Morbidity and Mortality WITH DR. Ludmer
Posterior Reversible Encephalopathy Syndrome (PRES)
PRES is characterized by subcortical edema most commonly in the posterior fossa on imaging. The etiology of the edema is thought to be due to endothelial dysfunction although the exact etiology is unclear. It is thought that rapid fluctuations in blood pressure play a role in this disease process. It is important to note that up to 20% of patients presenting with PRES will not present with hypertension.
Management of PRES should focus on treating the underlying etiology, managing HTN, and treating seizures.
Abdominal Aortic Aneurysm (AAA)
Only 21% of patients present with the classic AAA triad of abdominal or back pain, pulsatile mass, and hypotension. Most AAAs are diagnosed on routine screening exams or as incidental findings on other imaging.
As more and more imaging studies are ordered in the Emergency Department more incidental findings are being identified. Of all major incidental findings only 21% are reported in a provider's medical decision making, about 15% are referred for follow up, and about 5% of patients follow up within two years. It is unknown what affect this has on patient outcomes.
Lemierre's Syndrome was initially described in the 1940s as a septic thrombophelitis of the internal jugular vein in the setting of the ENT infection. Providers should consider the diagnosis of Lemierre's Syndrome when patients present with ENT infection, IJ thrombus, and evidence of embolic foci. Peritonsillar abscess is the most common cause of Lemierre's Syndrome. Infection is thought to be due to bacterial superinfection following a viral URI. Most cases occur in patients under 40 years of age. Patients can also present with Horner syndrome on physical exam.
There is no good evidence documenting the incidence of focal neurologic symptoms in the setting of Lemierre's Syndrome. Consider anticoagulation in the setting of extensive thrombus or in the setting of septic emboli. Diagnostic imaging of choice is CTA of the neck.
Patient reported symptoms are generally unreliable in the diagnosis for septic arthritis. Leukocytosis is unreliable in the diagnosis of septic joint. ESR and CRP are also largely unreliable unless they are significantly elevated, ESR >100 and CRP >200.
Ruling in gout as the etiology of monoarticular arthritis does not rule out infectious etiology. The evidence suggests that 1.5% of all gouty flares have concomitant septic arthritis.
Heparin Induced Thrombocytopenia (HIT)
HIT is due to antibody formation against heparin and platelet factor 4 (PF4). These antibodies then bind to platelets causing thrombosis and thrombocytopenia. Although significantly less common, this still can occur in the setting of low molecular weight heparin. Classically, HIT occurs 5-10 days after initial heparin exposure. However in patients who have previously been exposed to heparin, HIT can occur within 24-72 hours. Thrombocytopenia can occur rapidly and is characterized by a 50% drop in platelet count. Thrombosis occurs most commonly in the venous system by can occur in the arterial system as well. The 4Ts score can be used when evaluating a patient for HIT.
Taming the SRU: The Dyspnic Patient WITH DR. Randolph
When evaluating the dyspneic patient it is important to consider upper airway, pulmonary, cardiac, neurologic, hematologic, endocrine and toxicological etiologies. In the undifferentiated dyspneic patient the differential is broad.
Ventilation is due to aeration of the lungs. Perfusion is based on the blood the reaches the alveoli. V/Q mismatch occurs when the ventilation and perfusion of are not evenly matched. V/Q matching is necessary for ideal gas exchange.
A-a gradient stands for the aveolar-arterial gradient. The A-a gradient can be helpful when evaluating the patient with refractory hypoxia. In hypoxic patients with a normal A-a gradient this is concerning of global hypoventilation and normal underlying lung parenchymea. Often these patients will have an elevated pCO2. A hypoxic patient with an elevated A-a gradient considered V/Q mismatch, right to left shunt, or increased O2 extraction as possible etiologies for hypoxia.