broken faces

Monday, March 2, 2015

“You can’t put anything on the internet if it isn’t true.”

It’s a funny commercial for State Farm Insurance but when it comes to medicine, everything must be taken with a grain of salt. Just because the website is reputable or the speaker is well credentialed, does not mean that the information is correct. When it comes to analyzing medicine in the news, fact checking can be difficult since the information source may or may not be reliable. And that’s how I came to yell at my computer screen when reading about the facial injury sustained by Oklahoma Thunder’s Russell Westbrook.

The play was accidental, within seconds of the end of the game, and Mr. Westbrook’s face collided with a teammate’s knee. His face lost and a visible dent could be seen. A quick trip for x-rays, perhaps a face CT, and the diagnosis of zygomatic arch fracture was made. The surgery to repair it has already been completed. My frustration began and increased as I read descriptions of the fractured bone and the complications associated with the injury. Unfortunately, the commentary confused zygomatic arch with the zygoma. Two totally different structures within the face and their injuries are cared for in different ways.

The zygoma or zygomatic bone forms the lateral part of the face and the prominence of the cheek. It also forms the lateral wall and floor of the orbit, where the eye is located. This is a different bone than the zygomatic arch, which is formed by a prominence of the zygomatic bone in combination with the frontal bone.

Zygomatic_bone_anterior Zygomatic_bone_lateral

Zygomatic bone

The zygomatic bone helps form the structure of the face and orbit. It supports the eye socket and the muscles located within. There are also foramens (tunnels or holes) that allow arteries, veins and nerves to enter and exit the face and the orbit.

zygomatic arch

The arch, which Russell Westbrook broke is the prominent part of the cheekbone and part of its job to form protect the face against strong blows.It extends behind or poserior from the zygomatic bone and is rather strong because of its arch design. However, its most import responsibility is its location where the muscles of chewing and facial expression attach. And as a bonus, it allows the temporalis muscle to pass under the arch to allow the jaw to move appropriately.

When injured, the face can break in many ways but isolated injuries to the orbital bones including the zygoma and maxilla can occur. By the way, the orbit is also made up of the frontal, sphenoid, ethmoid, palatine, and lacrimal bones. The worry is all about the eye and its function, the sinuses that are located adjacent to those bones and the nerves that enter and exit through the bones. No matter what prominent websites report, the zygomatic arch has no relationship to these structures.

The zygomatic arch can break in association with other bones or it can be an isolated injury. When the arch is broken, the muscles that attach to it go into spasm and make be difficult to open the mouth (trismus). There is asymmetry and flattening of the face but usually no other major disasters. Its purpose is to protect more important facial structures and by collapsing the arch, it has performed its duty.

Treatment of the zygomatic bone fracture is meant to restore the symmetry of the face, make certain that the eye moves normally in the orbit and address any potential nerve damage. Up to 50% of these fractures will heal with no surgery required.

Treating the zygomatic arch fracture depends upon whether it is displace or caved in. If the bone is in the appropriate alignment, not much else is required. But in cases like Mr. Westbrook, where the arch is caved in, surgery is required to restore facial symmetry and to allow the temporalis muscle to pass under the arch unimpeded so jaw movement and chewing can be normalized.

Medicine isn’t that hard once you know anatomy and physiology and can match the two. It might be acceptable for the press to confuse one bone with another…or not. Fact checking is part of the job, just as it is in medicine. By knowing the structures of the body and their purpose, it is easier to look for potential complications. It is also easier to explain to the patient and family what options for treatment are reasonable. Sometimes the discussion gets confusing when the patient has done some research and the information that they read on the internet wasn’t necessarily true and may conflict with the bedside opinion they have just heard. That said, perhaps the best advice is not to rely of reporters for their medical knowledge, or you can just scream at your compute like I did.

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pulmonary embolus

Monday, February 23, 2015

If only patients would read the textbook and always have the same complaints and physical findings for an illness or disease. That would make diagnosis much easier. But real life is never easy when it comes to diagnosis and treatment. Consider the sad stories of Chris Bosh and Jerome Kersey.

Mr. Bosh, in the prime of his career as an NBA superstar notices some pain in his chest and for a few days doesn’t feel quite right. He sees his doctor and after a few tests, the diagnosis is made of pulmonary embolus, blood clots in his lungs. Mr. Kersey, at age 52 a retired basketball star, has one of the common presenting complaints for pulmonary embolus (PE). He dies suddenly with no warning and the diagnosis is made by the coroner. Mr. Kersey is not alone. Pulmonary embolus is the second only to cardiac arrest as the most common cause of sudden death.

There may be close to a million people each year in the US who suffer from PE, but it’s a hard diagnosis to make and the frequency may be even higher. Consider that autopsy studies of people who die in the hospital found that up to 60% had PEs and the diagnosis was missed 70% of the time. And for that reasons, doctors have a high worry factor when it comes to making the diagnosis. Patients show up complaining to their doctor about chest pain, worrying about their hearts, but as it turns out, lots more things cause chest pain that just heart disease.

Modern medicine hasn’t yet figured out how to help patients like Mr. Kersey who die without warning, but Mr. Bosh is a different story. His diagnosis is made and his doctors can high five themselves for not missing the potentially lethal disease. Now comes the tough decisions about treatment options. They all have to do with anticoagulation or thinning the blood. The blood clots in the lung, and there may be one or many, are actually located in the pulmonary arteries. Those are the large blood vessels where blood is pumped from the heart to the lungs, so that oxygen can be attached to red blood cells and then circulated to the rest of the body. Clots in the artery act like a dam and it makes it tough for the heart to pump against resistance. This can strain the heart muscle. If that isn’t enough of a problem, if enough clot is present, blood can’t get into the lung tissue and get loaded with oxygen. The potential exists for shock, hypotension (low blood pressure) and death.

pulmonary artery

The diagnosis is often made by CT and the amount of blood clot can be seen. The patient’s vital signs are monitored and their stability is assessed. The treatment for pulmonary embolus is anticoagulation or thinning the blood with medications. The first questions is whether the patient is so unstable that clotting busting drugs need to be used to dissolve the emboli that are already there. Usually, the answer is no and routine anticoagulation medication can be used. The second question to be answered is whether the patient can be treated at home. Many patients with PEs are stable and will need to be on blood thinning medication for a prolonged period of time. There are different medications available to use as an outpatient and the decision needs to be made whether to use a combination of enoxaparin (Lovenox) and warfarin (Coumadin) or the newer anticoagulants like apixaban (Eliquis) or rivaroxiban (Xarelto).

So how does one decide stability? It’s all about the vital signs. If the patient is tachycardic (rapid heart rate), tachypneic (rapid respiratory rate) and/or hypoxic (low blood oxygen), hospitalization and observation may be appropriate, even if the patient would get the same medications as they would if they were an outpatient. Abnormal vital signs presume that the heart and lungs are not working as well as they should and cannot deliver an adequate oxygen load to the body. Blood tests may be able to quantify how sick. Arterial blood gasses can measure how much oxygen is getting loaded into the blood stream and whether, the lungs are able to remove waste products from the blood. Troponin levels, normally a marker used to check for heart attack, can also help decide whether the heart muscle is being strained because it has to squeeze harder to push blood past the pulmonary artery clots. An echocardiogram, or ultrasound of the heart can also help assess heart strain.

Medications are also evolving and treatment strategies depend upon patient situation and physician comfort in using the newer anticoagulation medications like Eliquis and Xarelto. Classically, warfarin is used and blood levels have to be measured routinely to make certain the blood is adequately thinned. Warfarin dosing is adjusted based on those blood test results. That means patients have to go to the lab routinely, the doctors and nurses have to follow up on the tests and adjust medications. Studies suggest that patient blood is inadequately thinned more that 30% of the time. The new drugs do not need adjustment, blood tests or much follow up. Their downside: price is much more expensive than warfarin (but there is no need for blood tests or office visits) and…the anticoagulation cannot be emergently reversed in a bleeding emergency or if emergency surgery is required. Warfarin can be.

Finally, the question most basketball fans were asking: how long does a patient have to be anticoagulated, because on blood thinners, contact sports are out of the question because of the risk of fatal bleeding from trauma, especially to the head. The easy answer is at least three months. The real answer is…it depends. Questions that need to be asked have to do with the reason for the clot, the patients’ underlying risk of bleeding, if it is a recurrent clot and what other medical issues are present. The American College of Chest Physicians publishes guidelines for the diagnosis and treatment of blood clots and the summary is 47 pages long.

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