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Oral Antivirals for Treatment of Mild-Moderate COVID-19 Infection

Background

Two new oral agents were given Emergency Use Authorization to be used in patients with mild-moderate COVID-19 at high risk of progression to severe infection, molnupiravir and nirmatrelvir/ritonavir (Paxlovid) [1,2]. Prior to this authorization, most evidence-based COVID therapies were parenteral and required significant healthcare resources to coordinate and administer.

Comparison

Nirmatrelvir/ritonavir [3]Molnupiravir [4]
Mechanism

Protease inhibitor leadings to interruption of viral replication

Ritonavir has no role in treating COVID-19, it is only included to boost levels of nirmatrelvir via CYP3A4 inhibition

Increased frequency of RNA mutations and impaired replication [5]
Efficacy vs Placebo (Hospitalization or Death)0.8% vs 6.3% (CI -7.21 to -4.03)6.8% vs 9.7% (CI -5.9 to -0.1)
Drug InteractionsCYP3A4 inducers, inhibitors, and substrates

May decrease efficacy of hormonal contraceptives, non-hormonal contraceptives should be considered

Contraindicated medications include: amiodarone, carbamazepine, clozapine, colchicine, dihydroergotamine, dronedarone, flecainide, lovastatin, ranolazine, sildenafil, simvastatin

Many other important interactions exist so care should be taken to assess all medication interactions

N/A
Cost*Patient: $0

US government: $530 [6]

Patient: $0

US Government: $700 [7]

Dose300 mg/100 mg BID for 5 days

Must be started within 5 days of symptom onset

800 mg BID for 5 days

Must be started within 5 days of symptom onset

NotesApproved for patients ≥ 12 years old AND ≥ 40 kg

Not approved for inpatient initiation

If patient is hospitalized, continuation is up to the discretion of the provider

Not used as pre-/post-exposure prophylaxis

Approved for patients ≥ 18 years

Not approved for inpatient initiation

If patient is hospitalized, continuation is up to the discretion of the provider

Not used as pre-/post-exposure prophylaxis

Renal/Hepatic Dose AdjustmentseGFR  ≥30 to <60 mL/min: 150 mg/100 mg BID

eGFR <30 mL/min: Not recommended

Child-Pugh class C: Not recommended

None

*Note: The US federal government has purchased 10 million doses of nirmatrelvir/ritonavir and 3 million doses of molnupiravir [8,9]. These supplies will be allocated to states and territories as needed and will be available to patients at no charge. 

Evidence:

Nirmatrelvir/ritonavir (Paxlovid)

Paxlovid was evaluated in the EPIC-HR trial, which is not fully published at this time [3]. This was a phase 2/3, double-blinded, randomized placebo controlled trial including nonhospitalized, unvaccinated patients adults with mild-moderate COVID-19 within 5 days of symptom onset with at least 1 risk factor† for development of severe illness from COVID-19. Exclusion criteria included patients with a history of COVID-19 infection or COVID vaccination. Patients were given Paxlovid 300 mg/100 mg or placebo BID for 5 days. The primary outcome was hospitalization or death at day 28. The modified intention-to-treat1 (mITT1) group excluded patients who did not receive nor were expected to receive COVID-19 mAb treatment. In the mITT1 group, the primary outcome occurred in 0.8% of patients receiving Paxlovid vs 6.3% of patients in the placebo group (8/1039 vs 66/1046, CI -7.21 to -4.03).

These results appear quite robust with a fragility index of 37. Additionally, in patients with detectable COVID antibodies there was less of an impact of the study medication. However, these patients still appeared to have some benefit (0.2% vs 1.5%, CI -2.45 to -0.23) which suggests that vaccinated patients may still benefit from Paxlovid.

†Risk factors for progression to severe disease: BMI >25, chronic lung disease, asthma, chronic kidney disease, current smoker, immunosuppressive disease or immunosuppressive treatment, cardiovascular disease, hypertension, sickle cell disease, neurodevelopmental disorders, active cancer, medically-related technological dependence, or age >60 years

Molnupiravir 

Molnupiravir was evaluated in the MOVe-OUT trial [10]. This was a phase 3, double-blinded, randomized, placebo controlled trial including nonhospitalized, unvaccinated adults with mild-moderate COVID-19 within 5 days of symptom onset with at least 1 risk factor‡ for development of severe illness from COVID-19. Exclusion criteria included anticipated hospitalization within 48 hours, eGFR <30 or dialysis dependent, pregnancy, and COVID vaccination. Patients were able to receive steroids but not monoclonal antibodies (mAbs) nor remdesivir. Patients were given molnupiravir 800 mg or placebo BID for 5 days. The primary outcome was hospitalization or death at 29 days. In the mITT population, the primary outcome occurred in 6.8% of patients in the study group vs 9.7% in the placebo group (48/709 vs 68/699, CI -5.9 to -0.1). Death occurred in 1 patient on molnupiravir and in 9 patients on placebo (0.1% vs 1.3%, RRR 89%, CI 14 to 99).

Despite the above results, this may not be the positive trial it initially appears. First of all, for the primary outcome, the fragility index is 0, meaning that if 1 more patient in the study group experienced the primary outcome then it would have changed the statistical significance. Additionally, when the mITT analysis was adjusted for sex, the absolute risk reduction remained 2.8% but the confidence interval was not significant (-5.7 to 0.1). Lastly, in the subgroup analysis, there was no benefit in patients that had positive COVID antibody tests and there was a slight preference towards placebo over molnupiravir (3.7% vs 1.4%, ARR 2.3, CI -1.7 to 7.1). This suggests that vaccinated patients may not benefit from this therapy as much (or at all) as compared to unvaccinated patients.

‡Risk factors for progression to severe disease: age >60 years, active cancer, chronic kidney disease, COPD, BMI ≥30, heart failure, coronary artery disease, cardiomyopathy, or diabetes mellitus

Note: Both the EPIC-HR and MOVe-OUT studies were funded by their respective pharmaceutical company.

Bottom Line:

  • Nirmatrelvir/ritonavir (Paxlovid) and molnupiravir are approved under FDA EUAs for patients with mild-moderate COVID infection at high risk of severe disease within 5 days of symptom onset
  • Both medications appear to reduce death or hospitalization within a month, with most benefit likely to be experienced by unvaccinated patients
  • Nirmatrelvir/ritonavir (Paxlovid) appears to be more effective but also has many more drug interactions and contraindications

Want to learn more about EM Pharmacology?

Read other articles in the EM Pharm Pearls Series and find previous pearls on the PharmERToxguy site.

References:

  1. O’Shaughenessy J. Food and Drug Administration. Molnupiravir Emergency Use Authorization 108. December 23, 2021. https://www.fda.gov/media/155053/download
  2. O’Shaughenessy J. Food and Drug Administration. Nirmatrelvir/ritonavir Emergency Use Authorization 105. December 22, 2021. https://www.fda.gov/media/155049/download
  3. Nirmatrelvir/ritonavir. Package insert. Pfizer, Inc. 2021. https://www.fda.gov/media/155050/download
  4. Molnupiravir. Package insert. Merck Sharp & Dohme Corp. 2021. https://www.merck.com/eua/molnupiravir-hcp-fact-sheet.pdf
  5. Kabinger F, Stiller C, Schmitzová J, et al. Mechanism of molnupiravir-induced SARS-CoV-2 mutagenesis. Nat Struct Mol Biol. 2021;28(9):740-746. doi: 10.1038/s41594-021-00651-0. PMID: 34381216.
  6. Mishra M. U.S. to buy 10 mln courses of Pfizer’s COVID-19 pill for $5.3 bln. Reuters. Accessed January 12, 2022. https://www.reuters.com/business/healthcare-pharmaceuticals/us-govt-buy-10-mln-courses-pfizers-covid-19-pill-529-bln-2021-11-18/
  7. Willyard C. How antiviral pill molnupiravir shot ahead in the COVID drug hunt. Nature. Published online October 8, 2021. doi: 10.1038/d41586-021-02783-1. PMID: 34625735.
  8. Paxlovid (nirmatrelvir/PF-07321332 and ritonavir). U.S. Department of Health & Human Services: Office of the Assistant Secretary of Preparedness and Response. Updated: January 12, 2022. Accessed January 12, 2022. https://www.phe.gov/emergency/events/COVID19/investigation-MCM/Paxlovid/Pages/default.aspx
  9. Molnupiravir (MK-4482). U.S. Department of Health & Human Services: Office of the Assistant Secretary of Preparedness and Response. Updated: January 12, 2022. Accessed January 12, 2022. https://www.phe.gov/emergency/events/COVID19/investigation-MCM/molnupiravir/Pages/default.aspx
  10. Jayk Bernal A, Gomes da Silva MM, Musungaie DB, et al. Molnupiravir for oral treatment of covid-19 in nonhospitalized patients. N Engl J Med. Published online December 16, 2021. doi: 10.1056/NEJMoa2116044. PMID: 34914868.
By |2022-01-15T19:00:38-08:00Jan 15, 2022|EM Pharmacy Pearls, Infectious Disease, Tox & Medications|
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SAEM Clinical Image Series: Painful Blue Arm

arm swelling

A 68-year-old male with a past medical history of hypertension, hyperlipidemia, and recent ileostomy secondary to small bowel obstruction presented for acute left arm swelling, discoloration, and numbness since last night. He endorses sudden onset of painful edema with the development of purple discoloration. He denies trauma, history of similar problems, chest pain, or shortness of breath. He endorses difficulty flexing at the elbow secondary to the amount of swelling, pain, and numbness to the arm. The patient had a peripherally inserted central catheter (PICC) line placed in the left upper extremity two weeks ago.

 

Vitals: T 37.1°C; HR 80; BP 154/82; RR 18; O2 sat 100% on RA

General: Moderate distress secondary to pain but non-toxic appearing

Cardiovascular: Regular rate and rhythm; no murmurs; left ulnar artery 2+; left radial artery 1+ to palpation; bedside doppler—triphasic left ulnar artery and biphasic left radial artery; capillary refill three seconds

Respiratory: Lungs clear to auscultation bilaterally; no adventitious breath sounds

Musculoskeletal: Left upper extremity with global nonpitting edema from fingers to shoulder; skin with purple cyanotic discoloration; moderately tender to palpation throughout the entire limb; no crepitus or bullae; pain is not out of proportion; soft compartments throughout the left upper extremity

Neurologic: Alert and oriented to person, time, and place; Glasgow Coma Scale 15; cranial nerves II-XII grossly intact; sensation decreased in left upper extremity; all other extremities intact

Complete blood count (CBC): Unremarkable

Partial thromboplastin time (PTT) and International normalized ratio (INR): Unremarkable

Phlegmasia cerulea dolens (PCD) of the Upper Extremity. It’s just a deep venous thrombosis (DVT) right?

PCD is not just another DVT, it’s a severe limb-threatening (12-25% amputation rate) and life-threatening (25-40% mortality rate) disease that presents with marked swelling in the extremity, pain, and cyanosis.

The pathophysiology of PCD involves complete obstruction of both superficial and deep venous return, resulting in increased interstitial tissue pressure, arrest of capillary flow, tissue ischemia, and ultimately, gangrene. Upper extremity involvement is rare and only occurs in approximately 2-5% of all phlegmasia cases. PCD presents with key characteristics: marked edema, severe pain, pathognomonic blue discoloration/cyanosis, and eventually ischemia.

Ultrasound is the best initial modality for suspected PCD and bedside ultrasound with two-point compression can be quickly performed by the emergency physician.

Management should include fluid resuscitation, systemic anticoagulation, and emergent vascular surgery or interventional radiology consult for possible thrombectomy or catheter-directed thrombolysis.

Take-Home Points

  • PCD is a rare, life-and-limb-threatening disease that can rapidly progress to gangrene and tissue death.
  • Phlegmasia cerulea dolens literally translates to “painful blue inflammation.” Large clot burden causes severe pain, cyanosis, and marked edema.
  • Prompt evaluation with ultrasound, treatment with anticoagulation, and emergent vascular surgery or interventional radiology consultation are essential.

  • Chaochankit W, Akaraborworn O. Phlegmasia Cerulea Dolens with Compartment Syndrome. Ann Vasc Dis. 2018 Sep 25;11(3):355-357. doi: 10.3400/avd.cr.18-00030. PMID: 30402189; PMCID: PMC6200621.
  • Kommalapati A, Kallam A, Krishnamurthy J, Tella SH, Koppala J, Tandra PK. Upper Limb Phlegmasia Cerulea Dolens Secondary to Heparin-induced Thrombocytopenia Leading to Gangrene. Cureus. 2018 Jun 21;10(6):e2853. doi: 10.7759/cureus.2853. PMID: 30148006; PMCID: PMC6104908.
  • Kou CJ, Batzlaff C, Bezzant ML, Sjulin T. Phlegmasia Cerulea Dolens: A Life-Threatening Manifestation of Deep Vein Thrombosis. Cureus. 2020 Jun 12;12(6):e8587. doi: 10.7759/cureus.8587. PMID: 32670722; PMCID: PMC7358928.
  • Onuoha CU. Phlegmasia Cerulea Dolens: A Rare Clinical Presentation. Am J Med. 2015 Sep;128(9):e27-8. doi: 10.1016/j.amjmed.2015.04.009. Epub 2015 Apr 22. PMID: 25910785.

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2021 SAEM Annual Meeting | Copyrighted by SAEM 2021 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

 

By |2022-01-04T11:48:50-08:00Jan 10, 2022|Cardiovascular, SAEM Clinical Images|
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Balanced Fluids in Diabetic Ketoacidosis

Background

Many guidelines and treatment algorithms for diabetic ketoacidosis (DKA) recommend sodium chloride 0.9% as the replacement fluid of choice, though alternative fluids may be a better option [1-4]. Randomized trials, in adult and pediatric patients, demonstrate faster resolution of DKA when using balanced solutions (e.g., PlasmaLyte-A, lactated Ringer’s) compared to sodium chloride [5-7]. Dr. Josh Farkas provides further review of this topic in 3 excellent and detailed EMCrit posts [8-10].

Evidence

A phase-2 study published in 2021, SCOPE-DKA, randomized 93 patients with severe DKA (median venous pH 7.0) to receive PlasmaLyte-148 (PlasmaLyte-A) or sodium chloride 0.9% [11]. During the first 48 hours of treatment, patients received a average of ~6.5 L of fluid. At 24-hours, more patients in the PlasmaLyte group had resolution of DKA (defined as base excess ≥ -3 mEq/L) as compared to the sodium chloride group (69% vs 36%, p=0.002). However, by 48-hours, both groups had similar rates of DKA resolution (96% vs 86%, p=0.111). The study authors concluded that PlasmaLyte-148 may lead to faster resolution of metabolic acidosis in patients with DKA without an increase in ketosis, in line with findings from previous studies, but these results need to be confirmed in a larger, Phase 3 trial.

To further explore the nuances, strengths, and weaknesses of this study, please read the REBEL EM review by Dr. Mark Ramzy [13].

Bottom Line

  • The available data suggests that balanced fluids are beneficial in mild, moderate, and severe DKA.
  • PlasmaLyte-148 (PlasemaLyte A) may lead to faster resolution of metabolic acidosis than sodium chloride 0.9%. Though these findings need confirmation in a large, Phase 3 trial.
  • Generally, the composition of the initial liter is less important than prompt administration. However, for subsequent liters, a balance crystalloid (e.g., PlasmaLyte-148, or lactated Ringer’s) should be used instead of sodium chloride 0.9%.

Want to learn more about EM Pharmacology?

Read other articles in the EM Pharm Pearls Series and find previous pearls on the PharmERToxguy site.

References:

  1. Wolfsdorf J, Glaser N, Sperling MA, American Diabetes Association. Diabetic ketoacidosis in infants, children, and adolescents: A consensus statement from the American Diabetes Association. Diabetes Care. 2006;29(5):1150-1159. PMID: 16644656. doi: 10.2337/diacare.2951150.
  2. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. Diabetes Care. 2009;32(7):1335-1343. PMID: 19564476. doi: 10.2337/dc09-9032.
  3. Canadian Diabetes Association Clinical Practice Guidelines Expert Committee, Goguen J, Gilbert J. Hyperglycemic emergencies in adults. Can J Diabetes. 2013;37 Suppl 1:S72-76. PMID: 24070967. doi: 10.1016/j.jcjd.2013.01.023.
  4. Joint British Diabetes Societies Inpatient Care Group. The Management of Diabetic Ketoacidosis in Adults. 2021; online publication. Accessed January 3, 2022. https://abcd.care/sites/abcd.care/files/site_uploads/JBDS_02%20_DKA_Guideline_amended_v2_June_2021.pdf.
  5. Mahler SA, Conrad SA, Wang H, Arnold TC. Resuscitation with balanced electrolyte solution prevents hyperchloremic metabolic acidosis in patients with diabetic ketoacidosis. Am J Emerg Med. 2011;29(6):670-674. PMID: 20825879. doi: 10.1016/j.ajem.2010.02.004.
  6. Williams V, Jayashree M, Nallasamy K, Dayal D, Rawat A. 0.9% saline versus Plasma-Lyte as initial fluid in children with diabetic ketoacidosis (SPinK trial): a double-blind randomized controlled trial. Crit Care. 2020;24(1):1. PMID: 31898531. doi: 10.1186/s13054-019-2683-3.
  7. Self WH, Evans CS, Jenkins CA, et al. Clinical effects of balanced crystalloids vs saline in adults with diabetic ketoacidosis: a subgroup analysis of cluster randomized clinical trials. JAMA Netw Open. 2020;3(11):e2024596. PMID: 33196806. doi: 10.1001/jamanetworkopen.2020.24596.
  8. Farkas J. Four DKA Pearls. 2014. Accessed January 3, 2022. https://emcrit.org/pulmcrit/four-dka-pearls.
  9. Farkas J. Dominating the acidosis in DKA. 2016. Accessed January 3, 2022. https://emcrit.org/pulmcrit/bicarbonate-dka.
  10. Farkas J. IBCC – Diabetic Ketoacidosis (DKA). 2021. Accessed January 3, 2022. https://emcrit.org/ibcc/dka.
  11. Ramanan M, Attokaran A, Murray L, et al. Sodium chloride or Plasmalyte-148 evaluation in severe diabetic ketoacidosis (Scope-dka): a cluster, crossover, randomized, controlled trial. Intensive Care Med. 2021;47(11):1248-1257. PMID: 34609547. doi: 10.1007/s00134-021-06480-5.
  12. Ramzy M. SCOPE-DKA: Normal Saline vs Plasmalyte in Severe DKA. 2021. Accessed January 3, 2022. https://rebelem.com/scope-dka-normal-saline-vs-plasmalyte-in-severe-dka.
By |2022-01-03T10:16:35-08:00Jan 8, 2022|EM Pharmacy Pearls, Endocrine-Metabolic, Tox & Medications|
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SAEM Clinical Image Series: Inguinal Masses

A 50-year-old female with a past medical history of gastritis and marijuana abuse presents to the Emergency Department (ED) with epigastric abdominal pain for one day. The patient reports she was seen in the ED one month prior for similar symptoms and had an ultrasound of the gallbladder, which was negative. She was discharged home with prescriptions for Pepcid, Carafate, and Zofran. Once discharged home she did not experience any symptoms until the day prior to presenting again to the ED. The patient denies nausea, vomiting, back pain, dysuria, hematuria, subjective fevers, chills, diarrhea, vaginal bleeding, vaginal discharge, chest pain, or shortness of breath. Of note, the patient also reports intermittent bilateral inguinal discomfort, stating she believed she had inguinal hernias, which would become tender without exertion or any notable inciting factor.

 

inguinal mass

Vitals: HR 82; T 97.1°F; BP 147/95; RR 20; O2 sat 100% on room air

General: No acute distress

Cardiovascular: Regular rate and rhythm; no murmur; bilateral upper extremity and lower extremity pulses palpable

Gastrointestinal: Soft; generalized tenderness, predominantly epigastric; no abdominal masses

Genitourinary: Pelvic exam deferred; normal external vaginal exam; bilateral inguinal masses, non-tender, no overlying cellulitis

White blood cell (WBC) count: 5.64 k

Hemoglobin (Hgb): 10.4 g/dL

Hematocrit (Hct): 33.0%

Platelet count: 279 k

Complete metabolic panel (CMP): Unremarkable

Urine pregnancy test (UPT): Negative

DDX: Bilateral inguinal hernias, abscess, undescended testicles.

The abnormal findings in this patient were consistent with undescended rudimentary testicles in a patient without a prior diagnosis of true hermaphroditism (an ovotesticular disorder of sex development [DSD]). Our patient was phenotypically a female, with developed breasts, vagina, uterus, and ovaries, although uterus and ovaries were noted to be diminutive on imaging. Our patient identified herself as a female of homosexual orientation.

True hermaphroditism is characterized as the presence of seminiferous tubules and ovarian follicles in the same individual. Genitalia is usually ambiguous; however, patients may appear phenotypically male or female. Reproductive organ differentiation is a complex process involving multiple pathways and receptors, predominantly antimüllerian hormone (AMH). When testes differentiate, the secretion of AMH will lead to regression of müllerian structures, and lack of AMH will result in progression of female organ development (e.g., fallopian tubes, uterus, cervix, and upper vagina). The vast majority of patients with hermaphroditism will have a uterus or uterine horn, and most patients have breast development, ovulation, and menstruation.

Patients should be educated about the importance of close follow-up and the possible complications involved with this diagnosis. Although some patients may be asymptomatic and therefore undiagnosed, undescended testicles are at a slightly increased risk for gonadal tumors and may also suffer from testicular torsion. Patients may need to have a biopsy of undescended testes to confirm testicular tissue and be required to have surgical removal of testes.

Take-Home Points

  • The differential diagnosis for bilateral inguinal masses in a phenotypically female patient includes undescended testicles.
  • Patient education is of utmost importance as undescended testicles are still at risk of testicular torsion and carry an increased risk of testicular cancer.

  • English RE, Tulloch DN, Blaquiere RM. The demonstration of true hermaphroditism by computed tomography. Clin Radiol. 1986 Nov;37(6):593-4. doi: 10.1016/s0009-9260(86)80035-6. PMID: 3791859.
  • van Niekerk WA, Retief AE. The gonads of human true hermaphrodites. Hum Genet. 1981;58(1):117-22. doi: 10.1007/BF00284158. PMID: 6895206.
  • Walker AM, Walker JL, Adams S, Shi E, McGlynn M, Verge CF. True hermaphroditism. J Paediatr Child Health. 2000 Feb;36(1):69-73. doi: 10.1046/j.1440-1754.2000.00432.x. PMID: 10723695.
  • White, P. C. (2012). Disorders of Sexual Development. In Goldman’s Cecil Medicine (pp. 1511–1519). Elsevier. https://doi.org/10.1016/B978-1-4377-1604-7.00241-4

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2021 SAEM Annual Meeting | Copyrighted by SAEM 2021 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

 

By |2022-01-01T23:43:19-08:00Jan 3, 2022|Genitourinary, SAEM Clinical Images|
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SAEM Clinical Image Series: I Have a Stomachache

stomachache

An 18-year-old male with no significant past medical history presents with diffuse abdominal pain and multiple episodes of non-bloody, non-bilious vomiting for three days. The patient was seen yesterday at another facility and states he was diagnosed with gastritis and discharged with Zofran, which provided no relief. He denies fever, diarrhea, or urinary symptoms and states his last bowel movement was two days ago and was consistent with his usual bowel movements.

 

 

Vitals: T 97.7ºF; HR 138; BP 122/98; RR 18; O2 sat 99% on RA

General: Thin male, appears uncomfortable

Abdominal: Mild distention with diffuse tenderness to palpation; no guarding or rebound tenderness

White blood cell (WBC) count: 13k

Complete metabolic panel (CMP): Mild hypokalemia; otherwise unremarkable

Lactate: 4.9

Urinalysis (UA): Mild ketonuria; no hematuria; no evidence of infection

Superior Mesenteric Artery (SMA) syndrome also known as Wilke’s or Cast Syndrome is a condition where the third section of the duodenum gets compressed between the superior mesenteric artery and the aorta leading to a proximal obstruction in the duodenum and stomach. The most common etiology of SMA syndrome is the loss of the mesenteric fat pad surrounding the SMA. This leads to an acute angulation between the SMA and the aorta, thus compressing the duodenum and causing a partial or complete obstruction. While the condition is rare, predisposing factors include sudden weight loss and chronic illnesses such as malabsorption syndromes, AIDS, and malignancy.

Treatment in the acute stage is conservative management including gastric decompression, IV fluids, correction of electrolyte abnormalities, and nutritional support, which may include temporary gastro-jejunostomy (GJ) tube placement. Severe refractory cases may require surgical intervention. This patient was admitted and treated conservatively, including a temporary GJ tube placement which was removed a few months later.

Take-Home Points

  • Consider SMA syndrome in patients with a history of sudden weight loss or chronic illness.
  • Look for very proximal obstruction on CT with significant gastric distension.
  • Acute management is conservative treatment.

  • Hamden, A. & Scovell, S. (2020). Superior Mesenteric Artery Syndrome. In K. Collins (Ed.), UpToDate. Retrieved January 4, 2021, from https://www.uptodate.com/contents/superior-mesenteric-artery-syndrome
  • Niknejad, M. & Ranschaert, E. (2018). Superior Mesenteric Artery Syndrome. Radiopedia.org. Retrieved January 4, 2021, from https://radiopaedia.org/articles/superior-mesenteric-artery-syndrome?lang=us
  • Karrer FM. (2017). Superior Mesenteric Artery Syndrome. Medscape Reference. Retrieved December 22, 2020, from http://emedicine.medscape.com/article/932220-overview Genetic and Rare Diseases Information Center. (2018). Superior Mesenteric Artery Syndrome. [Online]. Available at: https://rarediseases.info.nih.gov/diseases/7712/superior-mesenteric-artery-syndrome#:~:text=Superior%20mesenteric%20artery%20syndrome%20(SMAS,complete%20blockage%20of%20the%20duodenum

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2021 SAEM Annual Meeting | Copyrighted by SAEM 2021 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

 

By |2021-12-02T13:55:35-08:00Dec 20, 2021|Gastrointestinal, Pediatrics, SAEM Clinical Images|
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SAEM Clinical Image Series: Vomiting in the Pediatric Patient

vomiting

A 2-year-old boy with a past medical history of Hirschsprung disease presents to the emergency department (ED) with vomiting, abdominal distension, and inability to tolerate PO for one day. His parents had been instructed by their pediatric surgeon to perform rectal irrigations 2-3 times daily for the few days prior to presentation.

 

Vital signs within normal limits.

General: Appears lethargic

HEENT: Oral mucosa dry

Abdomen: Moderately distended; decreased bowel sounds

Skin: Normal turgor

Non-contributory

The differential diagnosis for pediatric patients presenting with vomiting is broad and includes but is not limited to gastritis, diabetic ketoacidosis, pyloric stenosis, appendicitis, intussusception, urinary tract infection, colic, toxic ingestion, volvulus, incarcerated hernia, and bowel obstruction. However, in a child with Hirschsprung disease who presents with vomiting, an emergency medicine physician must maintain a high degree of suspicion for Hirschsprung-associated enterocolitis (HAEC).

Hirschsprung disease is a rare congenital condition affecting approximately 1-in-5,000 births that refers to a functional intestinal obstruction due to the absence of ganglionic cells in the myenteric plexus of the distal colon. Life-threatening complications of Hirschsprung disease include bowel obstruction, Hirschsprung-associated enterocolitis (HAEC), and toxic megacolon. HAEC is the leading cause of morbidity and mortality in these patients. HAEC can present with vague symptoms such as fever, diarrhea, vomiting, rectal bleeding, constipation, and lethargy. Due to these nonspecific symptoms, it is necessary for emergency medicine physicians to maintain a high index of suspicion for HAEC. Once diagnosed, immediate resuscitation should begin with the placement of a rectal tube for decompression, initiation of broad-spectrum antibiotics and fluids, as well as urgent pediatric surgery consultation.

Take-Home Points

  • HAEC can present with nonspecific symptoms of diarrhea, vomiting, fever, lethargy, abdominal distension, and obstipation.
  • HAEC must be quickly identified in patients with Hirschsprung disease due to the risk of rapid decompensation from hypovolemic shock secondary to dehydration, septic shock from HAEC, and the development of toxic megacolon.
  • HAEC is the leading cause of morbidity and mortality in pediatric patients with Hirschsprung disease.

  • Guillaume AWD, Miller AC, Nguyen MC. Enterocolitis in a Child With Hirschsprung Disease. Pediatr Emerg Care. 2019 Jul;35(7):e131-e132. doi: 10.1097/PEC.0000000000001108. PMID: 28328696.
  • Demehri FR, Halaweish IF, Coran AG, Teitelbaum DH. Hirschsprung-associated enterocolitis: pathogenesis, treatment and prevention. Pediatr Surg Int. 2013 Sep;29(9):873-81. doi: 10.1007/s00383-013-3353-1. PMID: 23913261.
  • Gosain A. Established and emerging concepts in Hirschsprung’s-associated enterocolitis. Pediatr Surg Int. 2016 Apr;32(4):313-20. doi: 10.1007/s00383-016-3862-9. Epub 2016 Jan 19. PMID: 26783087; PMCID: PMC5321668.
  • Maloney, Patrick J. “Gastrointestinal Disorders.” Rosen’s Emergency Medicine: Concepts and Clinical Practice. 9th Edition. Chapter 171. Page 2126-2144. 2018.

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2021 SAEM Annual Meeting | Copyrighted by SAEM 2021 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

 

By |2021-12-02T13:34:44-08:00Dec 13, 2021|Gastrointestinal, Pediatrics, SAEM Clinical Images|
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