Author Archives → Editor

Erythrocytosis

Brief H&P:

A 39-year-old male with symptomatic hypogonadism on testosterone therapy presents to the emergency department at the request of his primary care physician after outpatient labs showed a hemoglobin of 22.0 g/dl. He denies chest pain, shortness of breath, extremity swelling, or neurologic symptoms such as changes in vision, motor function, or sensation. On evaluation, his vital signs and a detailed physical examination are normal. There are no other lab abnormalities.

The patient was discharged with outpatient primary care follow-up after collection of serum EPO and JAK2 levels – the former of which was elevated and findings were attributed to testosterone use.

Algorithm for the Evaluation of Erythrocytosis

An algorithm for the evaluation of erythrocytosis

References

  1. Tefferi A, Barbui T. Polycythemia vera and essential thrombocythemia: 2019 update on diagnosis, risk-stratification, and management. American Journal of Hematology. 2019;94(1):133-143. doi:10.1002/ajh.25303
  2. McMullin MF, Harrison CN, Ali S, et al. A guideline for the diagnosis and management of polycythaemia vera. British Journal of Haematology. 2019;184(2):176-191. doi:10.1111/bjh.15648
  3. Tintinalli JE, Ma OJ, Yealy DM, et al., eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 9th ed. McGraw-Hill Education; 2020.
This algorithm was developed by Dr. Leland Damron. Leland is an internal medicine resident at UCLA.

Lower Extremity Edema Ultrasound

Brief H&P:

Ultrasound image of heart with depressed ejection fraction

Depressed ejection fraction, image from The POCUS Atlas

An 44 year-old male with no reported medical history (though limited access to medical care) presents with lower extremity swelling. He states that the symptoms have been gradually worsening over the past 3 months. He notes occasional fatigue while at work but denies chest pain, shortness of breath, leg pain or changes in urination.

A point-of-care ultrasound is performed showing decreased left ventricular ejection fraction. The patient was admitted for further evaluation and management of new-onset congestive heart failure.

Algorithm for the Evaluation of Lower Extremity Edema with Ultrasound

An algorithm for the evaluation of lower extremity edema with ultrasound

Gallery

The POCUS Atlas
The ultrasound images and videos used in this post come from The POCUS Atlas, a collaborative collection focusing on rare, exotic and perfectly captured ultrasound images.
The POCUS Atlas
Nodular liver contour, ascites

Nodular liver contour, ascites

Ascites

Ascites

Cobblestoning

Cobblestoning

Cobblestoning

Cobblestoning

Longitudinal view of a ruptured Baker cyst

Longitudinal view of a ruptured Baker cyst

References

  1. Trayes KP, Studdiford JS, Pickle S, Tully AS. Edema: diagnosis and management. Am Fam Physician. 2013;88(2):102-110.
  2. Goyal A, Cusick AS, Bhutta BS. Peripheral Edema. [Updated 2022 Nov 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK554452/
  3. Smith, C. Clinical manifestations and evaluation of edema in adults. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. http://www.uptodate.com. Accessed 2/11/2023.
This algorithm was developed by Dr. Huakang Huang. Huakang is an emergency medicine resident at UTHealth Houston.

Monocular Painless Vision Loss

Brief H&P:

A 29 year-old female with no known medical history presents with vision changes for two weeks. She describes blurring and darkening of her vision in the left eye without associated pain after which her vision returns to normal. She notes occasional headaches which she describes as her usual migraines.

Physical examination including a detailed neurological examination, visual acuity, and visual fields is normal with the exception of bilateral optic disc edema. A non-contrast head CT is performed and is similarly normal. The patient underwent uncomplicated lumbar puncture with identification of elevated opening pressure with otherwise unremarkable cerebrospinal fluid analyses.

The patient’s evaluation was consistent with idiopathic intracranial hypertension, she was started on acetazolamide 500mg p.o. b.i.d and was discharged with close neurology follow-up.

An Algorithm for the Evaluation of Painless Monocular Vision Loss

An algorithm for the evaluation of painless monocular vision loss

This algorithm was developed by Dr. Lara Samarneh. Lara is an emergency medicine resident at UTHealth Houston. She attended medical school at UTHealth Houston McGovern Medical School and graduated from The University of Texas at Austin with a Bachelor’s degree in Biomedical Engineering. She is passionate about education and is currently serving as Vice Chief of Education.
Special thanks to Dr. Ore-ofe O. Adesina, MD , Associate Professor, Department of Ophthalmology and Visual Science – McGovern Medical School, Medical Director, Cizik Eye Clinic for his expertise and review of this algorithm.

References

  1. Fundoscopy images in the algorithm are sourced from Ophthalmic Atlas Images by EyeRounds.org, The University of Iowa which are licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License.
  2. Guluma, K, Lee, J. Ophthalmology. In Rosen’s Emergency Medicine: Concepts and Clinical Practice (10th ed., pp. 750-780). Philadelphia, PA: Elsevier.
  3. Sharma P, Sridhar J, Mehta S. Flashes and floaters. Prim Care. 2015;42(3):425-435.
  4. Bagheri N, Mehta S. Acute vision loss. Prim Care. 2015;42(3):347-361.
  5. Pula JH, Kwan K, Yuen CA, Kattah JC. Update on the evaluation of transient vision loss. Clin Ophthalmol. 2016;10:297-303.
  6. Dehghani A, Giti M, Akhlaghi MR, Karami M, Salehi F. Ultrasonography in distinguishing optic neuritis from nonarteritic anterior ischemic optic neuropathy. Adv Biomed Res. 2012;1:3.
  7. Prasad S, Galetta SL. Approach to the patient with acute monocular visual loss. Neurol Clin Pract. 2012;2(1):14-23.
  8. Abbatemarco JR, Patell R, Buccola J, Willis MA. Acute monocular vision loss: Don’t lose sight of the differential. Rutecki GW, ed. CCJM. 2017;84(10):779-787.
  9. Current management of amaurosis fugax. The amaurosis fugax study group. Stroke. 1990;21(2):201-208.

Flank Pain Ultrasound

Brief H&P:

A 63 year-old male with a history of hypertension, tobacco use, and nephrolithiasis presents with left-sided flank pain. He notes sudden-onset approximately 4 hours prior to presentation and describes radiation to his groin. Pain was associated with nausea, denies hematuria and states pain is different compared to prior kidney stones. On evaluation, vital signs are notable for tachycardia (114bpm), blood pressure measured at 112/65mmHg. The patient appears uncomfortable and examination is notable for a pulsatile abdominal mass above the umbilicus.

ED Course

Normal

Normal

Abdominal Aortic Aneurysm

Abdominal Aortic Aneurysm

A point-of-care ultrasound is performed which shows no hydronephrosis and an 8cm infrarenal abdominal aortic aneurysm. Vascular surgery was consulted and a CTA was performed revealing ruptured abdominal aortic aneurysm. Uncrossmatched blood products were administered en route to the operating room due to hypotension.

Algorithm for the Evaluation of Flank Pain with Ultrasound

Algorithm for the Evaluation of Flank Pain with Ultrasound

Gallery

The POCUS Atlas
The ultrasound images and videos used in this post come from The POCUS Atlas, a collaborative collection focusing on rare, exotic and perfectly captured ultrasound images.
The POCUS Atlas
Normal

Normal

Abdominal Aortic Aneurysm

Abdominal Aortic Aneurysm

Abdominal Aortic Aneurysm

Abdominal Aortic Aneurysm

Dissection Flap

Dissection Flap

  View Gallery

Normal

Normal

Subpleural Consolidation

Subpleural Consolidation

Pleural Effusion

Pleural Effusion

Pneumothorax

Pneumothorax

  View Gallery   View Algorithm

Normal

Normal

Mild Hydronephrosis

Mild Hydronephrosis

Moderate Hydronephrosis

Moderate Hydronephrosis

Severe Hydronephrosis

Severe Hydronephrosis

  View Gallery

Gallstones

Many gallstones

Gallbladder wall thickening

Pericholecystic fluid

Choledocholithiasis

Common bile duct dilation

  View Gallery   View Algorithm

References

  1. Moore CL, Daniels B, Singh D, Luty S, Molinaro A. Prevalence and clinical importance of alternative causes of symptoms using a renal colic computed tomography protocol in patients with flank or back pain and absence of pyuria. Acad Emerg Med. 2013;20(5):470-478.
  2. ​​Prince L.A., & Johnson G.A. (2020). Aneurysmal disease. Tintinalli J.E., & Ma O, & Yealy D.M., & Meckler G.D., & Stapczynski J, & Cline D.M., & Thomas S.H.(Eds.),Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw Hill.
  3. Bueschen AJ. Flank Pain. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 182. Available from: https://www.ncbi.nlm.nih.gov/books/NBK292/
  4. Carter MR, Green BR. Renal calculi: emergency department diagnosis and treatment. Emerg Med Pract. 2011;13(7):1-17;
  5. https://wikem.org/wiki/Abdominal_aortic_aneurysm
This algorithm was developed by Dr. Timothy George. Timothy is an emergency medicine resident at UTHealth Houston.

Anticoagulant Reversal in Intracranial Hemorrhage

Brief HPI:

A 65-year-old male with a past medical history of hypertension, diabetes mellitus, and atrial fibrillation presents after a mechanical fall with a posterior scalp hematoma and altered mental status. The patient’s family reports that the patient is taking apixaban with his last dose 4 hours prior to arrival. Physical examination reveals a GCS of 13, blood pressure of 175/99, and asymmetric pupils. The patient is taken to CT where head imaging reveals left sided subdural hematoma with midline shift and developing uncal herniation.

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CT Head:

Left cerebral convexity acute subdural hematoma producing substantial mass effect with midline shift and left uncal herniation.
Case courtesy of Dr Andrew Dixon, Radiopaedia.org. From the case rID: 32395

A nicardipine infusion is initiated and the head of the bed is elevated. Andexanet Alfa is not available, therefore an infusion of 4-Factor PCC is initiated. The patient is taken emergently to the operating room by neurosurgery for craniotomy and hematoma evacuation.

An Algorithm for the Reversal of Anticoagulation for Intracranial Hemorrhage 1-4

An Algorithm for Anticoagulant Reversal in Intracranial Hemorrhage

All Agents

For all agents, discontinue anticoagulation. Patients may require blood pressure control including anti-hypertensive infusions (goal SBP <140). Avoid reversal for intracranial hemorrhage associated with cerebral venous thrombosis. Use cautiously in patients with concomitant life-threatening ischemia, thrombosis, or severe DIC.

Vitamin K Antagonists (ex. warfarin)

Initial Dose

A fixed dose of 4F-PCC 1500 to 2000 units can be given as an initial dose with repeat dosing based on INR measurement 15 minutes after completion of infusion. Follow local institution guidelines if available.

Monitoring and Repeat Dosing

  • Vitamin K: if INR ≥1.4 at 12 hours 5
  • 4F-PCC: May consider repeat PCC dosing based on INR, though with increased DIC and thrombotic risk, it is recommended to correct further with FFP if INR remains ≥1.4 6

Direct Factor Xa Inhibitors (ex. rivaroxaban, apixaban)

Activated charcoal may be effective for up to six hours for apixaban 7 and eight hours for rivaroxaban 8.

*Andexanet alfa Regimens 9,10

  • Low-dose: rivaroxaban <10mg, apixaban <5mg, edoxaban <30mg or 8 or more hours since last dose
  • High-dose: If greater than above thresholds, or dose/timing unknown

Pentasaccharides (ex. fondaparinux)

Use high-dose Andexanet alfa regimen 12

Direct Thrombin inhibitors (ex. dabigatran)

Monitoring and Repeat Dosing

If ongoing significant bleeding after treatment, consider redosing idarucizumab and/or hemodialysis.

Alternative Regimens

If idarucizumab is not available, aPCC (50-80 units/kg) , 4F-PCC or 3F-PCC (50 units/kg) can be used in order of preference.

Unfractionated Heparin

Dosing

Determination of units of heparin is based on estimated active agent (half-life 1-2 hours)

  • Protamine sulfate 1mg/100 units IV, maximum dose 50mg
  • Alternatively, can give fixed dose of 25-50mg

Monitoring and Repeat Dosing

If aPTT is persistently elevated, repeat 0.5 mg/100 units

Low-Molecular Weight Heparin 13

Reversal is not indicated if more than 3-5 half-lives have passed since administration:

  • Enoxaparin mean half-life: 4-5 hours
  • Dalteparin mean half-life: 2.8 hours
  • Nadroparin mean half-life: 3.7 hours

If bleeding persists, or renal insufficiency, repeat dose .5 mg/1 mg enoxaparin or .5 mg/100 anti-Xa units.

This algorithm was developed by Dr. Taylor Martin. Taylor is an emergency medicine resident at McGovern Medical School at UTHealth Houston.

References

Guidelines & Reviews

  1. Greenberg SM, Ziai WC, Cordonnier C, et al. 2022 guideline for the management of patients with spontaneous intracerebral hemorrhage: a guideline from the american heart association/american stroke association. Stroke. Published online May 17, 2022:101161STR0000000000000407.
  2. Tomaselli GF, Mahaffey KW, Cuker A, et al. 2020 acc expert consensus decision pathway on management of bleeding in patients on oral anticoagulants: a report of the american college of cardiology solution set oversight committee. J Am Coll Cardiol. 2020;76(5):594-622.
  3. Frontera JA, Lewin JJ, Rabinstein AA, et al. Guideline for reversal of antithrombotics in intracranial hemorrhage: a statement for healthcare professionals from the neurocritical care society and society of critical care medicine. Neurocrit Care. 2016;24(1):6-46.
  4.  Freeman, W. David, Weitz, Jeffrey. “Reversal of anticoagulation in intracranial hemorrhage.” UpToDate. (2022) https://www.uptodate.com/contents/reversal-of-anticoagulation-in-intracranial-hemorrhage?search=anticoagulation%20reversal (Accessed on May 26, 2022)

Vitamin K Antagonists

  1. Ansell J, Hirsh J, Hylek E, Jacobson A, Crowther M, Palareti G. Pharmacology and management of the vitamin k antagonists: american college of chest physicians evidence-based clinical practice guidelines(8th edition). Chest. 2008;133(6 Suppl):160S-198S.
  2. Pabinger I, Brenner B, Kalina U, et al. Prothrombin complex concentrate (Beriplex p/n) for emergency anticoagulation reversal: a prospective multinational clinical trial. J Thromb Haemost. 2008;6(4):622-631.

Direct Factor Xa Inhibitors

  1. http://packageinserts.bms.com/pi/pi_eliquis.pdf
  2. https://www.bayer.com/sites/default/files/2020-11/xarelto-pm-en.pdf
  3. Demchuk AM, Yue P, Zotova E, et al. Hemostatic efficacy and anti-fxa (Factor xa) reversal with andexanet alfa in intracranial hemorrhage: annexa-4 substudy. Stroke. 2021;52(6):2096-2105.
  4. Cohen AT, Lewis M, Connor A, et al. Thirty-day mortality with andexanet alfa compared with prothrombin complex concentrate therapy for life-threatening direct oral anticoagulant-related bleeding. J Am Coll Emerg Physicians Open. 2022;3(2):e12655.
  5. Scaglione F. New oral anticoagulants: comparative pharmacology with vitamin K antagonists. Clin Pharmacokinet. 2013;52(2):69-82.

Pentasaccharides (ex. fondaparinux)

  1. Lu G, DeGuzman FR, Hollenbach SJ, et al. A specific antidote for reversal of anticoagulation by direct and indirect inhibitors of coagulation factor Xa. Nat Med. 2013;19(4):446-451.

Low-Molecular Weight Heparin

  1. Fareed J, Hoppensteadt D, Walenga J, et al. Pharmacodynamic and pharmacokinetic properties of enoxaparin : implications for clinical practice. Clin Pharmacokinet. 2003;42(12):1043-1057.

Wheezing and Stridor

Brief HPI:

A 66 year-old male with a history of hypertension and COPD presents with shortness of breath. He states that his symptoms are unimproved with home nebulizer treatments and denies fever, cough or new sputum production. On examination, he has stridor appreciated during inspiratory and expiratory phases.

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CT Chest:

1.9cm soft tissue thickening of the left tracheal wall at the level of the inferior thyroid gland. Luminal narrowing to 4 mm at this level.
Case courtesy of Dr Ian Bickle from Radiopaedia.org: 47677

Sound Characteristics

Stridor

An inspiratory, expiratory, or continuous monophonic sound that is loudest over the central airways.

Wheezing

A musical, high-pitched sound – more commonly expiratory. Requires sufficient airflow to induce airway oscillations.

Respiratory Phase

Inspiratory

Supraglottic: negative intratracheal pressure during inspiration causes airway collapse.

Biphasic

Glottic/Subglottic: fixed obstruction not impacted by changes in luminal/thoracic pressure.

Expiratory

Intrathoracic: increased pleural pressure compresses the narrowed airway.

An Algorithm for the Diagnosis of Wheezing and Stridor

An Algorithm for the Diagnosis of Wheezing and Stridor

Special thanks to Dr. Denna Zebda, Assistant Professor, Department of Otorhinolaryngology – McGovern Medical School for her expertise and review of this algorithm.

References

  1. Sicari V, Zabbo CP. Stridor. [Updated 2021 Jul 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK525995/
  2. Patel PH, Mirabile VS, Sharma S. Wheezing. [Updated 2021 May 12]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482454/
  3. Bohadana A, Izbicki G, Kraman SS. Fundamentals of lung auscultation. N Engl J Med. 2014;370(21):2053.
  4. Orient JM, Sapira JD. Sapira’s Art & Science of Bedside Diagnosis. 4th ed. Wolters Kluwer Health/Lippincott Williams & Wilkins; 2010.

Infographic: CT Chest

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Infographic: CT Chest Interpretation Full Size 960 downloads 2 MB
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Infographic: CT Chest Interpretation PDF 1188 downloads 25 MB

Examples

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Circulation: Dissection

Stanford type A aortic dissection. Flap extends cranially into the common trunk of the innominate/left common carotid arteries and proximal right subclavian artery. Caudally, extends to the abdominal aorta below the level of the superior mesenteric artery.

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Circulation: Penetrating Atherosclerotic Ulcer

Penetrating atherosclerotic ulcer of the ascending aorta with mediastinal hematoma and compression of the pulmonary artery.
Case courtesy of Dr Jens Christian Fischer, Radiopaedia.org. From the case rID: 12810

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Circulation: Intramural Hematoma

Intramural hematoma surrounding aortic root and ascending aorta with small hemopericardium.
Case courtesy of Dr David Preston, Radiopaedia.org. From the case rID: 27746

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Circulation: Filling Defects

Extensive bilateral pulmonary emboli involving nearly all branches distal to left/right main pulmonary arteries.

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Circulation: Complications

Saddle pulmonary embolism with pulmonary artery dilation and flattening of the interventricular septum suggestive of right ventricular strain.

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Breathing: Pleura

Pneumothorax

LVAD

Brief H&P:

A 48 year-old male with a history of congestive heart failure s/p left ventricular assist device is brought in by EMS with low-flow alarms. According to prehospital report, the patient had otherwise been in his usual state of health and had been shocked by his ICD multiple times prior to their arrival. No vital signs could be obtained en route.

On arrival in the emergency department, the patient was awake and responding appropriately to questions. His MAP was 80mmHg, an audible whir was auscultated from his device and the skin surrounding the percutaneous exit site appeared normal.

ECG

ECG with Ventricular Fibrillation

POCUS

Ultrasound showing parasternal long axis view of fibrillating heart

The patient’s device was inactivated with a magnet to prevent further ineffectual shocks. An arterial line was placed for continuous blood pressure measurement. He was sedated and externally defibrillated with return to normal sinus rhythm prior to admission to the CCU.

An Algorithm for the Evaluation of Unstable LVAD1

Algorithm for the Evaluation of Unstable LVAD

Reference

Stenberg R, Shenvi C. Targeted evaluation of patients with left ventricular assist devices and shock or hypotension. Ann Emerg Med. 2020;76(1):34-41.

BRUE

Brief H&P:

A 4 month-old male with no past medical history and fully-immunized is brought to the emergency department by her mother after an episode of breathing difficulty. She describes that just prior to presentation she noted her child had stopped breathing. She lifted him from the bed and noted some blue discoloration to the mouth with limp extremities. She began to stimulate him by rubbing his chest and abdomen and he began crying after approximately 30 seconds.

She states that he has since returned to normal and she was able to feed him upon arrival to the emergency department without apparent difficulty or vomiting. Prior to the episode, the patient had been in his usual state of health (normal oral intake, urine/stool). No family history of sudden death.

On physical examination, vital signs are normal. The child appears comfortable. Head is normocephalic and atraumatic with normal anterior fontanelle. Mucous membranes are moist, heart sounds are normal and lungs are clear. The abdomen is soft and without organomegaly. The remainder of a detailed physical examination is unremarkable.

The patient was placed on continuous pulse oximetry, remained well-appearing on serial reassessments and had no further episodes while continuing to feed normally. An ECG was obtained:

The patient’s mother was counseled regarding the diagnosis of low-risk BRUE and the reassuring evaluation and ED observation period. She states that she is able to present to her pediatrician the subsequent morning for evaluation. She was counseled regarding return precautions prior to discharge.

An Algorithm for the Evaluation and Management of Brief Resolved Unexplained Events (BRUE)1,2

An Algorithm for the Evaluation and Management of Brief Resolved Unexplained Events (BRUE)

Differential Diagnosis for BRUE3

Category Causes
Environmental Abuse/trauma
Toxicological
CNS Seizure
Intracranial mass
Cardiovascular Congenital heart disease
Arrhythmia
Pulmonary Airway obstruction
Central apnea
Apnea of prematurity
Pneumonia
Bronchiolitis
Pertussis
Gastrointestinal GERD
IEM Glycogen storage disease
Hyperinsulinism
Fatty acid oxidation defects
This algorithm was developed by Dr. Ali Sina Mirab. Dr. Mirab is a PGY-3 emergency medicine resident at the McGovern Medical School at the University of Texas Health Science Center at Houston (UTHealth).

Special thanks to Dr. Thomas McCarty, Assistant Professor and Pediatric Emergency Medicine Fellowship Director in the Department of Emergency Medicine at McGovern Med EM for his review of the algorithm.

References:

  1. Tieder JS, Bonkowsky JL, Etzel RA, et al. Clinical Practice Guideline: Brief Resolved Unexplained Events (Formerly Apparent Life-Threatening Events) and Evaluation of Lower-Risk Infants: Executive Summary. Pediatrics. 2016:137(5):e20160591.
  2. Merritt JL, Quinonez RA, Bonkowsky JL, et al. A framework for evaluation of the higher-risk infant after a brief resolved unexplained event. Pediatrics. 2019;144(2):e20184101.
  3. McGovern MC, Smith MBH. Causes of apparent life threatening events in infants: a systematic review. Arch Dis Child. 2004;89(11):1043-1048.

Headache

Brief HPI:

A 48 year-old male with hypertension and hyperlipidemia presents with headache. Notes onset of symptoms 8 hours prior to presentation, reaching maximal severity within seconds. Headache improved with over-the-counter analgesics. On examination, there are no neurological deficits, neck is supple. A CT head non-contrast is obtained:

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CT Head:

No acute intracranial process. Case courtesy of Assoc Prof Craig Hacking, Radiopaedia.org, rID: 37118

ED Course:

A lumbar puncture is performed, CSF sampling reveals xanthochromia – neurosurgery is consulted and the patient is admitted for angiography and possible intervention.

An Algorithm for the Evaluation of Headache

An Algorithm for the Evaluation of Headache

High-Risk Historical Features

  • Sudden onset (seconds/minutes), patient recalls activity at onset
  • Worst in life or change in character from established headache
  • Fever, neck pain/stiffness
  • Altered mental status
  • Malignancy
  • Coagulopathy: iatrogenic, hepatopathy, dialysis
  • Immunocompromised
  • Rare: CO exposure, jaw claudication, PCKD

Location of Pain

Headache Location

  1. Unilateral: migraine
  2. Periorbital: glaucoma, CVT, optic neuritis, cluster
  3. Facial/maxillary: trigeminal neuralgia, sinusitis
  4. Temporal: GCA
  5. Occipital: cerebellar stroke
  6. Nuchal: meningitis

Characteristics of Primary Headaches

Type Location Duration Quality Associated symptoms Comment
Migraine Unilateral Hours to days Throbbing Photophobia, phonophobia Atypical migraines with neurological findings (basilar, ophthalmoplegic, ophthalmic, hemiplegic)
Tension Bilateral Minutes to days Constricting None
Cluster Unilateral, periorbital Minutes to hours Throbbing Conjunctival injection, lacrimation, rhinorrhea, miosis, eyelid edema Males 90%, triggered by EtOH.

Physical Examination Findings

Vital Signs
Fever: present in 95% of patients with meningitis
Head
Trauma: signs of basilar skull fracture
Temporal artery tenderness/induration: GCA
Pericranial muscle tenderness: tension headache
Trigger point, Tinnel sign: occipital neuralgia
Eyes
Pupillary defects: aneurysm with CN III compression
Papilledema, absence of spontaneous venous pulsations: elevated intracranial pressure
EOM abnormalities: ICH, mass lesion, neuropathy (DM, Lyme)
Horner syndrome (ptosis, miosis, anhidrosis): carotid dissection
Visual field defect: stroke, atypical migraine
Conjunctival injection: glaucoma (fixed, mid-size pupil, elevated intraocular pressure), cluster headache
Mouth
Thrush: immunocompromise
Sinuses
Tenderness to palpation, abnormal transillumination: sinusitis
Neck
Resistance to supine neck flexion: meningitis
Kernig: supine position, hip flexed, knee flexed, resistance to knee extension
Brudzinski: supine position, neck flexion results in knee flexion
Jolt accentuation: patient rotates head side-to-side, 2-3 times/sec exacerbates headache

References:

  1. Russi, C. (2013). Headache. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 170-175). Elsevier Health Sciences.
  2. Godwin SA, Villa J. “Acute headache in the ED: Evidence-Based Evaluation and Treatment Options.” Emerg Med Pract 2001; 3(6): 1-32.
  3. Edlow, J. A., Panagos, P. D., Godwin, S. A., Thomas, T. L., & Decker, W. W. (2008). Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department With Acute Headache. Annals of emergency medicine, 52(4), 407–436. doi:10.1016/j.annemergmed.2008.07.001
  4. WikEM: Headache

Ear Pain

Brief HPI:

A 48 year-old female with a history of hypertension, diabetes, and hyperlipidemia presents with ear pain and discharge. She notes an associated headache and fevers. Examination demonstrates external auditory canal edema with granulation tissue along the floor. No cranial nerve abnormalities identified.

CT suggestive of malignant otitis externa

Image courtesy of Dr. Charlie Chia-Tsong Hsu, Radiopaedia.org case rID: 19938.

ED Course:

A CT was obtained which demonstrated edema of the external auditory meatus, pinna and periauricular soft tissue with fluid in the left mastoid sinuses without evidence of bone erosion. The patient was diagnosed with malignant otitis externa, started on intravenous ciprofloxacin and admitted with otolaryngology consultation.

An Algorithm for the Differential Diagnosis of Ear Pain1-5

An Algorithm for the Differential Diagnosis of Ear Pain

Otalgia Gallery

References

  1. Earwood JS, Rogers TS, Rathjen NA. Ear pain: diagnosing common and uncommon causes. Am Fam Physician. 2018;97(1):20-27.
  2. Coulter J, Kwon E. Otalgia. [Updated 2020 Aug 15]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK549830/
  3. Pfaff, J. A., & Moore, G. P. (2018). Rosen’s Emergency Medicine: Concepts and Clinical Practice. In 1325336653 972907711 R. M. Walls (Author), Rosen’s Emergency Medicine: Concepts and Clinical Practice (9th ed., Vol. 1, pp. 820-831). Philadelphia, PA: Elsevier.
  4. Safavi Naini A, Ghorbani J, Montazer Lotfe Elahi S, Beigomi M. Otologic manifestations and progression in patients with wegener’s granulomatosis: a survey in 55 patients. Iran J Otorhinolaryngol. 2017;29(95):327-331.
  5. Conover K. Earache. Emerg Med Clin North Am. 2013;31(2):413-442.

Infographic: CT Cervical Spine Interpretation

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Header: CT Interpretation C-SpineAlignmentSpacingArticulationsFractures: PrimaryFractures: SecondaryLung Apices

Examples

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Alignment

Note the sharp angle of the anterior vertebral line and associated asymmetric widening of the interspinous space.

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Articulations: Craniocervical

Powers ratio >0.9, increased basion-dens interval (BDI). Case courtesy of Assoc Prof Craig Hacking, Radiopaedia.org. From the case rID: 87570

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Articulations: Facets

Facet dislocation. Case courtesy of RMH Core Conditions, Radiopaedia.org. From the case rID: 33851

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Fractures: Primary

Vertebral body height variance, posterior longitudinal ligament malalignment. Case courtesy of Dr Jeremy Jones, Radiopaedia.org. From the case rID: 6150

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Fractures: Secondary

Prevertebral edema

CSF Shunt Complications

Brief HPI:

A 33 year-old female with a history of idiopathic intracranial hypertension and ventriculoperitoneal shunt placement presents with headache and confusion. She denies fever, trauma, neck pain or stiffness. She has not had symptoms like this since her shunt was placed 2 years ago. Imaging was obtained which showed ventriculomegaly and a fracture of the shunt at the level of the cervical spine. Neurosurgery was consulted and the patient was admitted for shunt repair.

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CT Head

Ventriculomegaly with dilatation of the temporal horns in particular. Right parietal approach ventricular drain. Case courtesy of Dr. Henry Knipe, Radiopaedia.org, rID: 39615

XR Shunt Series

XR Shunt Series

Shunt tubing fractured at the level of the upper cervical spine

An Algorithm for CSF Shunt Complications

An Algorithm for CSF Shunt Complications

References:

  1. Madsen MA. Emergency department management of ventriculoperitoneal cerebrospinal fluid shunts. Ann Emerg Med. 1986;15(11):1330-1343.
  2. Ferras M, McCauley N, Stead T, Ganti L, Desai B. Ventriculoperitoneal shunts in the emergency department: a review. Cureus. 2020;12(2):e6857.
  3. Paff M, Alexandru-Abrams D, Muhonen M, Loudon W. Ventriculoperitoneal shunt complications: A review. Interdisciplinary Neurosurgery. 2018;13:66-70.
  4. Pitetti R. Emergency department evaluation of ventricular shunt malfunction: is the shunt series really necessary? Pediatr Emerg Care. 2007;23(3):137-141.
  5. Fowler JB, De Jesus O, Mesfin FB. Ventriculoperitoneal Shunt. [Updated 2021 Feb 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK459351/
  6. Broggi M, Zattra CM, Schiariti M, et al. Diagnosis of ventriculoperitoneal shunt malfunction: a practical algorithm. World Neurosurg. 2020;137:e479-e486.

Hypoglycemia

Brief HPI:

A 40 year-old male with a history of diabetes presents after accidental insulin overdose. He reports inadvertently administering 50 units of rapid-acting insulin when intending to take his long-acting insulin 25 minutes prior to presentation. He is currently asymptomatic, has a normal physical examination and his point-of-care glucose is 65mg/dL.

ED Course

The patient’s insulin regimen was clarified:

  • Insulin glargine 50 units SQ once daily
  • Insulin aspart 1 unit per 5g carbohydrates SQ before meals

The patient administered an insulin dose sufficient to dispose of 250g of carbohydrates with an impending peak action within minutes. The required dose of parenteral dextrose would require potentially-toxic1,2 solution concentrations (one liter of D25 or 10 ampules of D50) and there was insufficient time for central venous catheter placement. Moreover, the patient was awake and asymptomatic – able to tolerate oral intake. Juice boxes containing 15g of carbohydrates each were located and the patient drank 16-17 boxes while undergoing serial glucose measurements. His blood glucose ranged between 70mg/dL and 150mg/dL and he was discharged after an uneventful 6-hour observation.

Insulin Pharmacokinetics3

Graph of insulin pharmacokinetics

Insulin and Carbohydrates

The effects of both insulin and carbohydrate ingestion on blood glucose are individualized. If known, the patient’s insulin:carbohydrate ratio can be used to anticipate the effect of overdose. Alternatively, their mealtime dose and carbohydrate allowance can be used.

Very broadly, one gram of carbohydrates increases blood glucose by 3-5mg/dL and one unit of insulin disposes of 10 grams of carbohydrates (or reduces blood glucose by 30-50mg/dL).4

Symptoms

  • Autonomic: tremor, palpitations, anxiety, diaphoresis
  • Neuroglycopenic: cognitive impairment, psychomotor, seizure, coma

Diagnosis

  • Serum glucose <60mg/dL
  • Generally symptomatic at <55mg/dL though threshold is variable depending on chronicity
  • Whipple Triad:
    • Symptoms suggestive of hypoglycemia
    • Low glucose
    • Resolution of symptoms after administration of glucose

Differential Diagnosis of Hypoglycemia

Differential Diagnosis of Hypoglycemia

Common Anti-hyperglycemic Drugs and Pharmacology

Drug Pharmacology
Onset Peak Duration
Rapid-acting insulin

  • Aspart (Novolog)
  • Lispro (Humalog)
 15-30min 1-2h 3-5h
Short-acting insulin

  • Regular
 30-60min 2-4h 6-10h
Intermediate-acting insulin

  • NPH
 1-3h 4-12h 18-24h
Long-acting insulin

  • Glargine (Lantus)
 2-4h None 24h
Sulfonylurea

  • Glimepiride
  • Glipizide (Glucotrol)
  • Glyburide (Glycron, Micronase)
 – 2-6h 12-24h

Evaluation of Hypoglycemia

Patients with known diabetes who are not systemically ill and can identify a clear precipitant, no extensive workup is required. In severely ill patients, consider:

  • BMP
  • LFT
  • EtOH
  • Infectious workup: CXR, UA, urine and blood cultures
  • ECG, troponin
  • Other studies: insulin, C-peptide, pro-insulin, glucagon, growth hormone, cortisol, B-OH, insulin antibodies

Management and Monitoring

An algorithm for the management and monitoring of hypoglycemia

Special thanks to Dr. Ryan Pedigo, Associate Residency Program Director at Harbor-UCLA Medical Center for his case submission and content review.
Twitter

References:

  1. Kuwahara T, Asanami S, Kubo S. Experimental infusion phlebitis: tolerance osmolality of peripheral venous endothelial cells. Nutrition. 1998;14(6):496-501.
  2. Wiegand R, Brown J. Hyaluronidase for the management of dextrose extravasation. Am J Emerg Med. 2010;28(2):257.e1-2.
  3. Hirsch IB. Insulin analogues. N Engl J Med. 2005;352(2):174-183.
  4. Your Insulin Therapy. (2004). Am Fam Physician, 70(3), 511-512.
  5. Self, W. H., & McNaughton, C. D. (2013). Hypoglycemia. In Emergency Medicine (2nd ed., pp. 1379-1390). Elsevier.
  6. Service, FJ. Hypoglycemia in adults: Clinical manifestations, definition, and causes. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. (Accessed on March 18, 2016.)
  7. Service FJ. Hypoglycemic disorders. N Engl J Med. 1995;332(17):1144–1152. doi:10.1056/NEJM199504273321707.
  8. Krinsley JS, Grover A. Severe hypoglycemia in critically ill patients: risk factors and outcomes. Critical Care Medicine. 2007;35(10):2262–2267. doi:10.1097/01.CCM.0000282073.98414.4B.
  9. Lacherade J-C, Jacqueminet S, Preiser J-C. An overview of hypoglycemia in the critically ill. J Diabetes Sci Technol. 2009;3(6):1242–1249.

Hyperammonemia

Brief H&P

A 38 year-old male with unknown medical history is brought to the emergency department by EMS with agitation and bizarre behavior. According to prehospital report, the patient was acting erratically – shouting incomprehensibly in the middle of a busy street with possible associated seizure activity.

On evaluation, the patient was found to be tachycardic, hypertensive, and markedly agitated. Physical examination with a focus on toxidromes was notable for the presence of rotary nystagmus suggestive of hallucinogen including phencyclidine toxicity. The patient required pharmacologic sedation to allow for a broad evaluation of altered mental status.

ED Course

The patient’s workup including core temperature, head imaging and laboratory tests (including AST/ALT, albumin, INR) were unremarkable with the exception of an ammonia level of 142 umol/L (normal range 16-53), slightly elevated CK, and urine toxicology screen with multiple positive agents. Over the course of several hours in the emergency department, the patient’s mental status gradually improved reaching normal level of alertness and orientation with normal neurological examination. He acknowledged PCP use as well as a prior history of seizures (possibly related to ethanol withdrawal) without routine anti-epileptic drug use. He denied known history of liver disease.

The patient’s hyperammonemia was attributed to a hypercatabolic state secondary to phencyclidine-induced agitation with possible seizure. He was discharged with resources for assistance with substance cessation.

An Algorithm for the Differential Diagnosis of Hyperammonemia:

Algorithm for the Differential Diagnosis of Hyperammonemia

References:

  1. Kalra A, Norvell JP. Cause for Confusion: Noncirrhotic Hyperammonemic Encephalopathy. Clin Liver Dis. 2020;15(6):223-227. doi:10.1002/cld.929
  2. Mallet M, Weiss N, Thabut D, Rudler M. Why and when to measure ammonemia in cirrhosis? Clin Res Hepatol Gas. 2018;42(6):505-511. doi:10.1016/j.clinre.2018.01.004
  3. Hassan AAI, Ibrahim W, Subahi A, Mohamed A. ‘All that glitters is not gold’: when hyperammonaemia is not from hepatic aetiology. Bmj Case Reports. 2017;2017:bcr-2017-219441. doi:10.1136/bcr-2017-219441
  4. Odigwe CC, Khatiwada B, Holbrook C, et al. Noncirrhotic Hyperammonemia Causing Relapsing Altered Mental Status. Bayl Univ Medical Cent Proc. 2017;28(4):472-474. doi:10.1080/08998280.2015.11929312
  5. Upadhyay R, Bleck TP, Busl KM. Hyperammonemia: What Urea-lly Need to Know: Case Report of Severe Noncirrhotic Hyperammonemic Encephalopathy and Review of the Literature. Case Reports Medicine. 2016;2016:1-10. doi:10.1155/2016/8512721
  6. Walker V. Severe hyperammonaemia in adults not explained by liver disease. Ann Clin Biochem. 2011;49(3):214-228. doi:10.1258/acb.2011.011206
  7. Laish I, Ari ZB. Noncirrhotic hyperammonaemic encephalopathy. Liver Int. 2011;31(9):1259-1270. doi:10.1111/j.1478-3231.2011.02550.x
  8. LaBuzetta JN, Yao JZ, Bourque DL, Zivin J. Adult Nonhepatic Hyperammonemia: A Case Report and Differential Diagnosis. Am J Medicine. 2010;123(10):885-891. doi:10.1016/j.amjmed.2010.02.029
  9. Clay AS, Hainline BE. Hyperammonemia in the ICU. Chest. 2007;132(4):1368-1378. doi:10.1378/chest.06-2940
  10. Weng T-I, Shih FF-Y, Chen W-J. Unusual causes of hyperammonemia in the ED. Am J Emerg Medicine. 2004;22(2):105-107. doi:10.1016/j.ajem.2003.12.011
  11. Hawkes ND, Thomas GAO, Jurewicz A, et al. Non-hepatic hyperammonaemia: an important, potentially reversible cause of encephalopathy. Postgrad Med J. 2001;77(913):717. doi:10.1136/pmj.77.913.717

Sedative-Hypnotic Withdrawal

Brief H&P

A 24 year-old male with no reported medical history is transferred from jail for altered mental status. The patient had been in jail for two days and was noted to develop worsening confusion and agitation.

On arrival in the emergency department, the patient was agitated, moving wildly requiring physical restraints and speaking incomprehensibly. Initial vital signs were notable for tachycardia (HR 145bpm) and hypertension (BP 140/100mmmHg), afebrile core temperature. Examination revealed dilated pupils and dry skin. Point-of-care glucose measured 70mg/dL. Midazolam 5mg IV was administered due to his severe agitation and inability to cooperate with detailed evaluation.

After administration of midazolam, the patient became somewhat more lucid though he appeared to be hallucinating. He reported a history of alprazolam use. The patient was treated with nutritional supplementation and escalating doses of benzodiazepines. The patient remained persistently agitated after administration of midazolam 40mg IV as a single dose so phenobarbital was administered and the patient was intubated for airway protection and anticipated clinical course. The patient was started on a midazolam infusion at 40mg/hour after which he became more calm and vital signs normalized. Laboratory tests were unremarkable with the exception of elevated CK. Head imaging was negative for acute intracranial processes. The patient was admitted to the intensive care unit where he was transitioned to propofol and dexmedetomidine infusions. He was eventually extubated and discharged on hospital day #3 with a chlordiazepoxide taper.

Algorithm for the Management of Sedative-Hypnotic Withdrawal

Algorithm for the Management of Sedative-Hypnotic Withdrawal

Special thanks to David A. Tanen, MD FAAEM FACMT, Professor of Emergency Medicine, Harbor-UCLA Medical Center for his expertise and review of this algorithm.

References

Treatment Algorithms

  1. Gold, J. A., Rimal, B., Nolan, A. & Nelson, L. S. A strategy of escalating doses of benzodiazepines and phenobarbital administration reduces the need for mechanical ventilation in delirium tremens Crit Care Med 35, 724–730 (2007).
  2. Schmidt, K. J. et al. Treatment of Severe Alcohol Withdrawal. Ann Pharmacother 50, 389–401 (2016).
  3. Santos, C., Olmedo, R. E. & Kim, J. Sedative-hypnotic drug withdrawal syndrome: recognition and treatment. Emerg Medicine Pract 19, S1–S2 (2017).

Gabapentin

  1. Myrick, H. et al. A Double‐Blind Trial of Gabapentin Versus Lorazepam in the Treatment of Alcohol Withdrawal. Alcohol Clin Exp Res 33, 1582–1588 (2009).
  2. Stock, C. J., Carpenter, L., Ying, J. & Greene, T. Gabapentin Versus Chlordiazepoxide for Outpatient Alcohol Detoxification Treatment. Ann Pharmacother 47, 961–969 (2013).

Barbiturates

  1. Hendey, G. W., Dery, R. A., Barnes, R. L., Snowden, B. & Mentler, P. A prospective, randomized, trial of phenobarbital versus benzodiazepines for acute alcohol withdrawal. Am J Emerg Medicine 29, 382–385 (2011).
  2. Rosenson, J. et al. Phenobarbital for Acute Alcohol Withdrawal: A Prospective Randomized Double-blind Placebo-controlled Study. J Emerg Medicine 44, 592-598.e2 (2013).

Textbook Chapters

  1. Cohen, J. P. et al. Alcohols. in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e (McGraw-Hill Education, 2020).
  2. Quan, D. et al. Benzodiazepines. in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e (McGraw-Hill Education, 2020).

Reviews

  1. Mayo-Smith, M. F. Pharmacological Management of Alcohol Withdrawal: A Meta-analysis and Evidence-Based Practice Guideline. Jama 278, 144–151 (1997).
  2. Mayo-Smith, M. F. et al. Management of Alcohol Withdrawal Delirium: An Evidence-Based Practice Guideline. Arch Intern Med 164, 1405–1412 (2004).
  3. DeBellis, R., Smith, B. S., Choi, S. & Malloy, M. Management of Delirium Tremens. J Intensive Care Med 20, 164–173 (2005).
  4. Amato, L., Minozzi, S., Vecchi, S. & Davoli, M. Benzodiazepines for alcohol withdrawal. Cochrane Db Syst Rev CD005063 (2010) doi:10.1002/14651858.cd005063.pub3.

Adrenal Insufficiency

Brief H&P:

A 65 year-old female with a history of hypertension, hyperlipidemia and rheumatoid arthritis presents with generalized weakness and nausea/vomiting for 3 days. She denies fever, focal weakness, numbness or speech difficulty.

HPA Axis

HPA Axis

Vital signs were notable for hypotension (72/48mmHg), her examination revealed diffuse weakness but no focal deficits and her abdominal examination was unremarkable. Laboratory tests were notable for hyponatremia (117 mEq/L) and new renal dysfunction. She received 2L of intravenous fluids but remained hypotensive.

Additional history revealed that the patient had been out of her home medications (including prednisone) for the past 1 week. Samples for laboratory tests (cortisol, ACTH) were drawn and she was treated with hydrocortisone 100mg IV with subsequent improvement in blood pressure – she was admitted to the ICU for adrenal crisis.

An Algorithm for the Evaluation and Management of Adrenal Insufficiency and Crisis

Algorithm for the Evaluation and Management of Adrenal Insufficiency and Crisis

Special thanks to Dr. Katrin Takenaka, Professor, Department of Emergency Medicine and Dr. Reem Al-Dallal, Assistant Professor, Division of Endocrinology, Department of Internal Medicine – McGovern Medical School for their expertise and review of this algorithm.

References:

  1. Idrose, A., Tintinalli, J., Ma, O., Yealy, D., Meckler, G., Stapczynski, J., Cline, D., Thomas, S. (2020). Adrenal Insufficiency Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e
  2. Carroll, T., Aron, D., Findling, J., Tyrrell, J., Gardner, D., Shoback, D. (2017). Glucocorticoids and Adrenal Androgens Greenspan’s Basic & Clinical Endocrinology, 10e
  3. Dineen, R., Thompson, C., Sherlock, M. (2019). Adrenal crisis: prevention and management in adult patients Therapeutic Advances in Endocrinology and Metabolism 10(), 2042018819848218. https://dx.doi.org/10.1177/2042018819848218
  4. Rushworth, R., Torpy, D., Falhammar, H. (2019). Adrenal Crisis New England Journal of Medicine 381(9), 852-861. https://dx.doi.org/10.1056/nejmra1807486
  5. Amrein, K., Martucci, G., Hahner, S. (2018). Understanding adrenal crisis Intensive Care Medicine 44(5), 652-655. https://dx.doi.org/10.1007/s00134-017-4954-2
  6. Oelkers, W. (1996). Adrenal Insufficiency The New England Journal of Medicine 335(16), 1206-1212. https://dx.doi.org/10.1056/nejm199610173351607
  7. Tucci, V., Sokari, T. (2014). The Clinical Manifestations, Diagnosis, and Treatment of Adrenal Emergencies Emergency Medicine Clinics of North America 32(2), 465-484. https://dx.doi.org/10.1016/j.emc.2014.01.006
  8. Bleicken, B., Hahner, S., Ventz, M., Quinkler, M. (2010). Delayed Diagnosis of Adrenal Insufficiency Is Common: A Cross-Sectional Study in 216 Patients The American Journal of the Medical Sciences 339(6), 525-531. https://dx.doi.org/10.1097/maj.0b013e3181db6b7a
  9. Broersen, L., Pereira, A., Jørgensen, J., Dekkers, O. (2015). Adrenal Insufficiency in Corticosteroids Use: Systematic Review and Meta-Analysis The Journal of Clinical Endocrinology & Metabolism 100(6), 2171-2180. https://dx.doi.org/10.1210/jc.2015-1218
  10. Joseph, R., Hunter, A., Ray, D., Dixon, W. (2016). Systemic glucocorticoid therapy and adrenal insufficiency in adults: A systematic review Seminars in Arthritis and Rheumatism 46(1), 133-141. https://dx.doi.org/10.1016/j.semarthrit.2016.03.001

Toxidromes

Case 1:

A 20 year-old male with a history of polysubstance use, depression and seasonal allergies presents via ambulance for altered mental status. According to prehospital report, EMS were contacted by the patient’s roommate who noted that he had been acting strangely after being alone in his room for several hours. Vital signs are notable for fever (T 103.2°F) and tachycardia. The patient was confused, unable to follow commands – pupils were dilated.

The initial impression was concerning for sympathomimetic toxicity, the patient was treated with cooled intravenous fluids and required pharmacologic sedation and physical restraints to obtain blood samples. ECG, initial laboratory tests and urine toxicology screen were unremarkable. A non-contrast CT head was normal.

The patient remained altered and a repeat examination was performed which revealed multiple, opened blister packs of diphenhydramine and dry, flushed skin.

Anti-cholinergic toxicity was presumed, likely exacerbated by the administration of butyrophenones for sedation. He was treated with benzodiazepines, additional evaporative cooling measures and was admitted to the intensive care unit.

Case 2:

A 32 year-old female with a history of depression was brought to the emergency department by family members who were concerned about bizarre behavior and muscle stiffness. They note that the patient was recently started on a new antidepressant though they are unsure of the name. They describe occasional alcohol consumption but no illicit drug use.

In the emergency department, vital signs were notable for fever and hypertension. Examination demonstrated increased muscle tone and sustained clonus in bilateral lower extremities.

The patient’s presentation was concerning for serotonin syndrome, she was treated with benzodiazepines and intravenous fluids with gradual improvement in mental status and hypertonicity. Upon awakening, she reported doubling her medication dose recently due to persistent feelings of hopelessness as well as increased wine consumption.

An Algorithm for the Evaluation of Toxidromes

An Algorithm for the Evaluation of Toxidromes

Diagnostic Tests

All Patients Most Patients Critical Patients
POC glucose

Core temperature

ECG

Urine hCG

 BMP

UA

Acetaminophen

Salicylate

Ethanol

 LFT

Lipase

Serum osmolarity

Ionized calcium

Magnesium

GI Decontamination

Activated charcoal

Activated charcoal (1g/kg) within 1-hour post-ingestion and if the patient is awake and cooperative (or via enteric tube if intubated).

Not recommended

  1. Heavy metals
  2. Ions (ex. lithium)
  3. Corrosives
  4. Hydrocarbons
  5. Alcohols

Whole-bowel irrigation

Indicated for sustained-release formulations, expulsion of body packing materials, or ingestion of agent not absorbed by activated charcoal.

Serum alkalinization

For certain ingestions (salicylate, phenobarbital, methotrexate), serum alkalinization through infusion of sodium bicarbonate targeting serum pH 7.5 (and urine pH 8.0) may promote elimination.

Intralipid emulsion

May be useful for local anesthetic toxicity, b-blocker, and calcium channel blocker overdose.

Electrocardiographic Toxidromes

 

QT Prolongation QRS Prolongation
Anti-emetic Diphenhydramine
Anti-psychotic Cocaine
Anti-microbials (fluoroquinolone, macrolide) Diltiazem, verapamil
Anti-depressant (TCA, SSRI) Propranolol
Anti-arrhythmic Amantadine
Carbamazepine

Gap-producing Toxidromes

Osmolar Gap

  • Toxic alcohol
    • Ethanol
    • Methanol
    • Ethylene glycol
    • Isopropyl alcohol
  • Drug stabilizing agents
    • Mannitol
    • Propylene glycol
    • Glycerol

Anion Gap

  • Salicylate
  • Iron
  • Isoniazid
  • Methanol
  • Ethylene glycol
  • Cyanide

References

  1. Meehan, T. J. (2018). Approach to the Poisoned Patient. In Rosens emergency medicine: concepts and clinical practice (pp. 1813–1822). Philadelphia, PA: Elsevier.
  2. Holstege, C., Borek, H. (2012). Toxidromes Critical Care Clinics 28(4), 479-498. https://dx.doi.org/10.1016/j.ccc.2012.07.008
  3. Mégarbane, B. (2014). Toxidrome-based Approach to Common Poisonings Asia Pacific Journal of Medical Toxicology 3(1), 2-12. https://dx.doi.org/10.22038/apjmt.2014.2463
  4. Rasimas, J., Sinclair, C. (2017). Assessment and Management of Toxidromes in the Critical Care Unit. Critical care clinics 33(3), 521-541. https://dx.doi.org/10.1016/j.ccc.2017.03.002
  5. Thompson, T., Theobald, J., Lu, J., Erickson, T. (2014). The general approach to the poisoned patient Disease-a-Month 60(11), 509-524. https://dx.doi.org/10.1016/j.disamonth.2014.10.002
This algorithm was co-developed by Dr. Chigozie Dike, and Dr. Katrina Nemri.

Dr. Dike is a Houstonian true and true, born across the street at Ben Taub Hospital and proud to have the support of her family and friends through her medical school and emergency medicine training at McGovern Med EM at UT Health. She is a big foodie and loves music. In her free time she’s exploring local restaurants, traveling to new cities, and practicing yoga.

Dr. Nemri is currently a second year emergency medicine resident at McGovern Med EM at UT Health. Her interests are in medical education and critical care. She is a local Houstonian who hopes to stay in the city after residency.

Isolation Precautions

An Algorithm for the Determination of Isolation Precautions

An Algorithm for the Determination of Isolation Precautions

References

  1. Siegel, J., Rhinehart, E., Jackson, M., Chiarello, L., Committee, H. (2007). 2007 Guideline for Isolation Precautions: Preventing Transmission of Infectious Agents in Health Care Settings American Journal of Infection Control 35(10), S65-S164. https://dx.doi.org/10.1016/j.ajic.2007.10.007
  2. Liang, S., Theodoro, D., Schuur, J., Marschall, J. (2014). Infection Prevention in the Emergency Department Annals of Emergency Medicine 64(3), 299-313. https://dx.doi.org/10.1016/j.annemergmed.2014.02.024
  3. Liang, S., Riethman, M., Fox, J. (2018). Infection Prevention for the Emergency Department: Out of Reach or Standard of Care? Emergency medicine clinics of North America 36(4), 873-887. https://dx.doi.org/10.1016/j.emc.2018.06.013
  4. Gottenborg, E., Barron, M. (2016). Isolation Precautions in the Inpatient Setting Hospital Medicine Clinics 5(1), 30-42. https://dx.doi.org/10.1016/j.ehmc.2015.08.004
  5. Harding, A., Almquist, L., Hashemi, S. (2011). The use and need for standard precautions and transmission-based precautions in the emergency department. Journal of emergency nursing: JEN : official publication of the Emergency Department Nurses Association 37(4), 367-73; quiz 424-5. https://dx.doi.org/10.1016/j.jen.2010.11.017