 hours and initial 02 saturation >94%. Exclusion criteria included 02 saturations <94%, AMS, and oxygen administration prior to randomization. Primary end points for the study were infarct size measured by Troponin T (TnT) and CK-MB. Secondary endpoints were recurrent myocardial infarction, cardiac arrhythmia and myocardial infarct size assessed by cardiac magnetic resonance (CMR) imaging at 6 months. There were 638 patients randomized, of which 441 were confirmed STEMI who underwent primary endpoint analysis (218 in oxygen group vs. 223 in no oxygen group). The baseline characteristics were similar except for 38% in the oxygen group had anterior infract vs. 33 % in no oxygen group. There was a statistically significant increase in mean CK-MB, however mean TnT was similar. There was an increase in the rate of recurrent myocardial infarction in the oxygen group compared to the no oxygen group (5.5% vs. 0.9%, P=0.006) along with increase in frequency of cardiac arrhythmia (40.4% vs. 31.4%; P=0.05). At 6 months, the oxygen group (139 patients) had an increase in myocardial infarct size on CMR (20.3grams vs. 13.1grams; P=0.04) (11).

The AVOID trail concludes that supplemental oxygen in normoxic STEMI patients increased myocardial injury along with cardiac arrhythmia, and recurrent MI. It was also associated with larger myocardial infarct size. However, the study is not without its flaws. The use of 02 at 8L/min seems excessive and could account for the differences. Also, patients in no oxygen group were given oxygen either during catheterization or in the hospital stay (if 02 saturation dropped below 94%).

Where do we go from here? It seems that every patient who arrives via EMS with complaint of chest pain is placed on a NRB. The literature does not support this notion, and we may in fact be doing disservice to our patients. If there is to be a change in practice, it has to come from both pre-hospital setting as well as ED. There is no denying the importance of oxygen in patients who are hypoxic and having AMI. However, for normoxic patients it might be prudent to stay away from oxygen.


  1. Steele C. Severe angina pectoris relieved by oxygen inhalations. BMJ1900, 2:1568.
  2. Keefer CS, Resnik WH. Angina pectoris: a syndrome caused by anoxemia of the myocardium. Arch Intern Med 1928, 41:769-807.
  3. Russek HI, Regan FD, Naegele CF. One hundred percent oxygen in the treatment of acute myocardial infarction and severe angina pectoris. JAMA 1950, 144:373-375.
  4. MacKenzie GJ, Flenley DC, Taylor SH, McDonald AH, Stanton HP, Donald KW. Circulatory and respiratory studies in myocardial infarction and cardiogenic shock. Lancet 1964, 2:825-832.
  5. Thomas M, Malmcroma R, Shillingford J. Haemodynamic effects of oxygen in myocardial infarction. Brit Heart J 1965,27:401-407.
  6. Neill WA. Effects of arterial hypoxemia and hyperoxia on oxygen availability for myocardial metabolism: patients with and without coronary artery disease. Am J Cardiol 1969, 24:166-171.
  7. Bourassa MG, Campeau L, Bois MA, Rico O. The effects of inhalation of 100 percent oxygen on myocardial lactate metabolism in coronary heart disease. Am J Cardiol 1969, 24:172-177.
  8. Rawles JM, Kenmure AC:Controlled trial of oxygen in uncomplicated myocardial infarction. Br Med J 1976, 1:1121-1123.
  9. McNulty PH, Robertson BJ, Tulli MA, Hess J, Harach LA, Scott S, Sinoway LI. Effect of hyperoxemia and vitamin C on coronary blood flow in patients with ischemic heart disease. J Appl Physiol 2007, 102:2040-2045.
  10. Cabello JB, Burls A, Emparanza JI, Bayliss S, Quinn T:Oxygen therapy for acute myocardial infarction. Cochrane Database Syst Rev2013, 8:
  11. Stub D, Smith K, Bernard S, Bray JE, Stephenson M, Cameron P, Meredith I, Kaye DM: A randomized controlled trial of oxygen therapy in acute myocardial infarction Air Verses Oxygen In myocarDial infarction study (AVOID Study). American Heart Journal 2012, Volume 163, Issue 3, 339 – 345.e1.





Fever, abd pain in a patient on pred, mtx

A 50s F with hx RA on methotrexate cc fever x 2-3 days.  She denies cough, sob, chest pain, dysuria, or flank pain.  She has epig / LUQ pain with nausea, vomiting x 1, no diarrhea.  She has no other pmh.  Her meds include pred, metformin, lantus, metoprolol, and simvastatin.  She has no psh.  On exam, she has HR 80, RR 14, BP 130 / 74, T 103, RA sat is 100.  Her exam is normal with minimal LUQ tenderness, if any.  She is obese.

What work-up do we do?

What is her treatment and dispo?

Facial Pain answer



Facial pain usually comes from a tooth, sinuses, tmj, lymph nodes, and less commonly ears.  The remaining structure is the parotid.  Very rarely, facial pain is due to a bony skull lesion.


The patient’s pain is where her parotid is.  To verify the dx, you can (1) do a CT, (2) try to push pus out of Stensen’s duct [I never see this, largely because most parotitis is not purulent], or (3) do nothing.  I usually scan if I feel a lump (mass/abscess).

The dx of common childhood contagious disease nowadays is so complicated, requiring blood tests, imaging, etc.  There was a measles case in the nejm that got a ridiculous amount of tests (http://www.nejm.org/doi/full/10.1056/NEJMcps1413402).  In the old days, your doctor probably said, “oh you have measles, mumps, etc.” and sent you home with a lollipop.

Most parotitis I see are viral, but not mumps.  I have not had a mumps outbreak in my area despite occasional spikes in cases of parotitis and other salivary gland infections.  Most patients get better with ibuprofen, though there is a temptation to throw abx at the patient.  I usually send these patients for ent follow-up.  Most pcps have no idea what to do with parotitis nowadays.

On this patient’s scan, the L parotid is obviously enlarged, despite the lack of swelling on exam.  I do iv contrast in case there’s an abscess.  She was sent home with ibuprofen and got better after a few days.