Musculoskeletal pain is a common ED presentation and emergency providers can often manage it with NSAIDs alone.1 On the other hand, when patients present with small localized areas of intense muscle spasm called trigger points, NSAIDs won’t cut it. A trigger point injection (TPI), however, is a safe and easy way to treat the underlying cause of trigger point pain, and requires only basic equipment already available in most the EDs.
The Emergency Department (ED) is the frontline of the opioid crisis, treating patients with opioid-related infections, opioid withdrawal, and overdose. These encounters can be difficult or even downright confrontational. But that does not have to be the case! With the use of buprenorphine, we can “flip the script” for these encounters, encouraging patient-provider collaboration in the treatment of opioid addiction as medical disease.
Ethanol withdrawal is a complex disease state. Two of the main players are GABA (an inhibitory neurotransmitter) and glutamate (an excitatory transmitter that can act on NMDA receptors). Simplistically, chronic ethanol use leads to a down-regulation of GABA receptors and an up-regulation in glutaminergic receptors, such as NMDA. When ethanol is abruptly discontinued, we are left with a largely excitatory state with less ability for GABA-mediated inhibition and more capacity for NMDA/glutamate-mediated excitation. While much of the treatment of severe ethanol withdrawal is focused on GABA, there are agents, such as phenobarbital and propofol, that can suppress the glutaminergic response. Ketamine seems like it should confer benefit, as well, due to its NMDA antagonist properties. Until recently there was only one clinical study using ketamine for severe ethanol withdrawal.1 Now there are three.2,3
A patient presents to the ED for management of a spider bite. Which of the following statements is correct regarding a bite from the spider pictured?
Intracranial hemorrhage (ICH) is associated with significant disability and mortality. Although evidence-based guidelines exist, many hospitals have their own institutional practice patterns, which can make it difficult to care for these patients in the ED. Dr. Debbie Yi Madhok, an emergency physician and neurointensivist, sat down with Dr. Derek Monette, the ALiEM Deputy Editor in Chief, to discuss updates in the management of ICH. This interview follows up her original popular 2017 ALiEM post on dilemmas in ICH management, and takes a deeper dive into the nuances of seizure prophylaxis, blood pressure control, and platelet transfusions. We present the podcast and key learning points.
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The Toxicologist Mindset series features real-life cases from the San Francisco Division of the California Poison Control System.
Case: A previously healthy 49-year-old woman presented to the emergency department (ED) with acute onset of confusion. Family members noticed her to have unsteady gait and she complained of blurry vision and difficulty urinating. She denied the use of any drugs or alcohol and took no medications. In the ED, her vital signs were: T 98.7, BP 95/59, P 130, RR 16, and O2 sat 100% on room air. Her pupils were 7 mm and reactive and her skin was dry. Bowel sounds were present. She had no focal neurological findings, but appeared “very confused” and “frightened.”
Serum electrolytes, CBC, and liver function tests were all unremarkable. She had a negative urine drug screen and alcohol level. The ECG demonstrated sinus tachycardia with normal intervals, and the brain CT was normal.
What are your next thought processes?
A middle-aged man with a history of diabetes and hypertension presents with nausea, vomiting, and shortness of breath. His laboratory testing is remarkable for a leukocytosis, ketonemia, and an anion gap acidosis (pH of 7.13). The EM resident caring for this patient is surprised to find that the blood glucose is 121 mg/dL.
Which home medication is likely responsible for this presentation?
The patient’s presentation is consistent with diabetic ketoacidosis (DKA) in the absence of hyperglycemia. This entity is known at euglycemic DKA and it is increasingly recognized for an association with a newer oral diabetic medication class, SGLT2 inhibitors. Examples include:
The FDA has approved these three SGLT2 inhibitors for Type 2 diabetics, and at times, they are prescribed off-label for Type 1. The mechanism involves decreasing glucose reabsorption in the nephron’s proximal tubule (via inhibition of the sodium-glucose linked cotransporter-2 protein). This results in increased urinary excretion of glucose that is independent of the body’s insulin secretion.1
Other potential benefits of this class of medications include:1–3
In 2015 the FDA issued a warning, however, that SGLT2 inhibitors may cause ketoacidosis, urinary tract infections, and urosepsis.4 Since then, multiple case reports have been published showing an association between SGLT2 inhibitors and the development of euglycemic DKA.
Euglycemic DKA is an uncommon and likely under-diagnosed phenomenon, best defined as DKA with a lower than expected blood glucose (less than 250 mg/dL according to the American Diabetes Association).4–6
Potential precipitants, in addition to SGLT2 inhibitors, include:7
EPs may delay diagnosis, given the modest glucose levels at the time of presentation. This, however, is false reassurance because DKA is not defined by an absolute blood glucose. Interestingly, patients with euglycemic DKA may have a normal mental status despite marked ketoacidosis, and vomiting seems to be a common complaint.5
Euglycemic DKA treatment is the same as traditional DKA, and includes hydration, insulin, and supportive care. Patients with euglycemic DKA may also need a dextrose infusion given the lower glucose levels.
The mechanisms by which SGLT2 inhibitors cause or predispose to euglycemic DKA are unclear and likely complex. SGLT2 inhibitors may lead to a decrease in either endogenous or exogenous insulin, and an increase in glucagon production.8 This insulin deficiency or resistance may be mild in Type 2 diabetics, however, preventing the profound spike in blood glucose seen in traditional DKA.7
The evidence suggesting a link between SGLT2 inhibitors and euglycemic DKA remains limited to case reports. Both the FDA and the European Medicine Agency have reported cases of DKA with unusually low glucose levels.4,9 Peters et al. reported 13 episodes euglycemic DKA in patients taking SGLT2 inhibitors, though most were Type 1 diabetics.10 In Japan, 28 cases of DKA or ketoacidosis in patients taking SGLT2 inhibitors have been reported as of 2015. Of these, the initial blood glucose is known in only 14 cases, but in 9 cases, it was <300 mg/dL.8