Its 7:01am. Your shift in your department’s high acuity area is just beginning, and you are waiting to receive sign out. There hasn’t even been time to get your first sip of coffee. Just as you are lifting your cup to your lips, the charge nurse grabs you and says, “Doctor, I need you! This patient isn’t looking so good!” [...]
Editor’s note: This post was listed in the LITFL Review 153‘s “Best of #FOAMed” category.
Venous thromboembolism (VTE) (deep vein thrombosis or pulmonary embolism) has an incidence of roughly 1 in 1,000 with an incidence of PE with or without DVT of 2.3 per 10,000.
One major factor to consider is that VTE is much more common in the elderly and has a mortality highly associated with co-morbidities such as cancer and underlying cardiovascular disease.
In the distant past any diagnosis of DVT and/or PE would result in admission for heparin bridging to oral anticoagulation therapy. This was largely due to a fear that outpatient management would lead to an increase in fatal embolic or major bleeding events. However, there is a great amount of literature that has established the safety of outpatient management of “low-risk” DVT; outpatient treatment has become standard of care for these patients.
“Low-risk” patients were those with no prior VTE, no PE, no prior heparin use, and no confounding co-morbidities (cancer, infection, stroke, etc).
So what about PE?
If outpatient management is standard of care for a select group of DVT patients, then can we treat PE as an outpatient? [...]
As an EM physician, it is difficult to have working knowledge of the hundreds of different types of rashes that exist. However, I argue that it is not the job of the EM physician to diagnose every rash that comes in the ED. That is the job of the dermatologist who has the luxury of time and biopsies. Rather, it is our duty, just like chest pain and syncope, to rule out the life-threatening causes of skin lesions, quickly identify a potentially lethal rash, and provide the appropriate initial stabilization, resuscitation and disposition (ICU, surgery).
The left bundle branch arises from the Bundle of His, and subsequently is divided into the anterior and posterior fascicles. The anterior fascicle is usually supplied by septal perforators from the Left Anterior Descending artery, and the posterior fascicle typically has a dual supply from septal perforators from the Left Anterior Descending artery and the Posterior Descending artery (arising from the Right Coronary).
Electrocardiographically, a LBBB is defined as QRS duration greater than or equal to 120 ms; a broad-notched or slurred R wave in leads I, aVL, V5, and V6; absent Q waves in leads I, V5, and V6; and an R peak time >60 ms in leads V5 and V6 but normal in leads V1 to V3 (1). LBBB can be transient and/or rate-related (1). These morphologic changes make it difficult to discern whether or not a patient presenting to the emergency department with chest pain is experiencing a STEMI. [...]
A New Way to Think About Subarachnoid Hemorrhage:
It is helpful to remember that while a subarachnoid hemorrhage is in fact a “bleed”, it is also a stroke. When compared to ischemic strokes, hemorrhagic strokes tend to have an increased risk death in the acute phase, but for those patients that don’t die, their overall prognosis for return-to-baseline is somewhat better than ischemic events. Why is this? During hemorrhagic strokes (i.e. bleeds), an artery bursts, bathing brain cells in blood. The cells become “stunned”, but there is rarely significant cell death surrounding these events. If the total volume of hemorrhage is small, a patient has a chance at making a full, or near-full recovery (depending on extent of injury and any herniation symptoms).
In ischemic events, lack of blood flow to brain cells causes cellular destruction, and a watershed “penumbra” effect can cause large swaths of brain cell death relative to the small area of initial ischemia. In ischemic cell death, brain cells don’t remodel or regain function, which is why ischemic stroke patients have a high likelihood of residual neurologic deficit. This terminal cell death is also why there is such a push for early identification of ischemic stroke, and why thrombolytics and other neurologic intervention procedures have gained such momentum.
Patients presenting with headaches are worrisome because it can be difficult to sift through so many associated symptoms to determine who has benign pathology and who has a catastrophe brewing in their brain. It is my goal to give you the needed strategy to be a rock star when it comes to evaluating headache patients. [...]