Questions of the Week for 3/12/2024

Q: You have a pediatric patient who presents in DKA. They are toxic appearing and do not open their eyes spontaneously but open them to pain and groan. They are moving all four extremities equally and following commands. You are concerned that they may have cerebral edema. What is the next step in managing this?

  • This patient should be treated with either mannitol (1 g/kg) or hypertonic saline (5 mL/kg of 3% NaCl) for presumed cerebral edema. It is controversial which of these is preferred. There has been retrospective evidence that 3% NaCl is associated with worse outcomes, but this is subject to bias.17 Mannitol has diuretic effects, which may promote volume depletion and hypotension in an already hypovolemic patient. At this point, there does not seem to be a clear consensus on which is preferred.

    The patient should also undergo an emergent head CT but treatment should not be delayed for imaging. If you are concerned enough to image, then treat them while awaiting results. They should be treated with standard DKA treatments such as fluid resuscitation and insulin. Historically, there was concern that certain IV fluids may worsen outcomes, however recent studies seem to indicate that fluid type and rate of administration probably does not have a significant effect on cerebral edema outcomes.18 If possible, it is generally best to avoid intubation in DKA patients unless airway protection is necessary from a mental status or airway protection perspective.

Q: You have a 27-year-old male patient with no reported past medical history who has had two days of hematemesis. Their BP is 130/80, HR 75 with the remainder of their vitals within normal limits. Their hemoglobin is 11 g/dL and their BUN is 25 mg/dL (unclear baseline). Their rectal exam has brown stool with no melena or blood. What is the recommended disposition for this patient?

  • Based on the Glasgow Blatchford bleeding score for upper GI bleeds, this patient would be classified as “high risk” and should be admitted. This patient gets points for their anemia and elevated BUN, which can represent digested heme from an upper GI bleed. The score also includes analysis of vital signs, recent syncope, and cardiac/hepatic disease.

    The American College of Gastroenterology (ACG) published a guideline in 2021 that encourages the use of this score and suggests (though with a conditional recommendation and low quality of evidence) that patients with a score of 0-1 should be considered candidates for discharge with outpatient follow up and patients with a score greater than 1 should be admitted.

Q: You admit a patient with an upper GI bleed to the intensive care unit and consult GI for endoscopy. They are happy to see the patient but ask what dose of proton pump inhibitor (PPI) will you give this patient?

  • Interestingly the ACG does not have a firm recommendation for or against PPI before endoscopy but recommends “high dose” PPI therapy after endoscopy. They do note that pre-endoscopic PPI “may modestly reduce need for endoscopic treatment”. It seems reasonable to start this from the ED and realistically essentially all GI consultants will ask for it. The guidelines support either continuous or intermittent dosing. For continuous, they recommend an 80 mg bolus followed by a continuous infusion at 8 mg/hr. Our institution tends to use an intermittent bolus strategy. The dosing for this is a bit less clear, however the ACG guidelines suggest an 80 mg IV bolus followed by 40 mg IV 2-4 times daily. Our institution usually uses pantoprazole, but esomeprazole and omeprazole are also acceptable options.

Q: You are taking care of a patient who presents with bright red blood per rectum. They are overall very well appearing and have only had one episode of bright red blood in the toilet earlier today. They are a 70-year-old male with no previous lower GI bleeds and no gross blood or hemorrhoids on their rectal exam. Their heart rate is 75 and their blood pressure is 140/90. Their hemoglobin is 13 (no baseline available). They are not on any anticoagulation and do not have any comorbidities. What should the disposition for this patient be?

  • According to the ACG guidelines for Management of Patients with Acute Lower Gastrointestinal Bleeding, this patient should probably be admitted for inpatient evaluation of their suspected lower GI bleed. Their Oakland Score for Safe Discharge After Lower GI Bleed is 10, which places them in a higher risk category.5 The ACG suggests (conditional recommendation, low quality of evidence) that patients with an Oakland score greater than 8 are likely higher risk and may not be safe for discharge. Some authors have suggested that increasing the threshold to 10 may allow for more safe discharges without a significant increase in adverse events but this remains somewhat controversial. As always, the ability to obtain prompt follow up and patient factors may significantly impact this decision.

Q: You are taking care of a patient who is in cardiac arrest. Per EMS they had a witnessed arrest which was initially ventricular fibrillation but has now changed to asystole. What key benefits can TEE provide in this case?

  • TEE can help provide vital information on chest compression location and quality, improving perfusion during CPR. Additionally, this patient may actually have fine ventricular fibrillation which is not clearly visualized on the cardiac monitor but may be seen on ultrasound. Identification of fine VF may significantly change your management in this case. TEE can also help provide additional information regarding the etiology of the arrest such as pericardial tamponade, wall motion abnormalities (once ROSC is achieved), right heart strain, etc and has been shown to be associated with lower pauses in compressions during rhythm/pulse checks.

Q: You have a patient who presents with shortness of breath, new atrial fibrillation with rapid ventricular response and chest discomfort. You decide to rule out pulmonary embolism and send them for a CT PE study. A few hours after the CT is done they are awaiting an inpatient bed but are now very hypertensive with increased tachycardia and a new fever. What could be going on?

  • Exacerbation of hyperthyroidism leading to thyroid storm is a known complication of iodinated contrast and has been reported to occur within an hour of contrast administration10. This phenomenon is called the Jod-Basedow effect and is due to the large exogenous iodine load in a susceptible patient (someone with known or undiagnosed hyperthyroidism). The incidence of iodinated contrast induced hyperthyroidism (not necessarily storm) is estimated to be around 0.5 to 5%11.

Q: How would you manage this patient’s atrial fibrillation?

  • Supportive care with optimization of volume status, electrolyte repletion (particularly magnesium and potassium) and anti-pyretic therapy is important as always. Recall that a significant portion of patients with thyroid storm have myocardial dysfunction and that the classically recommended Propranolol can be dangerous if given too aggressively. Consider starting your rate control strategy with the shorter acting Esmolol (recommended by Japanese guidelines)15. Use your bedside echo and clinical picture to help you. Remember that amiodarone also contains iodine and is well known to cause hyperthyroidism, though generally over the course of days to weeks.12 Most authors seem to think that amiodarone use in thyroid storm is acceptable if given in conjunction with (preferably after) anti-thyroid medications.13,14 Some degree of permissive tachycardia is likely preferred for most patients in thyroid storm as over aggressive rate control can lead to hypotension and insufficient perfusion to meet the patient’s metabolic needs. Most patients with a heart rate > 150 probably need rate control but 110-130 may be acceptable.15 As always, consider electrical cardioversion if the patient is unstable and atrial fibrillation is thought to be contributing to their instability. Keep in mind that it may be challenging to convert and keep the patient in sinus rhythm until their underlying pathology is addressed.

References:

  1. Laine L, Barkun AN, Saltzman JR, Martel M, Leontiadis GI. ACG Clinical Guideline: Upper Gastrointestinal and Ulcer Bleeding [published correction appears in Am J Gastroenterol. 2021 Nov 1;116(11):2309]. Am J Gastroenterol. 2021;116(5):899-917. doi:10.14309/ajg.0000000000001245

  2. Blatchford O, Murray WR, Blatchford M. A risk score to predict need for treatment for upper-gastrointestinal haemorrhage. Lancet. 2000;356(9238):1318-1321. doi:10.1016/S0140-6736(00)02816-6

  3. Oakland K, Kothiwale S, Forehand T, et al. External Validation of the Oakland Score to Assess Safe Hospital Discharge Among Adult Patients With Acute Lower Gastrointestinal Bleeding in the US. JAMA Netw Open. 2020;3(7):e209630. Published 2020 Jul 1. doi:10.1001/jamanetworkopen.2020.9630

  4. Garcia-Iglesias P, Machlab S, Martinez-Bauer E, et al. Diagnostic accuracy of the Oakland score versus haemoglobin for predicting outcomes in lower gastrointestinal bleeding. Gastroenterol Hepatol. Published online February 8, 2024. doi:10.1016/j.gastrohep.2024.02.002

  5. Sengupta N, Feuerstein JD, Jairath V, et al. Management of Patients With Acute Lower Gastrointestinal Bleeding: An Updated ACG Guideline. Am J Gastroenterol. 2023;118(2):208-231. doi:10.14309/ajg.0000000000002130

  6. Limb C, Siddiqui MA. Apparent asystole: are we missing a lifesaving opportunity?. BMJ Case Rep. 2015;2015:bcr2014208364. Published 2015 Mar 16. doi:10.1136/bcr-2014-208364

  7. Cummins RO, Austin D Jr. The frequency of 'occult' ventricular fibrillation masquerading as a flat line in prehospital cardiac arrest. Ann Emerg Med. 1988;17(8):813-817. doi:10.1016/s0196-0644(88)80561-4

  8. Amaya S, Langsam A. ‘Ultrasound detection of ventricular fibrillation disguised as asystole’. Ann Emerg Med 1999;33:344–6. 10.1016/S0196-0644(99)70372-0

  9. Ewy GA, Dahl CF, Zimmermann M, Otto C. Ventricular fibrillation masquerading as ventricular standstill. Crit Care Med. 1981;9(12):841-844. doi:10.1097/00003246-198112000-00008

  10. Thumma, Soumya MD1; Manchala, Venkata MD1,2; Mattana, Joseph MD1,2. Radiocontrast-Induced Thyroid Storm. American Journal of Therapeutics 26(5):p e644-e645, September/October 2019. | DOI: 10.1097/MJT.0000000000000844

  11. Basida B, Zalavadiya N, Ismail R, Krayem H. Weathering the Storm: Thyroid Storm Precipitated by Radioiodine Contrast in Metastatic Thyroid Carcinoma. Cureus. 2021;13(3):e14219. Published 2021 Mar 31. doi:10.7759/cureus.14219

  12. Tsang W, Houlden RL. Amiodarone-induced thyrotoxicosis: a review. Can J Cardiol. 2009;25(7):421-424. doi:10.1016/s0828-282x(09)70512-4

  13. Parmar MS. Thyrotoxic atrial fibrillation. MedGenMed. 2005;7(1):74. Published 2005 Jan 4.

  14. Reddy V, Taha W, Kundumadam S, Khan M. Atrial fibrillation and hyperthyroidism: A literature review. Indian Heart J. 2017;69(4):545-550. doi:10.1016/j.ihj.2017.07.004

  15. Satoh T, Isozaki O, Suzuki A, et al. 2016 Guidelines for the management of thyroid storm from The Japan Thyroid Association and Japan Endocrine Society (First edition). Endocr J. 2016;63(12):1025-1064. doi:10.1507/endocrj.EJ16-0336

  16. Muir AB, Quisling RG, Yang MC, Rosenbloom AL. Cerebral edema in childhood diabetic ketoacidosis: natural history, radiographic findings, and early identification. Diabetes Care. 2004;27(7):1541-1546. doi:10.2337/diacare.27.7.1541\

  17. Decourcey DD, Steil GM, Wypij D, Agus MS. Increasing use of hypertonic saline over mannitol in the treatment of symptomatic cerebral edema in pediatric diabetic ketoacidosis: an 11-year retrospective analysis of mortality*. Pediatr Crit Care Med. 2013;14(7):694-700. doi:10.1097/PCC.0b013e3182975cab

  18. Kuppermann N, Ghetti S, Schunk JE, et al. Clinical Trial of Fluid Infusion Rates for Pediatric Diabetic Ketoacidosis. N Engl J Med. 2018;378(24):2275-2287. doi:10.1056/NEJMoa1716816

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