Emergency Medical Minute Emergency Medical Minute

Contributor: Travis Barlock MD
Educational Pearls:
Thrombolytic therapy (tPA or TNK) is often used in the ED for strokes
Use of anticoagulants with INR > 1.7 or  PT >15
Warfarin will reliably increase the INR
Current use of Direct thrombin inhibitor or Factor Xa inhibitor 
aPTT/PT/INR are insufficient to assess the degree of anticoagulant effect of Factor Xa inhibitors like apixaban (Eliquis) and rivaroxaban (Xarelto) 
Intracranial or intraspinal surgery in the last 3 months
Intracranial neoplasms or arteriovenous malformations also increase the risk of bleeding
Current intracranial or subarachnoid hemorrhage
History of intracranial hemorrhage from thrombolytic therapy also contraindicates tPA/TNK
Recent (within 21 days) or active gastrointestinal bleed
Hypertension
BP >185 systolic or >110 diastolic
Administer labetalol before thrombolytics to lower blood pressure
Timing of symptoms
Onset > 4.5 hours contraindicates tPA
Platelet count BGL Potential alternative explanation for stroke-like symptoms obviating need for thrombolytics
References
1. Fugate JE, Rabinstein AA. Absolute and Relative Contraindications to IV rt-PA for Acute Ischemic Stroke. The Neurohospitalist. 2015;5(3):110-121. doi:10.1177/1941874415578532
2. Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the Early Management of Patients with Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke a Guideline for Healthcare Professionals from the American Heart Association/American Stroke Association. Vol 50.; 2019. doi:10.1161/STR.0000000000000211
Summarized by Jorge Chalit, OMSII | Edited by Jorge Chalit

Contributor: Ricky Dhaliwal, MD
Educational Pearls:
Takotsubo cardiomyopathy, also known as "broken heart syndrome,” is a temporary heart condition that can mimic the symptoms of a heart attack, including troponin elevations and mimic STEMI on ECG.
The exact cause is not fully understood, but it is often triggered by severe emotional or physical stress. The stress can lead to a surge of catecholamines which affects the heart (multivessel spasm/paralysed myocardium).
The name "Takotsubo" comes from the Japanese term for a type of octopus trap, as the left ventricle takes on a distinctive shape resembling this trap during systole. The LV is dilated and part of the wall becomes akenetic. These changes can be seen on ultrasound.
The population most at risk for Takotsubo are post-menopausal women.
Coronary angiography is one of the only ways to differentiate Takotsubo from other acute coronary syndromes.
Most people with Takotsubo cardiomyopathy recover fully.
References
Amin, H. Z., Amin, L. Z., & Pradipta, A. (2020). Takotsubo Cardiomyopathy: A Brief Review. Journal of medicine and life, 13(1), 3–7. https://doi.org/10.25122/jml-2018-0067
Bossone, E., Savarese, G., Ferrara, F., Citro, R., Mosca, S., Musella, F., Limongelli, G., Manfredini, R., Cittadini, A., & Perrone Filardi, P. (2013). Takotsubo cardiomyopathy: overview. Heart failure clinics, 9(2), 249–x. https://doi.org/10.1016/j.hfc.2012.12.015
Dawson D. K. (2018). Acute stress-induced (takotsubo) cardiomyopathy. Heart (British Cardiac Society), 104(2), 96–102. https://doi.org/10.1136/heartjnl-2017-311579
Kida, K., Akashi, Y. J., Fazio, G., & Novo, S. (2010). Takotsubo cardiomyopathy. Current pharmaceutical design, 16(26), 2910–2917. https://doi.org/10.2174/138161210793176509
Summarized by Jeffrey Olson MS2 | Edited by Jorge Chalit, OMSII

Contributor: Ricky Dhaliwal MD
Educational Pearls:
Primary adrenal insufficiency (most common risk factor for adrenal crises)
An autoimmune condition commonly known as Addison's Disease
Defects in the cells of the adrenal glomerulosa and fasciculata result in deficient glucocorticoids and mineralocorticoids
Mineralocorticoid deficiency leads to hyponatremia and hypovolemia
Lack of aldosterone downregulates Endothelial Sodium Channels (ENaCs) at the renal tubules
Water follows sodium and generates a hypovolemic state
Glucocorticoid deficiency contributes further to hypotension and hyponatremia
Decreased vascular responsiveness to angiotensin II
Increased secretion of vasopressin (ADH) from the posterior pituitary
An adrenal crisis is defined as a sudden worsening of adrenal insufficiency
Presents with non-specific symptoms including nausea, vomiting, fatigue, confusion, and fevers
Fevers may be the result of underlying infection
Work-up in the ED includes labs looking for infection and adding cortisol + ACTH levels
Emergent treatment is required
100 mg hydrocortisone bolus followed by 50 mg every 6 hours
Immediate IV fluid repletion with 1L normal saline
The most common cause of an adrenal crisis is an acute infection in patients with baseline adrenal insufficiency
Often due to a gastrointestinal infection
References
1. Bancos I, Hahner S, Tomlinson J, Arlt W. Diagnosis and management of adrenal insufficiency. Lancet Diabetes Endocrinol. 2015;3(3):216-226. doi:10.1016/S2213-8587(14)70142-1
2. Bornstein SR, Allolio B, Arlt W, et al. Diagnosis and Treatment of Primary Adrenal Insufficiency: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2016;101(2):364-389. doi:10.1210/jc.2015-1710
3. Cronin CC, Callaghan N, Kearney PJ, Murnaghan DJ, Shanahan F. Addison disease in patients treated with glucocorticoid therapy. Arch Intern Med. 1997;157(4):456-458.
4. Feldman RD, Gros R. Vascular effects of aldosterone: sorting out the receptors and the ligands. Clin Exp Pharmacol Physiol. 2013;40(12):916-921. doi:10.1111/1440-1681.12157
5. Hahner S, Loeffler M, Bleicken B, et al. Epidemiology of adrenal crisis in chronic adrenal insufficiency: the need for new prevention strategies. Eur J Endocrinol. 2010;162(3):597-602. doi:10.1530/EJE-09-0884 
Summarized by Jorge Chalit, OMSII | Edited by Meg Joyce & Jorge Chalit
 

Contributor: Travis Barlock, MD
Educational Pearls:
Cancer-related emergencies can be sorted into a few buckets:
Infection
Cancer itself and the treatments (chemotherapy/radiation) can be immunosuppressive. Look out for conditions such as sepsis and neutropenic fever.
Obstruction
Cancer causes a hypercoagulable state. Look out for blood clots which can cause emergencies such as a pulmonary embolism, stroke, superior vena cava (SVC) syndrome, and cardiac tamponade.
Metabolic
Cancer can affect the metabolic system in a variety of ways. For example, certain cancers like bone cancers can stimulate the bones to release large amounts of calcium leading to hypercalcemia. Tumor lysis syndrome is another consideration in which either spontaneously or due to treatment, tumor cells will release large amounts of electrolytes into the bloodstream causing hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia.
Medication side effect
Immunomodulators can have strange side effects. A common one to know is Keytruda (pembrolizumab), which can cause inflammation in any organ. So if you have a cancer patient on immunomodulators with any inflammatory changes (cystitis, colitis, pneumonitis, etc), talk to oncology about whether steroids are indicated.
Chemotherapy can cause tumor lysis syndrome (see above), and multiple chemotherapeutics are known to cause heart failure (doxorubicin, trastuzumab), kidney failure (cisplatin), and pulmonary toxicity (bleomycin).
References
Campello, E., Ilich, A., Simioni, P., & Key, N. S. (2019). The relationship between pancreatic cancer and hypercoagulability: a comprehensive review on epidemiological and biological issues. British journal of cancer, 121(5), 359–371. https://doi.org/10.1038/s41416-019-0510-x
Gyamfi, J., Kim, J., & Choi, J. (2022). Cancer as a Metabolic Disorder. International journal of molecular sciences, 23(3), 1155. https://doi.org/10.3390/ijms23031155
Kwok, G., Yau, T. C., Chiu, J. W., Tse, E., & Kwong, Y. L. (2016). Pembrolizumab (Keytruda). Human vaccines & immunotherapeutics, 12(11), 2777–2789. https://doi.org/10.1080/21645515.2016.1199310
Wang, S. J., Dougan, S. K., & Dougan, M. (2023). Immune mechanisms of toxicity from checkpoint inhibitors. Trends in cancer, 9(7), 543–553. https://doi.org/10.1016/j.trecan.2023.04.002
Zimmer, A. J., & Freifeld, A. G. (2019). Optimal Management of Neutropenic Fever in Patients With Cancer. Journal of oncology practice, 15(1), 19–24. https://doi.org/10.1200/JOP.18.00269
Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit, OMSII
 

Contributor: Travis Barlock MD
Educational Pearls:
There are three indications for IV albumin in the ED
Spontaneous bacterial peritonitis (SBP)
Patients with SBP develop renal failure from volume depletion
Albumin repletes volume stores and reduces renal impairment
Albumin binds inflammatory cytokines and expands plasma volume
Reduced all-cause mortality if IV albumin is given with antibiotics
Hepatorenal syndrome
Cirrhosis of the liver causes the release of endogenous vasodilators
The renin-angiotensin-aldosterone system (RAAS) fails systemically but maintains vasoconstriction at the kidneys, leading to decreased renal perfusion
IV albumin expands plasma volume and prevents failure of the RAAS
Large volume paracentesis
Large-volume removal may lead to circulatory dysfunction
IV albumin is associated with a reduced risk of paracentesis-associated circulatory dysfunction
There are many other FDA-approved conditions for which to use exogenous albumin but the data are conflicted about the benefits on mortality
References
1. Arroyo V, Fernandez J. Pathophysiological basis of albumin use in cirrhosis. Ann Hepatol. 2011;10(SUPPL. 1):S6-S14. doi:10.1016/s1665-2681(19)31600-x
2. Bai Z, Wang L, Wang R, et al. Use of human albumin infusion in cirrhotic patients: a systematic review and meta-analysis of randomized controlled trials. Hepatol Int. 2022;16(6):1468-1483. doi:10.1007/s12072-022-10374-z
3. Batool S, Waheed MD, Vuthaluru K, et al. Efficacy of Intravenous Albumin for Spontaneous Bacterial Peritonitis Infection Among Patients With Cirrhosis: A Meta-Analysis of Randomized Control Trials. Cureus. 2022;14(12). doi:10.7759/cureus.33124
4. Kwok CS, Krupa L, Mahtani A, et al. Albumin reduces paracentesis-induced circulatory dysfunction and reduces death and renal impairment among patients with cirrhosis and infection: A systematic review and meta-analysis. Biomed Res Int. 2013;2013. doi:10.1155/2013/295153
5. Sort P, Navasa M, Arroyo V, et al. Effect of Intravenous Albumin on Renal Impairment and Mortality in Patients with Cirrhosis and Spontaneous Bacterial Peritonitis. N Engl J Med. 1999;341(6):403-409.
Summarized by Jorge Chalit, OMSII | Edited by Meg Joyce & Jorge Chalit
 

Contributor: Ricky Dhaliwal, MD
Educational Pearls:
What are DKA and HHS?
DKA (Diabetic Ketoacidosis) and HHS (Hyperosmolar Hyperglycemic State) are both acute hyperglycemic states.
DKA
More common in type 1 diabetes.
Triggered by decreased circulating insulin.
The body needs energy but cannot use glucose because it can’t get it into the cells.
This leads to increased metabolism of free fatty acids and the increased production of ketones.
The buildup of ketones causes acidosis.
The kidneys attempt to compensate for the acidosis by increasing diuresis.
These patients present as dry and altered, with sweet-smelling breath and Kussmaul (fast and deep) respirations.
HSS
More common in type 2 diabetes.
In this condition there is still enough circulating insulin to avoid the breakdown of fats for energy but not enough insulin to prevent hyperglycemia.
Serum glucose levels are very high – around 600 to 1200 mg/dl.
Also presents similarly to DKA with the patient being dry and altered.
Important labs to monitor
Serum glucose
Potassium
Phosphorus
Magnesium
Anion gap (Na - Cl - HCO3)
Renal function (Creatinine and BUN)
ABG/VBG for pH
Urinalysis and urine ketones by dipstick
Treatment
Identify the cause, i.e. Has the patient stopped taking their insulin?
Aggressive hydration with isotonic fluids.
Normal Saline (NS) vs Lactated Ringers (LR)?
LR might resolve the DKA/HHS faster with less risk of hypernatremia.
Should you bolus with insulin?
No, just start a drip.
0.1-0.14 units per kg of insulin.
Make sure you have your potassium back before starting insulin as the insulin can shift the potassium into the cells and lead to dangerous hypokalemia.
Should you treat hyponatremia?
Make sure to correct for hyperglycemia before treating. This artificially depresses the sodium.
Should you give bicarb?
Replace if the pH Don’t intubate, if the patient is breathing fast it is because they are compensating for their acidosis.
References
Andrade-Castellanos, C. A., Colunga-Lozano, L. E., Delgado-Figueroa, N., & Gonzalez-Padilla, D. A. (2016). Subcutaneous rapid-acting insulin analogues for diabetic ketoacidosis. The Cochrane database of systematic reviews, 2016(1), CD011281. https://doi.org/10.1002/14651858.CD011281.pub2
Chaithongdi, N., Subauste, J. S., Koch, C. A., & Geraci, S. A. (2011). Diagnosis and management of hyperglycemic emergencies. Hormones (Athens, Greece), 10(4), 250–260. https://doi.org/10.14310/horm.2002.1316
Dhatariya, K. K., Glaser, N. S., Codner, E., & Umpierrez, G. E. (2020). Diabetic ketoacidosis. Nature reviews. Disease primers, 6(1), 40. https://doi.org/10.1038/s41572-020-0165-1
Duhon, B., Attridge, R. L., Franco-Martinez, A. C., Maxwell, P. R., & Hughes, D. W. (2013). Intravenous sodium bicarbonate therapy in severely acidotic diabetic ketoacidosis. The Annals of pharmacotherapy, 47(7-8), 970–975. https://doi.org/10.1345/aph.1S014
Modi, A., Agrawal, A., & Morgan, F. (2017). Euglycemic Diabetic Ketoacidosis: A Review. Current diabetes reviews, 13(3), 315–321. https://doi.org/10.2174/1573399812666160421121307
Self, W. H., Evans, C. S., Jenkins, C. A., Brown, R. M., Casey, J. D., Collins, S. P., Coston, T. D., Felbinger, M., Flemmons, L. N., Hellervik, S. M., Lindsell, C. J., Liu, D., McCoin, N. S., Niswender, K. D., Slovis, C. M., Stollings, J. L., Wang, L., Rice, T. W., Semler, M. W., & Pragmatic Critical Care Research Group (2020). Clinical Effects of Balanced Crystalloids vs Saline in Adults With Diabetic Ketoacidosis: A Subgroup Analysis of Cluster Randomized Clinical Trials. JAMA network open, 3(11), e2024596. https://doi.org/10.1001/jamanetworkopen.2020.24596
Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit, OMSII