TEMPORAL ARTERY EXAMINATION: PART OF THE HEADACHE EXAMINATION IN THE ELDERLY

A patient presents with jaw pain.  At triage, 100.4 is found to be her temperature.  She is a poor historian. You ask specific, targeted questions in an effort to narrow the differential diagnosis.  She answers each by redoubling her description of the pain. Routine examination is unrevealing.  The dentition appears normal.  She has difficulty localizing the pain. You palpate for pre and postauricular lymph nodes and note she has scalp tenderness.  Could this be temporal arteritis?

 

Temporal arteritis is actually a misnomer, as it tends to affect any of the cranial vessels from the aortic arch.  The pathologic diagnosis, and the modern preferred term, is “giant cell arteritis.” It is strongly associated with polymyalgia rheumatica, a periarticular synovitis presenting with pain and morning stiffness of the shoulder girdle, but can also affect the neck and pelvic girdle.(Salvarani NEJM 2002)

 

Giant cell arteritis presents with four categories of symptoms:

1) Cranial arteritis – stroke, amaurosis fugax, diplopia, etc.

2) Extracranial arteritis – headache and scalp tenderness, jaw claudication, etc.

3) Systemic symptoms – fatigue, anorexia, fever, malaise, weight loss, fever etc.

4) Polymalgia rheumatica – synovitis of the periarticular structures of the shoulder and other musculoskeletal units, especially hand edema.

 

Temporal arteritis is a pathologic diagnosis, and this pathology is actually something that can be directly examined. The temporal artery emerges preauricularly and forks into the frontal branch and parietal branch. Palpate in these areas.  Does it feel inflamed? Is there tenderness?  Dilation?  Absence of a pulse?  Any of these abnormalities might indicate temporal arteritis.

 

The 1990 American College of Rheumatology criteria for diagnosis starts with age,  headache, and any temporal artery abnormality on physical examination.(Hunter Arthritis Rheum 1990)

 

The original description by Hutchison in 1890 tells you what you might see: red linear streaks on the head, painful, swollen temporal arteries, which eventually become firm and pulseless.

 

Take home points:

-The temporal artery is accessible to palpation

-Temporal arteritis can be recognized at the bedside by inspection and palpation of the temporal artery

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SHOULDER DYSTOCIA

A patient presents to the emergency department in labor.  You check and as you look, she pushes the head out which you catch just in time with some counter-pressure to control delivery. But now things stop and the shoulder won’t deliver. You run your finger between the neck and shoulder – no nuchal cord. What do you do next?

 

The goal is to get the baby out as soon as possible and prevent hypoxic ischemic encephalopathy and brachial plexopathy (Gurewitsch Clin Ob Gyn 2007). You have about 6-8 minutes of “head-to-body” time until brain injury can occur (time the head is sitting on the perineum). Try a maneuver for shoulder dystocia, but if it does not lead to easy delivery then it did not work and quickly go to the next one.  This is the right kind of haste.  The wrong kind of haste is to jerk the child out, which risks brachial plexopathy.  Finesse is needed, not force.

 

Most of the risk of brachial plexopathy is from lateral traction on the neck.  Axial traction is much safer.  If one finds that lateral traction would be needed, it usually means positioning of the fetus is not yet ideal.

 

In recent years, suprapubic pressure (intended to push the obstructed shoulder posteriorly) and McRoberts maneuver (hyperflexion of the hips) are emphasized.  These maternal maneuvers do work 25-40% of the time. Additionally, McRoberts can help open up passage of the fetus deeper into the pelvis and improve the transit. However, a few generations ago in the 1940s fetal manipulation was used predominantly, and rates of brachial plexopathy were actually lower. (Gurewitsch 2007)

 

Rotational manipulation of the fetus is safe and effective, and should be turned to quickly in cases of dystocia, long before lateral traction is considered.

 

You try suprapubic pressure and the child’s shoulder moves slightly.  You then rotate the infant and the delivery follows spontaneously.

 

Take home points:

-For shoulder dystocia, fetal manipulation can be more effective than maternal manipulation

-if one maneuver does not fully solve the problem, go to the next maneuver

-Lateral traction of the neck is to be avoided

BPPV WITHOUT NYSTAGMUS

The traditional teaching is that one must not diagnose benign paroxysmal positional vertigo (BPPV) unless geotropic nystagmus is seen on Dix-Hallpike maneuver. But in the emergency department, we commonly see patients with classic paroxysms of vertigo, classic positional triggers, and yet Dix-Hallpike is normal. What is the basis for the traditional view that requires for the diagnosis of BPPV a positive Dix-Hallpike maneuver?

 

A critically appraised review found that only one study has “tested the test,” finding a sensitivity of 79% and a specificity of 75% (Halker, Neurologist, 2008). Supporting this is the reporting in a review that repositioning maneuvers were effective in 50-97% of these patients (Alvarenga, Braz J Otorhinolaryngol 2011).

 

Remember of course that Epley is for posterior canal BPPV. So some of these patients with a history that says BPPV and no confirming tests will have a different canal affected. Go ahead and try Epley but if it does not work, consider testing for alternate canals, or, more simply, refer to otolaryngology.

 

Take home points:

-Use the Epley maneuver in BPPV without nystagmus

-Refer non-responders to the otolaryngologist for consideration of anterior or horizontal canal variants.

HYPOXEMIA: A PHYSIOLOGIC DIFFERENTIAL DIAGNOSIS

You are taking care of a patient with sepsis of unclear cause and find hypoxemia.  The chest x-ray is normal.  What is causing the hypoxemia?

When the history and physical examination do not reveal an explanation for hypoxemia, it helps to think physiologically. Air, chest vasculature, and blood all are essential.

Classically, hypoxemia is caused by:

Low PiO2 (example, altitude)

Lungs: Impaired diffusion (now thought to be an uncommon contribution)

Alveolar hypoventilation

V/Q mismatch (diseases of the chest)

Shunt (a type of V/Q mismatch with theoretically zero ventilation)

Dead space (a type of V/Q mismatch with theoretically zero perfusion)

At the bedside, the relevant differentiation is alveolar hypoventilation from V/Q mismatch.  Is the patient alert and breathing adequately? Order an arterial blood gas if there is doubt, and look for elevated CO2 as an indicator of underventilation.  For everything else, consider the lungs and the heart.

In this case, further questioning of the patient revealed longstanding tobacco use and subsequent chronic obstructive pulmonary disease.  The patient has chronic V/Q mismatch.

Take home points:

For unexplained hypoxemia, assess ventilation

If ventilation is normal, pursue diseases of the chest

INCARCERATED HERNIA

A patient presents with pain in his ventral hernia.  You wonder whether it could be strangulated. Does the bedside examination help?  Sure. Check for tenderness, localized peritoneal signs, assess appetite, ability to eat and drink, bowel habits.  Does this answer the question as to whether there is strangulation?  Probably not.

 

There is no question that strangulated hernias need immediate surgery.  And there is no question that reducible hernias, if there is no concern for infarction, do not need admission to the hospital.  But it seems that there is some debate over incarcerated hernias.  Many surgeons, at least in southern California, want to send patients with “incarcerated but non-strangulated hernias” home.  They will tell the emergency physician over the phone that there is no strangulation.

 

The problem is that there is no way to reliably identify this category of patient. The gold standard for diagnosis of strangulation is the surgeon’s eye and hands on the bowel.  This means looking at the bowel for color, signs of venous congestion, and peristalsis.  Some choose to do this laparoscopically through the hernia site (Ferzli Surg Endosc 2004). A study of 147 patients with incarcerated hernia found at operation that 61 were strangulated and 85 were merely incarcerated (Alvarez Hernia 2004). 41% of these patients experienced complications after surgery.  There are no studies I found that say physical diagnosis can reliably discriminate strangulation from mere incarceration.

 

Incarceration and acute pain suggests venous obstruction.  Even if one could be assured there is no strangulation, untreated venous congestion disrupts the health of the bowel and puts the patient at risk for local adhesions (Kingsnorth A Fundamentals of Surgical Practice 2011).  Surgeons, before telling emergency physicians to send patients home with incarcerated hernias, need to cite evidence for why this is safe.  A search today on pubmed for “outpatient incarcerated hernia” reveals that outpatient management of incarcerated hernias never been studied.

 

If you are the emergency physician what can you do?  Reduce the reducible hernias.  Give good analgesia, try to pull traction on the hernia and then compress it to evacuate the extra venous blood.  If it still doesn’t reduce, then this is a case where you call the surgeon and request surgery, or at least admission for observation.

 

Take home points:

Using physical diagnosis to decide strangulation is usually not possible

Using physical diagnosis to decide incarceration is easy

Patients with incarcerated hernias need surgical evaluation

TACHYCARDIA: A PHYSIOLOGIC DIFFERENTIAL DIAGNOSIS

A patient is found to have unexpected tachycardia.  What is the cause?  We use associated symptoms and signs to guide the diagnostic approach.  When that isn’t clear, a physiologic approach might enhance bedside diagnostic reasoning:

 

Cardiac output (CO) = stroke volume (SV) x heart rate (HR)

 

Although the simple equation in a living organism belies much deeper complexity, we can reason that an increase in heart rate means one of three things:

 

1. Stroke volume is decreased

a. Decreased preload (hypovolemia, pulmonary embolism)

b. Decreased inotropy (congestive heart failure)

c. Increased afterload (hypertensive congestive heart failure)

2. Cardiac output is increased

3. Primary disturbance in heart rate

 

Using this approach generates its own differential diagnosis, and may help in subtle presentations.

 

Take home points:

-CO = SV x HR

-An increased heart rate suggests increased cardiac output or decreased stroke volume