Teaching Shifts

This post is based on Teaching Shifts From Dr Christophe, Dr Taitt, and Dr Berland

Case 1:

A 24-year-old female with no medical problems presents with abdominal pain, nausea, and vomiting. Her LMP was last week. She denies alcohol use but admits to daily marijuana use. When you peruse her chart, you notice that she has had multiple similar presentations to the ED. She denies recent travel, sick contacts, or exposure to suspicious foods. She has not had diarrhea, urinary symptoms, vaginal discharge, fevers, or chills. VS HR 105 BPM, RR 22, BP 112/80, T 37.1C, FS 75 mg/dL. The abdomen is soft with minimal tenderness in the epigastric area.

Cannabinoid hyperemesis syndrome (CHS) is a disease frequently encountered by emergency practitioners. As with any nausea-inducing condition, one of the key dangers lies in continued emesis and PO intolerance, leading to dehydration and potential electrolyte derangements.

Although in the ED we typically see patients in the hyperemesis phase of CHS, patients typically pass through three overlapping, yet distinct stages; prodrome, hyperemesis, and recovery. The prodrome can last for several days and consists of nausea, decreased appetite, and abdominal discomfort. The acute hyperemesis phase, which often lasts only one day, consists of frequent vomiting with abdominal pain. Symptoms finally improve during the recovery phase.

CHS should be considered a diagnosis of exclusion, patients often have multiple other substance use disorders, and are at risk of developing other pathology secondary to prolonged and forceful vomiting. Additionally, other intraabdominal pathology might be missed due to the history of marijuana use and premature closure on CHS as a diagnosis.

The most important aspect of treatment for CHS is the discontinuation of marijuana use. In the acute setting, however, management is aimed at control of pain and vomiting. Dopamine antagonists such as haloperidol or droperidol are often used as first-line agents for the hyperemesis phase. Benzodiazepines can also be used during the hyperemesis phase in the emergency department, but these medications can lead to over-sedation. Finally, topical capsaicin applied to the abdomen has some data to suggest utility in resolving acute episodes of CHS, and there is some evidence that suggests compulsive hot showers can help relieve symptoms.

Response to dopamine antagonists shouldn’t be considered diagnostic, and patients should be frequently re-evaluated. Further, patients may have contraction alkalosis with starvation ketosis. Intravenous fluids, preferably a balanced crystalloid containing dextrose, should be used for resuscitation, and thiamine should be considered for patients with a prolonged episode or concurrent alcohol use disorder. 

Case 2:

A 32-year-old male with a history of schizophrenia is brought in by EMS for altered mental status. You find him lying on the stretcher staring straight ahead and not moving. He does not answer you or even look in your direction when you speak, though he does respond to noxious stimuli. His vital signs are stable, and his physical exam is otherwise unremarkable except for a tendency to hold his arm in a raised position when you lift it, however, there is no noted rigidity, cogwheeling, or hyperreflexia.

Catatonia is a clinically-defined syndrome that occurs in a variety of psychiatric conditions. Although it is typically associated with staring and immobility, it actually can occur in two forms; the retarded form consisting of a lack of response to external stimuli (mutism, anorexia), and the excited form consisting of severe agitation. 

Retarded catatonia is by far the more common of the two forms. Among other conditions, the differential for a patient presenting with retarded catatonia should include intoxication, CVA, and non-convulsive status epilepticus (NCSE). As such, routine investigations such as  ECG, bloodwork, CT head, and EEG should be considered.

The treatment for either excited or retarded catatonia is benzodiazepines. Most practitioners prefer to use lorazepam given either intramuscularly or sublingually. Patients may respond to small doses in a matter of minutes, though those with more prolonged courses of catatonia may require larger doses (response to benzodiazepines isn’t diagnostic as it could still be NCSE). Once a clinical improvement has been noted, this dose must be continued at regular intervals until psychiatry has had the opportunity to treat the patient for underlying conditions, as relapse may otherwise occur.

Case 3: 

A 2-month, 2-week-old-child with a history of SBO s/p ex lap with ligation of the ligament of teres and appendectomy presents with 2 days of vomiting and 2 weeks since the last BM. On presentation, the child has tachycardia, dry mucous membranes, decreased level of activity, grunting, and abdominal distension. Suspicion for SBO is high. Surgery performs a bedside disimpaction. Further evaluation leads to suspicion of Hirschsprung’s Disease and Hirschsprung’s-associated Enterocolitis (HAEC).

Images from: Heuckeroth RO. Hirschsprung disease — integrating basic science and clinical medicine to improve outcomes. Nat Rev Gastroenterol Hepatol. 2018;15(3):152-167. doi:10.1038/nrgastro.2017.149

Images from: Heuckeroth RO. Hirschsprung disease — integrating basic science and clinical medicine to improve outcomes. Nat Rev Gastroenterol Hepatol. 2018;15(3):152-167. doi:10.1038/nrgastro.2017.149

Case 4:

A 40-year-old female with a history of cigarette smoking comes to the ED with Shortness of breath. She is febrile with a cough and tachycardia. A chest x-ray shows a tortuous aorta with widened mediastinum, so the team decides to get a CTA of both the thoracic aorta and the abdominal aorta. A CTA then shows an ascending fusiform aortic aneurysm measuring a maximum of 4.2 cm without evidence of hematoma or dissection. What is the management for this patient?

For ascending aortic aneurysm, annual monitoring with CTA/MRA if within 3.5-4.4 cm or semi-annual CTA/MRA

• • MRA/CTA if 4. 5-5.4 cm.
• • Surgery if >5.5 cm, symptomatic, or >0.5 cm/year growth

For descending aortic aneurysms a level of 5.5 cm is also used as an indication for surgery, and monitoring should be carried out similarly. As a note, these criteria don’t apply to dissections, which are often found with aortic aneurysms.

Case 5:

You have an altered patient that is found to have a fingerstick glucose of “>500”. Vital signs are 124/min BP 110/75 mm Hg, RR 20/min, Temp 37.3C. The exam is notable for a patient that has no focal neuro deficits but is disoriented and not following commands, with sunken eyes and dry mucous membranes. ED Echo shows normal EF with hyperdynamic heart and collapsible IVC. NCHCT shows no acute infarct, and the rest of the labs have a pH of 7.48, Na 140, K 5.0, Cl100, CO2 35, BUN 40, Cr 1.8, Glucose 1250, serum osmolality 375. Your diagnosis is HHS (hyperosmolar hyperglycemic state). The MICU resident says they can’t be dehydrated, and don’t give them fluids, because they calculated the free water deficit using: Equation 1: 0.6 × 60kg × [1 − (140 ÷ Na+)] = Free Water Deficit, 0.6*60[1-(140/140)] = 0L.

However, you know that this patient is severely dehydrated based on their HR and sono. When you calculate the free water deficit using the serum osm rather than sodium: equation 2: 0.6 × 60kg × [1 − (290 ÷ Posm)] = Free Water Deficit, 0.6*60[1-(290/375)] = 8L. You are able to say they are definitively severely dehydrated. Alternately, if you don’t have serum osmolarity you can consider using the corrected sodium in the traditional sodium-based free water deficit formula. Remember the 1.6 for each 100 of glucose above 100 was shown to be less accurate than 2.4 by Hiller in 1999. By substituting the corrected sodium of 168 in equation 1 you get a free water deficit of 6L, much closer to the 8L from equation 2. This is not in the literature, but the correction is needed because glucose is an osmol and impacts the measured value of sodium. By correcting for this, you are taking into account the osm difference. You equally could calculate serum osmolarity and use that in place of the measured serum osmolality, but this might not account for the complete picture of the patient’s fluid status.

References

1. 1. Cheuvront SN, Kenefick RW, Sollanek KJ, Ely BR, Sawka MN. Water-deficit equation: systematic analysis and improvement. Am J Clin Nutr. 2013;97(1):79-85. doi:10.3945/ajcn.112.046839
2. 2. Hiratzka LF, Bakris GL, Beckman JA, et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the Diagnosis and Management of Patients With Thoracic Aortic Disease: Executive Summary. Circulation. 2010;121(13):1544-1579. doi:10.1161/CIR.0b013e3181d47d48
3. 3. Hillier TA, Abbott RD, Barrett EJ. Hyponatremia: evaluating the correction factor for hyperglycemia. Am J Med. 1999;106(4):399-403. doi:10.1016/s0002-9343(99)00055-8
4. 4. Expert Panel on Vascular Imaging:, Bennett SJ, Dill KE, et al. ACR Appropriateness Criteria® Suspected Thoracic Aortic Aneurysm. J Am Coll Radiol. 2018;15(5S):S208-S214. doi:10.1016/j.jacr.2018.03.031
5. 5. Rasmussen SA, Mazurek MF, Rosebush PI. Catatonia: Our current understanding of its diagnosis, treatment and pathophysiology. World J psychiatry. 2016;6(4):391-398. doi:10.5498/wjp.v6.i4.391
6. 6. Richards JR. Cannabinoid Hyperemesis Syndrome: Pathophysiology and Treatment in the Emergency Department. J Emerg Med. 2018;54(3):354-363. doi:10.1016/j.jemermed.2017.12.010
7. 7. Dean DJ, Sabagha N, Rose K, et al. A Pilot Trial of Topical Capsaicin Cream for Treatment of Cannabinoid Hyperemesis Syndrome. Acad Emerg Med. June 2020:acem.14062. doi:10.1111/acem.14062
8. 8. Chang YH, Windish DM. Cannabinoid hyperemesis relieved by compulsive bathing. Mayo Clin Proc. 2009;84(1):76-78. doi:10.1016/S0025-6196(11)60811-2
9. 9. Frykman PK, Short SS. Hirschsprung-associated enterocolitis: prevention and therapy. Semin Pediatr Surg. 2012;21(4):328-335. doi:10.1053/j.sempedsurg.2012.07.007
10. 10. Heuckeroth RO. Hirschsprung disease — integrating basic science and clinical medicine to improve outcomes. Nat Rev Gastroenterol Hepatol. 2018;15(3):152-167. doi:10.1038/nrgastro.2017.149

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Noah Berland

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