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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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

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.

00_ct_csf_shunt
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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

Opioid Withdrawal

Brief HPI:

A 28 year-old female with a history of IV drug use presents to the emergency department with back pain and fever. During evaluation for spinal epidural abscess, she develops vomiting and diarrhea. Examination reveals diaphoresis, mydriasis and hyperactive bowel sounds – she states that her last heroin use was 18-hours ago.

The patient was interested in guidance with cessation of opioid dependence and was evaluated by a recovery support specialist in the emergency department and provided with an appointment for outpatient follow-up. She was treated with buprenorphine-naloxone 8mg sublingual and her symptoms resolved. Her diagnostic evaluation was normal and she was discharged with a prescription for buprenorphine-naloxone 16mg daily until follow-up.

An Algorithm for the Management of Opioid Withdrawal1-4

An Algorithm for the Management of Opioid Withdrawal

Signs

  • Mydriasis
  • Piloerection
  • Diaphoresis
  • Hyperactive bowel sounds

COWS Calculator

Symptoms

  • Dysphoria
  • Rhinorrhea
  • Myalgias, arthralgias
  • Nausea, vomiting, diarrhea
  • Abdominal cramps

Buprenorphine Considerations

Buprenorphine is a high-affinity, opioid partial agonist. The administration of buprenorphine may displace lower-affinity opioids.5 When used for the treatment of acute opioid withdrawal, special care must be taken to ensure that sufficient time has elapsed since last use (evidenced by the presence of moderate withdrawal symptoms) as the immediate displacement of existing opioids can precipitate severe withdrawal. In addition to provoking the maximum severity of the symptoms for which treatment was sought, this can generate mistrust in an otherwise effective medication and the healthcare system more broadly. The combination of buprenorphine with naloxone is intended to deter parenteral abuse – oral/sublingual naloxone is poorly bioavailable.

The initiation of medication-assisted treatment for opioid dependence from the emergency department should be dependent on the availability of outpatient follow-up and addiction treatment programs.6

Supportive Care4,6-7

Symptom Agent Dose
Nausea, Vomiting Promethazine 25mg IM
Diarrhea Loperamide 4mg PO
Octreotide 50mcg SQ
Muscle cramps Baclofen 5mg PO
Anxiety, Dysphoria Lorazepam 1-2mg IV
Diazepam 2-10mg PO, IM, IV
Pain, Myalgia Acetaminophen 650mg – 1,000mg PO
Ibuprofen 600mg PO

Unobserved Induction Guide8

The following guide is adapted from the Yale Department of Emergency Medicine ED-Initiated Buprenorphine Program and is available free for use.
Home Induction Guide Preview

This algorithm was developed with Dr. Drew Silver. Drew is an emergency medicine resident at McGovern Medical School at the University of Texas Health Science Center at Houston (UTHealth).

References

  1. Strayer R, Hawk K, Hayes B, Herring A et al. Management of Opiate Misuse Disorder in the Emergency Department: A White Paper Prepared for the American Academy of Emergency Medicine. American Academy of Emergency Medicine.
  2. ED-Initiated Buprenorphine. Retrieved July 17, 2020, from https://medicine.yale.edu/edbup/Algorithm_338052_5_v2.pdf
  3. Su, M., Lopez, J., Crossa, A., Hoffman, R. (2018). Low dose intramuscular methadone for acute mild to moderate opioid withdrawal syndrome The American Journal of Emergency Medicine 36(11), 1951-1956. https://dx.doi.org/10.1016/j.ajem.2018.02.019
  4. Stolbach A, Hoffman R. Opioid withdrawal in the emergency setting. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc.
  5. Boas, R., Villiger, J. (1985). Clinical actions of fentanyl and buprenorphine. The significance of receptor binding. British journal of anaesthesia 57(2), 192-6. https://dx.doi.org/10.1093/bja/57.2.192
  6. D’Onofrio, G., Chawarski, M., O’Connor, P., Pantalon, M., Busch, S., Owens, P., Hawk, K., Bernstein, S., Fiellin, D. (2017). Emergency Department-Initiated Buprenorphine for Opioid Dependence with Continuation in Primary Care: Outcomes During and After Intervention Journal of General Internal Medicine 32(6), 660-666. https://dx.doi.org/10.1007/s11606-017-3993-2
  7. Gowing, L., Farrell, M., Ali, R., White, J. (2016). Alpha2‐adrenergic agonists for the management of opioid withdrawal Cochrane Database of Systematic Reviews https://dx.doi.org/10.1002/14651858.cd002024.pub5
  8. Home Initiated Buprenorphine. Retrieved July 17, 2020, from https://medicine.yale.edu/edbup/quickstart/Home_Buprenorphine_Initiation_338574_42801_v1.pdf
  9. Wesson DR, Ling W. The Clinical Opiate Withdrawal Scale (COWS). J Psychoactive Drugs. 2003;35(2):253-259. doi:10.1080/02791072.2003.10400007

Hypoxia

Brief H&P:

A 67 year-old male with a history of hypertension and diabetes presents to the emergency department after a syncopal episode. He had been completing his normal morning routine when he developed a sensation of lightheadedness and awoke on the ground of his kitchen. He denies associated chest pain, palpitations, diaphoresis, or recent illness. He has no known sick contacts nor exposures to individuals undergoing evaluation for COVID-19.

On arrival in the emergency department, the patient was noted to be hypoxic with pulse oximetry measuring 74%. He was placed on supplemental oxygen via non-rebreather with improvement of oxygen saturation to 94%. Examination demonstrated diminished alertness (requiring constant stimulation for responses) and generalized motor weakness. Cardiac and pulmonary examinations were unremarkable with the exception of tachypnea and no extremity edema was appreciated.

A chest radiograph was obtained which demonstrated platelike atelectasis. An arterial blood gas was obtained with PaO2 of 72mmHg suggesting a prominent A-a gradient. CT pulmonary angiography was obtained:

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CT Pulmonary Angiography:

Bilateral pulmonary emboli. Case courtesy of Associate Prof Frank Gaillard, Radiopaedia.org, rID: 19636

Upon return, the patient’s mental status worsened associated with hypotension and he was intubated for airway protection and received systemic thrombolysis. He was subsequently taken for emergent endovascular treatment of massive pulmonary embolus.

An Algorithm for the Differential Diagnosis of Hypoxemia & Hypoxia1-7

Hypoxemia is defined as low PaO2 while hypoxia is insufficient global or local tissue oxygen content.

An Algorithm for the Differential Diagnosis of Hypoxemia and Hypoxia

References

  1. Stapczynski J. Respiratory Distress. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e New York, NY: McGraw-Hill; . http://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=219642010. Accessed April 12, 2020.
  2. Gas Transport & pH. In: Barrett KE, Barman SM, Brooks HL, Yuan JJ. eds. Ganong’s Review of Medical Physiology, 26e New York, NY: McGraw-Hill; . http://accessmedicine.mhmedical.com/content.aspx?bookid=2525&sectionid=204297654. Accessed April 12, 2020.
  3. Loscalzo J. Hypoxia and Cyanosis. In: Jameson J, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. eds. Harrison’s Principles of Internal Medicine, 20e New York, NY: McGraw-Hill; . http://accessmedicine.mhmedical.com/content.aspx?bookid=2129&sectionid=192012521. Accessed April 12, 2020.
  4. West NE, Lechtzin N. Chapter 93. Hypoxia. In: McKean SC, Ross JJ, Dressler DD, Brotman DJ, Ginsberg JS. eds. Principles and Practice of Hospital Medicine New York, NY: McGraw-Hill; 2012. http://accessmedicine.mhmedical.com/content.aspx?bookid=496&sectionid=41304065. Accessed April 12, 2020.
  5. Pulmonary Physiology. In: Kibble JD, Halsey CR. eds. Medical Physiology: The Big Picture New York, NY: McGraw-Hill; 2014. http://accessmedicine.mhmedical.com/content.aspx?bookid=1291&sectionid=75576764. Accessed April 12, 2020.
  6. Petersson, J., Glenny, R. (2014). Gas exchange and ventilation–perfusion relationships in the lung European Respiratory Journal 44(4), 1023-1041. https://dx.doi.org/10.1183/09031936.00037014
  7. Morchi, R. (2011). Diagnosis Deconstructed: The Case of the Patient with No Chief Complaint Emergency Medicine News XXXIII(3)
    Rodríguez-Roisin, R., Roca, J. (2005). Mechanisms of hypoxemia Intensive Care Medicine 31(8), 1017-1019. https://dx.doi.org/10.1007/s00134-005-2678-1

COVID-19

Brief HPI:

A 38 year-old male with a history of hypertension presents to the emergency department with fever, cough and shortness of breath. He notes 4 days of symptoms which have been gradually worsening despite over-the-counter treatments. He denies recent travel or sick contacts. While he attempted to remain isolated – his symptoms grew intolerable.

On arrival in the emergency department, vital signs were notable for tachycardia and hypoxia (SpO2 85%, improving to 92% on 4L by nasal cannula). Physical examination demonstrated tachypnea and accessory muscle use but clear lung fields, and no extremity edema nor jugular venous distension. A chest radiograph revealed patchy airspace opacities. A presumptive diagnosis of COVID-19 pneumonia was made.

While awaiting hospitalization, the patient’s hypoxia worsened though he remained otherwise alert and oriented. He was placed on 15L via non-rebreather and instructed regarding self-prone positioning. He was admitted to the intensive care unit.

An Algorithm for the Management of COVID-19 Hypoxic Respiratory Failure1-6

An algorithm for the management of COVID-19 respiratory failure

References

  1. Whittle, J., Pavlov, I., Sacchetti, A., Atwood, C., Rosenberg, M. (2020). Respiratory Support for Adult Patients with COVID‐19 Journal of the American College of Emergency Physicians Open https://dx.doi.org/10.1002/emp2.12071
  2. Hui, D., Chow, B., Chu, L., Ng, S., Lee, N., Gin, T., Chan, M. (2012). Exhaled Air Dispersion during Coughing with and without Wearing a Surgical or N95 Mask PLoS ONE  7(12), e50845. https://dx.doi.org/10.1371/journal.pone.0050845
  3. Hui, D., Chow, B., Lo, T., Ng, S., Ko, F., Gin, T., Chan, M. (2015). Exhaled Air Dispersion During Noninvasive Ventilation via Helmets and a Total Facemask Chest  147(5), 1336-1343. https://dx.doi.org/10.1378/chest.14-1934
  4. Hui, D., Chow, B., Lo, T., Tsang, O., Ko, F., Ng, S., Gin, T., Chan, M. (2019). Exhaled air dispersion during high-flow nasal cannula therapy versus CPAP via different masks European Respiratory Journal  53(4), 1802339. https://dx.doi.org/10.1183/13993003.02339-2018
  5. Sun, Q., Qiu, H., Huang, M., Yang, Y. (2020). Lower mortality of COVID-19 by early recognition and intervention: experience from Jiangsu Province Annals of Intensive Care  10(1), 33. https://dx.doi.org/10.1186/s13613-020-00650-2
  6. Roca, O., Caralt, B., Messika, J., Samper, M., Sztrymf, B., Hernández, G., García-de-Acilu, M., Frat, J., Masclans, J., Ricard, J. (2018). An Index Combining Respiratory Rate and Oxygenation to Predict Outcome of Nasal High-Flow Therapy American Journal of Respiratory and Critical Care Medicine  199(11), 1368-1376. https://dx.doi.org/10.1164/rccm.201803-0589oc

Pneumomediastinum

Brief HPI:

A 34-year-old male with a history of rheumatoid arthritis and interstitial lung disease presents to the emergency department with joint pain unimproved with home medications. He suspects the precipitant is a recent illness, describing cough and nasal congestion. He also noted a “crunching” sensation when turning his neck not otherwise associated with fevers, recurrent vomiting, chest pain, abdominal pain or difficulty breathing.

A chest radiograph was obtained which demonstrated pneumomediastinum.

Chest x-ray showing pneumomediastinum

Imaging from several months prior to presentation is shown below:

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Prior CT Chest:

Extensive peripheral reticular and ground glass opacities and traction bronchiectasis predominates in the lower lobes. Imaging findings are most suggestive of usual interstitial pneumonia. Small focus of pneumomediastinum at carina.

The patient was placed on supplemental oxygen, a repeat chest CT was obtained.

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Current CT Chest:

Large pneumomediastinum extends superiorly into the bilateral lower neck and bilateral anterior and posterior chest walls. It extends inferiorly to the anterior diaphragmatic space. This most likely represents spontaneous pneumomediastinum in the clinical setting of interstitial lung disease. Pneumorrhachis is seen, related to pneumomediastinum.

The etiology of the patient’s spontaneous pneumomediastinum was deemed to be related to his underlying interstitial lung disease provoked by viral respiratory tract infection related coughing. He was observed for two days without decompensation and was discharged with outpatient follow-up.

Pathophysiology of Pneumomediastinum

Spontaneous pneumomediastinum results from the rupture of terminal alveoli with subsequent tracking of gas along the bronchovascular tree through interstitial lung tissue to the mediastinum and adjacent structures (pleural, pericardial, retropharyngeal, retroperitoneal, intraperitoneal and subcutaneous spaces)1.

Secondary pneumomediastinum arises from non-alveolar sources including the gastrointestinal tract (most gravely, esophageal rupture though also from other intraperitoneal sources2), and upper respiratory tract (including facial fractures3).

Management of Pneumomediastinum5-7

The management of spontaneous pneumomediastinum focuses on treatment of the underlying precipitant, supportive care, administration of supplemental oxygen (to promote gas reabsorption) and observation for complications including rare progression to tension pneumomediastinum4.

Secondary pneumomediastinum is of significantly more concern and should be suspected in patients with any of the following features:

Symptoms

  • History of forceful vomiting
  • Dysphagia

Signs

  • Fever
  • Hemodynamic instability
  • Left-sided pleural effusion
  • Abdominal tenderness
  • Leukocytosis

Management is aggressive including resuscitation, maintenance of NPO status, broad-spectrum antibiotics, and emergent surgical consultation.

Differential Diagnosis of Pneumomediastinum5-11

An Algorithm for the Evaluation of Pneumomediastinum

References:

  1. Macklin, M., Macklin, C. (1944). Malignant Interstitial Emphysema of the Lungs and Mediastinum as an Important Occult Complication in Many Respiratory Diseases and Other Conditions: an Interpretation of the Clinical Literature in the Light of Laboratory Experiment Medicine 23(4)
  2. Fosi, S., Giuricin, V., Girardi, V., Caprera, E., Costanzo, E., Trapano, R., Simonetti, G. (2014). Subcutaneous Emphysema, Pneumomediastinum, Pneumoretroperitoneum, and Pneumoscrotum: Unusual Complications of Acute Perforated Diverticulitis Case Reports in Radiology 2014(), 1-5. https://dx.doi.org/10.1155/2014/431563
  3. Luca, G., Petteruti, F., Tanga, M., Luciano, A., Lerro, A. (2011). Pneumomediastinum and Subcutaneous Emphysema Unusual Complications of Blunt Facial Trauma Indian Journal of Surgery 73(5), 380-381. https://dx.doi.org/10.1007/s12262-011-0310-x
  4. Shennib, H., Barkun, A., Matouk, E., Blundell, P. (1988). Surgical Decompression of a Tension Pneumomediastinum Chest 93(6), 1301-1302. https://dx.doi.org/10.1378/chest.93.6.1301
  5. Bakhos, C., Pupovac, S., Ata, A., Fantauzzi, J., Fabian, T. (2014). Spontaneous pneumomediastinum: an extensive workup is not required. Journal of the American College of Surgeons 219(4), 713-7. https://dx.doi.org/10.1016/j.jamcollsurg.2014.06.001
  6. Iyer, V., Joshi, A., Ryu, J. (2009). Spontaneous Pneumomediastinum: Analysis of 62 Consecutive Adult Patients Mayo Clinic Proceedings 84(5), 417-421. https://dx.doi.org/10.4065/84.5.417
  7. Takada, K., Matsumoto, S., Hiramatsu, T., Kojima, E., Shizu, M., Okachi, S., Ninomiya, K., Morioka, H. (2009). Spontaneous pneumomediastinum: an algorithm for diagnosis and management. Therapeutic advances in respiratory disease 3(6), 301-7. https://dx.doi.org/10.1177/1753465809350888
  8. Al-Mufarrej, F., Badar, J., Gharagozloo, F., Tempesta, B., Strother, E., Margolis, M. (2008). Spontaneous pneumomediastinum: diagnostic and therapeutic interventions. Journal of cardiothoracic surgery 3(1), 59. https://dx.doi.org/10.1186/1749-8090-3-59
  9. Takada, K., Matsumoto, S., Hiramatsu, T., Kojima, E., Watanabe, H., Sizu, M., Okachi, S., Ninomiya, K. (2008). Management of spontaneous pneumomediastinum based on clinical experience of 25 cases Respiratory Medicine 102(9), 1329-1334. https://dx.doi.org/10.1016/j.rmed.2008.03.023
  10. Bejvan, S., Godwin, J. (1996). Pneumomediastinum: old signs and new signs. American Journal of Roentgenology 166(5), 1041-1048. https://dx.doi.org/10.2214/ajr.166.5.8615238
  11. Langwieler, T., Steffani, K., Bogoevski, D., Mann, O., Izbicki, J. (2004). Spontaneous pneumomediastinum The Annals of Thoracic Surgery 78(2), 711-713. https://dx.doi.org/10.1016/j.athoracsur.2003.09.021

Numbness

Case 1

Brief HPI:

A 66-year-old male with a history of hypertension, diabetes, hyperlipidemia and prior stroke presents with acute-onset right-sided numbness. Examination demonstrates decreased sensation to light touch and pinprick in right upper- and-lower extremities as well as right face. Strength, cranial nerve and cerebellar testing is normal.

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MRI Brain:

Small focus of restricted diffusion within the left insular subcortical white matter consistent with acute lacunar infarct.1

Discussion:

Infarction of the ventral posterolateral nucleus of the thalamus disrupts relays from the medial lemniscus and spinatholamic tracts extending to the cortex.

Case 2

Brief HPI:

A 34-year-old female with no significant medical history presents with headache and neck pain. Examination is notable for decreased strength with decreased sensation to pinprick (and preserved light touch) in bilateral upper extremities.

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MRI C-Spine:

Chiari I malformation with associated cervical syringomyelia (79mm length, 11mm anteroposterior diameter) extending from C3 to T1.2

Discussion:

The central cord lesion affects the adjacent, medial fibers of the corticospinal tract resulting in upper extremity weakness. Disruption of crossing spinothalamic tract fibers results in diminished pain and temperature sensation at the level of the lesion.

Anatomy3,4

Dorsal column and spinothalamic tracts

Sensory information is gathered from specialized receptors in skin and soft-tissues which detect a variety of stimuli including temperature, pressure, vibration, and pain. This is subsequently transmitted through peripheral nerves which in certain regions coalesce into larger bundles before entering the spinal cord through the dorsal nerve root. Upon entering the spinal cord, sensory information is divided into two tracts:

  1. Spinothalamic: Small, poorly-myelinated fibers carrying pain, temperature and touch stimuli synapse with second-order neurons over several levels in the ipsilateral dorsal horn crossing to the contralateral side in the anterior commissure anterior to the central canal. Touch information ascends in the anterior spinothalamic tract while pain and temperature information ascends in the lateral spinothalamic tract.
  2. Dorsal column: Large, myelinated fibers carrying vibration and proprioception information ascend in the ipsilateral posteromedial spinal cord. Fibers from the thoracic and lumbar region occupy the more medial (gracile) column, while fibers from the cervical region occupy the more lateral (cuneate) column. These fibers synapse in their respective nuclei in the medulla before crossing to the contralateral medial lemniscus.

Both tracts proceed to the ventral posterolateral (VPL) nucleus of the thalamus, through the internal capsule before terminating in the somatotopically-arranged primary somatosensory cortex in the parietal lobe.

Understanding the neuroanatomy supports a systematic approach to the evaluation of sensory disturbances. It is important to note that the transmission of light touch sensation involves both pathways and offers less localizing value when compared to specific assessment of proprioception or pain detection. Sensory disturbances are often accompanied by motor abnormalities  which can further aid with localization. Other key distinguishing features include acuity of onset wherein abrupt presentations may suggest ischemia or infarction, compared to more indolent processes with broader differentials (including compressive mass lesions, demyelination, or autoimmune disease).

An Algorithm for the Evaluation of Sensory Disturbances5

References

  1. Case courtesy of Dr Bruno Di Muzio, Radiopaedia.org, rID: 45066
  2. Case courtesy of Dr Bahman Rasuli, Radiopaedia.org, rID: 65655
  3. Aminoff MJ. Numbness, Tingling, and Sensory Loss. In: Kasper D, Fauci A, Hauser S, Longo D, Jameson J, Loscalzo J. eds. Harrison’s Principles of Internal Medicine, 19e New York, NY: McGraw-Hill; 2014. http://accessmedicine.mhmedical.com/content.aspx?bookid=1130&sectionid=79724797. Accessed February 07, 2020.
  4. Sensory Disorders. In: Simon RP, Aminoff MJ, Greenberg DA. eds. Clinical Neurology, 10e New York, NY: McGraw-Hill; . http://accessmedicine.mhmedical.com/content.aspx?bookid=2274&sectionid=176234164. Accessed February 07, 2020.
  5. Berkowitz AL. Numbness: A Localization-Based Approach. In: McKean SC, Ross JJ, Dressler DD, Scheurer DB. eds. Principles and Practice of Hospital Medicine, 2e New York, NY: McGraw-Hill; . http://accessmedicine.mhmedical.com/content.aspx?bookid=1872&sectionid=146977205. Accessed February 07, 2020.