A patient presents with difficulty feeding for the past month.  Specifically, she states that she is “unable” to swallow.  How do we perform the bedside examination so as to take this presentation to the highest degree of resolution?


Swallowing can be divided into 2 processes: oropharyngeal and esophageal.


The oropharyngeal process moves the food bolus from the back of the tongue to the pharynx, where the pharynx squeezes it into the upper esophagus.  This event involves the soft palate closing of the nasopharynx, the epiglottis closing of the tracheal entrance, and the upper esophageal sphincter transiently relaxing to accommodate the food bolus.  This is a complex neurological event, and oropharyngeal dysphagia is usually caused by a neurological disease.  Telltale signs include nasal and tracheal aspiration, as well as inability to propel food out of the pharynx.


The esophageal process moves food from the upper esophageal sphincter (cricopharyngeus) to the lower esophageal sphincter.  Disruption can be anatomic (obstruction) or physiologic (motility). It presents with the feeling that food gets stuck in the esophagus. Patients feel these symptoms in the chest.


Dysphagia to solids only (such as chewy meats) signifies an anatomic obstruction. Gastroenterologists use marshmallows to bring this out, and call it a “viscous swallow.” Typical causes of anatomic obstruction include stricture, ring, or cancer.


Dysphagia to liquids and solids signifies a physiologic motility disorder. These can be localized to the lower esophageal sphincter, such as achalasia, or can be diffuse, such as diffuse esophageal spasm. Motility orders can also be secondary to inflammation, such as in gastroesophageal reflux disease.


By clarifying which part of the swallow process is disordered as well as noting whether liquids are affected helps considerably narrow the differential diagnosis of dysphagia.



-Inability to swallow or aspiration indicates oropharyngeal dysphagia, and is usually neurologic.

-Dysphagia to solids indicates obstruction.

-Dysphagia to liquids and solids indicates a motility disorder.



You see a patient with pleuritic chest pain.  The EKG shows ST segment elevation in the inferior leads as well as V2-V5. The closest cardiac catheterization laboratory is 120 miles away, and you normally give thrombolytics for STEMI.  But is this STEMI or pericarditis?  Can the history and physical examination help?

It has been estimated that as many as 5% of emergency department patients with noninfarction chest pain have pericarditis. (NEJM 2004)

Recognizing pericarditis is important because administration of thrombolytics may lead to hemorrhagic complications and even death.

The diagnosis of pericarditis rests on the right clinical story along with a confirmatory finding on physical examination, EKG, or echocardiogram. Describing the sensitivity and specificity of these findings is difficult because there is often no independent gold standard for diagnosis and there are no known large studies on the clinical findings in pericarditis in the emergency department.

Classic symptoms include pain localized at the area of the heart. The pain is classically pleuritic and worse with inspiration.  It is relieved with leaning forward. The pain can radiate to any cardiac referral area, but pain referred to the trapezius ridge might be more specific, caused by irritation of the phrenic nerve(NEJM 2004).

The incidence of a friction rub appears to be somewhat low, perhaps 18-34%(Cohen). It is easier to hear at the left lower sternal border with the patient leaning forward at end expiration.  In the emergency department, however, an additional maneuver for improving audibility is lowering ambient noise.  The rub is often transient and serial examination improves the sensitivity. (NEJM 2004, Spodick JAMA 2003).  Because of the poor sensitivity and specificity of clinical diagnosis, adjunctive testing is generally needed for diagnosis.

Electrocardiographic findings depend on the stage of illness.  Classically the disease starts with diffuse ST-segment elevation, which then resolves, followed by diffuse T-wave inversions, which then resolves. Diffuse PR segment depression may in fact be earlier and more sensitive than ST elevation.

Laboratory support for the diagnosis is said to include elevation in C-reactive protein and erythrocyte sedimentation rate.  However, the sensitivity and specificity for these laboratory markers for pericarditis in emergency department patients with chest pain is not known.  Troponin elevations occur in 35 to 50% , so this can not always help differentiate myocardial infarction from pericarditis.(NEJM)

Finally, an echocardiogram can be used when there is doubt about the differential diagnosis of myocardial infarction and pericarditis.  Regional wall motion abnormalities would support myocardial infarction whereas pericardial effusion, present in 58% of cases, would support pericarditis (Cohen 2008)

The patient’s pain is pleuritic but there are no additional specific signs of pericarditis.  You call the cardiologist and ask for an echocardiogram to ensure no regional wall motion abnormalities.  The cardiologist comes and though there is no effusion, there is also no regional wall movement abnormalities, so you both decide not to give thrombolytics.  Because of diagnostic uncertainty however, you transfer the patient for cardiac catheterization, and the arteries turn out to be clean. The patient’s discharge diagnosis is pericarditis.  The clinical diagnosis of pericarditis and the decision to withhold thrombolytics was felt to be courageous but well-justified, and ultimately protected the patient from exposure to hemorrhagic risks.

Summary: Confirmatory findings include

Exam – Pericardial friction rub

EKG – Classic diffuse ST elevation

Echo – Pericardial effusion


I hear trainees express diffidence about the clinical diagnosis of vaginitis in the emergency department.  While our bedside diagnostic certainty might be limited, studies suggest that it is limited for the specialists as well.  In fact, even after testing for pH, amines, and wet preparation microscopy, 30% of patients remain undiagnosed (Lowe 2009).   Thus, judgment is required.


The initial differential diagnosis centers on the three most common conditions, bacterial vaginosis, candidiasis, and trichomoniasis.  The treatment for the first and third is the same, metronidazole for 7 days.


Thus, the treatment decisions come down to a decision about antifungals.  In general, if the history and physical examination does not give evidence of candidiasis, the patient should be treated with seven days of metronidazole and then referred to the gynecologist for further care.  Although candida is commonly recognized by the cottage cheese discharge, keep in mind that severe cases of candidiasis can present with erythema and fissures. Bacterial vaginosis does not (Sobel 2007).


Sometimes the best thing we do for health of the patient is give helpful lifestyle advice.  Some patients suffer from recurrent vaginitis because of overutilization of antibiotics for winter colds or other practices whose harm is unperceived to them.  Optimal vaginal acidity is maintained by lactobacillus.  Women who suffer from recurrent vaginitis need to do all they can to maintain lactobacillus. Preventable disturbances include douching, frequent introduction of alkaline sperm, and overutilization of antibiotics.


There are several other considerations, especially in the patient with chronic disease, but this at least serves as a reminder that emergency physicians can approach this acute presentation with confidence and make a difference for our patients.



Extraocular movements: intact and painless

Visual fields: intact

Lids/Lacrim: nl, no edema

Conjunctivae/sclera: nl, no injection

Cornea: clear, no ulcers, no uptake of fluorescein

Anterior chamber: clear

Pupils: equally round, reactive to light, no direct or consensual photophobia. No afferent pupillary defect

Fundoscopy: intact red reflex, sharp disc

Intraocular pressure:


A patient presents with eye pain and redness. Does palpation help raise or lower the probability of acute glaucoma?  Is this physical examination finding worth pursuing?

First, it should be stated that many physical findings we pursue lack sufficient specificity to rule in a diagnosis.  Others lack the sensitivity to rule it out.  Palpation of globe pressure has not been studied prospectively as a physical finding in the acute painful eye population.

However, many opthalmologists consider it a useful finding.  If one palpates an asymmetrically rock hard globe on one side then the differential diagnosis can be narrowed substantially.  All that is required is confirmation through tonometry.

It is reasonable for emergency physicians to cultivate this as a bedside skill.  Have the patient look down, and palpate the superior portion of the globe through a closed lid.  See how much force is required to indent the wall. (Heidary 2010).  Use tonometry as the gold standard and hone your skills.

Update: Since first writing this post I heard from a colleague who had a severe trauma patient with GCS 3 and proptosis. Ocular palpation led her to the diagnosis of orbital compartment syndrome. During lateral canthotomy she had trouble with the inferior cantholysis, and again it was the palpation that led her to keep going until the eye softened and she was assured of successful release of pressure.