An example of a comprehensive coma exam in a patient with psychogenic coma:



-description – lying supine, well-dressed

-breathing pattern – normal

-breath odor – normal

Head atraumatic normocephalic


-eyes midline and conjugate without deviation

-pupils 2mm, equally reactive

-eyes squint to bright light

-fundoscopy – unable to perform due to eye movement

-purposeful movements detected

Oropharynx – mucus membranes moist

Neck – no meningismus

Chest cta bilat

Heart rrr no mrg

Abd soft, nt, no om

Extremities – warm, no atrophy

Neurologic examination:

Mental status:

-level of consciousness – unreactive

-no receptive or expressive language


-muscle tone normal, not atonic, not increased

-not following motor commands


-withdraws to pain in all 4 extremities


-DTRs symmetrical

-Babinski down bilaterally

Cranial nerves:

II – visual threat – blinks. Eye squints to bright light.

III, IV, VI – does not track.  Oculocephalic reflexes reveal intact motor movements.

V – corneal reflex intact, nares tickling provokes grimace

VII – supraorbital nerve compression yields symmetrical facial grimace

VIII – voice stimulation in ear provokes flinch

IX/X – gag reflex intact

XI/XII – not possible to reliably examine


Motor: purposeful movement to pain

Verbal – no response

Eyes – closed

Coma tests:

Cold calorics reveal nystagmus with fast phase away from the ice



A patient presented with chest pain radiating to the back. She has chronic eczema covering the thorax. The day before she had a full work-up, including CT scan of the chest.  The resident suspects shingles.  “How would you demonstrate that in a patient like this?” you ask the resident. The resident draws vertical lines with Q-tips on her chest and allodynia is detected at upper and lower borders of a band-like distribution.  No vesicles were seen through the eczematous tissue, but gentle rubbing unroofed vesicles in this band-like area but not the remainder of the chest. “Well done!”


The clues to the diagnosis in some of the more challenging cases we see in emergency medicine arise from unique characteristics of nerves.  Ravi Morchi in “Diagnosis Deconstructed” (Emergency Medicine News, December 2011) describes a case where a patient presented with anterior thigh pain which traced out to the area of the femoral nerve. He gently pinched the skin off the thigh and it still hurt, indicating allodynia and the absence of deeper pathology in this area. This ultimately led him upstream to the iliopsoas abscess that was irritating the femoral nerve.


Nerve-related pain is identified through the following steps:

1) Topography

Trace the boundaries of the painful area.  If they correspond to a dermatome or peripheral nerve then this is suspicious for nerve-mediated pain. Of course, the painful area can spread outside of the area of the specific dermatome, so one should not be rigid in the interpretation of this pattern.(Oaklander, Archives of Neurology, 1999)

2) Allodynia

A painful response to nonpainful stimuli suggests neuropathic pain, in the absence of other disease.  A gentle touch of the finger is sufficient to provoke this.  Any modality can exhibit this pattern.  One author describes punctate hyperalgesia as abnormal pain from pinprick, static hyperalgesia from blunt pressure, heat hyperalgesia from hot stimuli and cold hyperalgesia from cold stimuli.(Haanpaa, Am J Med, 2009)

3) Positive findings

In addition to allodynia, other positive nerve-mediated phenomena include paresthesia and lancinating transient sharp pain

4) Negative findings

Sensory deficits are common in neuropathic pain, and can include hypoesthesia to light touch, temperature, and vibration.


Take Home Points:

Map out areas of pain when nerve-related pain is a possibility.

Check for allodynia – the experience of pain in response to non-painful stimuli

Recognize positive and negative phenomena of nerve-related pain.


Acute aortic regurgitation is distinct from chronic aortic regurgitation.  The top three causes are endocarditis, aortic dissection, and blunt trauma.  Analogous to the situation with acute mitral regurgitation (see separate posting), there has not been time for compensatory dilation of the ventricle, so back pressures rise. The left ventricular pressure rises significantly, and patients present with heart failure.


Because the compensatory ventricular dilation and increase in stroke volume has not yet occurred, none of the peripheral signs of aortic insufficiency are seen. No water hammer pulse, no Duroziez sign (to-and-fro murmur over the femoral artery with femoral artery compression) and no exaggerated pulsations seen distally. And in fact, the long murmur of aortic regurgitation is shortened and softened and heard mainly in early diastole (Stout, Circulation, 2009).  It is heard best with the patient sitting and leaning forward.  Augmentation maneuvers include bilateral compression of the arms, with handgrip as a less specific alternative.  Don’t be discouraged though, a search for this sign may pay off in key situations.  The International Registry of Acute Aortic Dissections has shown that the diastolic murmur of aortic regurgitation is present in as many as 44% of patients.(Hagen JAMA 2000)


The treatment is surgical, though afterload reduction is an important temporizing measure.


Take home points:

Acute aortic regurgitation presents with congestive heart failure

The murmur is shorter and more subtle than the chronic form

Peripheral signs of aortic regurgitation typically are not seen


Acute mitral regurgitation is distinct from chronic mitral regurgitation.  The chronic state represents compensatory changes, including dilation of the left ventricle, which preserves cardiac output through increasing stroke volume.  In acute mitral regurgitation however, the left ventricle is typically normal in size, and the regurgitant streams shoots backward, leaving the ventricular volume pathologically low.   Forward flow is diminished, and these patients present with shock.  The retrograde flow causes pulmonary edema.

The classic teaching is that an acute murmur of mitral regurgitation suggests disruption or rupture of a leaflet, usually either from endocarditis or papillary muscle infarction.  But the murmur is different.  Sometimes it can be loud, but typically it is quieter.  The regurgitant blood quickly raises atrial pressure to equalize with the left ventricle.  Thus, regurgitation stops earlier and the murmur is earlier, shorter, and quieter (Stout, Circulation, 2009).

One other finding might help.  The pulmonary pressure is acute high, so P2 happens later.  Meanwhile the left ventricular volume is lower, so A2 happens earlier.  Thus, wide splitting of S2 is present, though this does not appear to have been well-studied recently.

The main point is that if the patient has shock and pulmonary edema without an explanation, look for signs of mitral regurgitation.  A new early systolic murmur or wide splitting of S2 is a sign that your patient may be heading to the operating room.

Take home points:

The murmur of acute mitral regurgitation may be subtle

Consider this diagnosis in unexplained shock and pulmonary edema

Listen for wide splitting of S2


A 2 week old is brought in severe distress and shock.  You suspect congenital heart disease with a ductal-dependent lesion.  Should you start prostaglandin E1?


The anatomy of congenital heart disease can be complex, but as one authority put it, “specific anatomical knowledge of the many complex lesions is not required for good early management.” (Brooks 2008)


The ductus arteriosus in the fetus bypasses the lungs, shunting blood from the pulmonary artery to the aorta.  After birth, the pulmonary resistance drops and it closes by smooth muscle contraction. This happens within the first two weeks, and that is when these patients present.


There are two types of ductal-dependent lesions.  Those that depend on the ductus for pulmonary flow and those that depend on the ductus for aortic flow. They present with cyanosis or shock, respectively. Prostaglandin E1 is indicated when the patient is unstable, and the examination suggests congenital heart disease.


Cyanosis: Apply the hyperoxia test. If the hypoxemia does not resolve with 100% oxygen, then it is assumed there is congenital heart disease.


Shock: Easily confused with sepsis and other systemic diseases. Specific signs of congenital heart disease should be sought, including pathological murmurs, abnormal pulses, rales, hepatomegaly, and cardiomegaly. If any of these are found, prostaglandin E1 is indicated.



-Cyanosis: Failing the hyperoxia test diagnoses congenital heart disease

-Shock: Asymmetric pulses, pathological murmurs, cardiomegaly, and signs of congestive heart failure diagnose congenital heart disease

-Prostaglandin E1 is indicated in the crashing neonate with any physical signs of congenital heart disease.