Penetrating Neck Trauma

Brief H&P

A young male presents to the emergency department after a self-inflicted stab wound to the neck. Examination revealed a knife handle protruding from the left lateral neck. A plain radiograph is shown below.

CXR: Radiopaque foreign body in left neck.

The patient was initially stable but developed shortness of breath upon attempting to lie flat for advanced imaging and was taken emergently to the operating room. Neck exploration showed no obvious neurovascular injuries, and the course of the 6cm blade was posterior to the trachea and esophagus. The knife was removed with “considerable force” as it was likely lodged within a portion of vertebral bone. The patient underwent esophagoscopy and bronchoscopy without identified tracheoesophageal injuries. The patient did well post-operatively and was discharged home.

Zones of Injury1-3

Previously, the evaluation and management of hemodynamically stable patients with penetrating neck injury was guided by the anatomic “zone” of injury. The affected zone guided the performance of additional diagnostic procedures including potentially morbid neck explorations.

Neck Zones of Injury

Understanding zone definitions remains important for the emergency physician to appreciate potentially implicated underlying structures. However, the advent of modern imaging modalities, specifically computed tomography with angiography, provides appropriate sensitivity for vascular and tracheoesophageal injuries when combined with detailed physical examination and maintenance of an appropriate threshold for the performance of additional studies if warranted by the clinical presentation (suboptimal imaging, concerning projectile trajectory, etc).

Zone Definition
I Clavicles/sternum to cricoid cartilage
II Cricoid cartilage to the angle of mandible
III Superior to the angle of mandible to the skull base

 

Algorithm for the Evaluation of Penetrating Neck Trauma

 

References

  1. Sperry JL, Moore EE, Coimbra R, et al. Western Trauma Association critical decisions in trauma: penetrating neck trauma. J Trauma Acute Care Surg. 2013;75(6):936-940. doi:10.1097/TA.0b013e31829e20e3.
  2. Brywczynski JJ, Barrett TW, Lyon JA, Cotton BA. Management of penetrating neck injury in the emergency department: a structured literature review. Emerg Med J. 2008;25(11):711-715. doi:10.1136/emj.2008.058792.
  3. Shiroff AM, Gale SC, Martin ND, et al. Penetrating neck trauma: a review of management strategies and discussion of the “No Zone” approach. Am Surg. 2013;79(1):23-29. doi:10.1007/978-3-662-49859-0_29.

 

Diplopia Applied

Brief H&P:

A young male with no past medical history presents to the emergency department after assault. He was punched multiple times in the face and has since noted double vision, worse with upward gaze. Examination revealed right peri-orbital edema with associated limitation to upward gaze.

Imaging:

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CT Maxillofacial Non-contrast

Inferior orbital wall fracture with herniation of the inferior rectus muscle.

Extraocular Muscle Actions:

Extra-ocular movement actions.

Affected Anatomic Sites in Diplopia:

Coordinated eye positioning is affected by voluntary movements (requiring cranial nerve control for conjugate eye movements), vergence (for depth adjustments), as well as reflexive adjustments for head movement (requiring vestibular input). As with any motor activity, neuromuscular control must be normal with unrestricted movement of the globe within the orbit.

Sites causing diplopia

Algorithm for the Evaluation of Diplopia:

Diplopia has been explored previously on ddxof. The earlier algorithm was focused on identifying the paretic nerve. This algorithm uses features of the history and physical examination to identify potential etiologic causes of diplopia.

Algorithm for the Evaluation of Diplopia

References:

  1. Rucker JC, Tomsak RL. Binocular diplopia. A practical approach. Neurologist. 2005;11(2):98-110. doi:10.1097/01.nrl.0000156318.80903.b1.
  2. Friedman DI. Pearls: diplopia. Semin Neurol. 2010;30(1):54-65. doi:10.1055/s-0029-1244995.
  3. Alves M, Miranda A, Narciso MR, Mieiro L, Fonseca T. Diplopia: a diagnostic challenge with common and rare etiologies. Am J Case Rep. 2015;16:220-223. doi:10.12659/AJCR.893134.
  4. Dinkin M. Diagnostic approach to diplopia. Continuum (Minneap Minn). 2014;20(4 Neuro-ophthalmology):942-965. doi:10.1212/01.CON.0000453310.52390.58.
  5. Marx J, Walls R, Hockberger R. Rosen’s Emergency Medicine – Concepts and Clinical Practice. 8 ed. Elsevier Health Sciences; 2013:176-183.
  6. Nazerian P, Vanni S, Tarocchi C, et al. Causes of diplopia in the emergency department: diagnostic accuracy of clinical assessment and of head computed tomography. Eur J Emerg Med. 2014;21(2):118-124. doi:10.1097/MEJ.0b013e3283636120.
  7. Low L, Shah W, MacEwen CJ. Double vision. BMJ. 2015;351:h5385. doi:10.1136/bmj.h5385.
  8. Danchaivijitr C, Kennard C. Diplopia and eye movement disorders. J Neurol Neurosurg Psychiatry. 2004;75 Suppl 4:iv24-iv31. doi:10.1136/jnnp.2004.053413.
  9. Huff JS, Austin EW. Neuro-Ophthalmology in Emergency Medicine. Emerg Med Clin North Am. 2016;34(4):967-986. doi:10.1016/j.emc.2016.06.016.

Cervical Spine Injuries

Brief H&P

A young patient with no past medical history is brought in by ambulance after a high-speed motor vehicle accident. Trauma survey demonstrates absent motor/sensation in bilateral lower extremities with sensory level at T3-T4. Computed tomography of the cervical spine was obtained and is shown below.

Imaging

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CT C-Spine

Fracture-dislocation at C6-C7 and C7-T1 with comminuted burst fracture to C7 and locked facet joint with resultant anterior migration of C6 over C7, unstable cervical spine fracture.

Anatomy

Atlas and Axis
Axis (C2 vertebra)
C-spine Lateral View
C-spine Radiographs
Skull base and C1/C2
Vertebral Columns

Flexion

C1/C2

Wedge fracture

  • Stretch on strong nuchal ligament transmits force to vertebral body.
  • Stability: Generally stable unless >50% compression or multiple contiguous.

Flexion-teardrop fracture

  • Severe flexion force, avulsion of fragment of anterior/inferior portion of vertebral body.
  • Stability: Unstable, involves anterior/posterior ligamentous disruptions.

Clay shoveler’s fracture

  • Oblique fracture of spinous process of lower cervical spine.
  • Stability: Stable

Subluxation

  • Pure ligamentous injury without associated fracture.
  • Imaging: Widening of interspinous and intervertebral spaces on lateral.
  • Stability: Potentially unstable.

Bilateral facet dislocation

  • Anterior displacement of spine above level of injury caused by dislocation of upper inferior facet from lower superior facet.
  • Imaging: Anterior displacement greater than ½ AP diameter of vertebral body.
  • Stability: Unstable

Odontoid process fracture

  • Head trauma with shear force directed at odontoid.
  • Sub-classification: Type I (above transverse ligament), type II (odontoid base), type III (extension to body of C2)
  • Stability: Types II, III unstable.

Flexion/Rotation

Rotary atlantoaxial dislocation

  • Imaging: Open-mouth odontoid, asymmetric lateral masses of C1.
  • Stability: Unstable

Unilateral facet dislocation

  • Flexion and rotation centered around single facet results in contralateral facet dislocation.
  • Imaging: AP radiograph shows spinous processes above dislocation displaced from midline, lateral radiograph shows anterior displacement of lower vertebra (less than ½ AP diameter of vertebral body).

Extension

Posterior neural arch fracture (C1)

  • Forced extension causes compressive force on posterior elements of C1 between occiput and C2.
  • Stability: Unstable

Hangman’s fracture (spondylolysis C2)

  • Abrupt deceleration causes fracture of bilateral pedicles of C2, potentially with associated subluxation. Rarely associated with SCI due to large diameter of neural canal at C2.
  • Imaging: May be associated with retropharyngeal space edema.
  • Stability: Unstable

Extension-teardrop fracture

  • Abrupt extension (ex. diving) results in stretch along anterior longitudinal ligament with avulsion of anterior/inferior fragment of vertebral body (usually C5-C7).
  • Imaging: May be radiographically similar to flexion-teardrop fracture.
  • Complications: Central cord syndrome
  • Stability: Unstable in extension

Vertical compression

Burst fracture

  • Force applied from above or below causes transmission of force to intervertebral disc and vertebral body.
  • Imaging: Comminuted vertebral body, >40% compression of anterior vertebral body.
  • Complications: Fracture fragments may impinge on spinal cord.
  • Stability: Stable

Jefferson fracture (C1)

  • Vertical force transmitted from occipital condyles to superior articular facets of atlas, resulting in fractures of anterior and posterior arches.
  • Imaging: Widening of predental space. Open-mouth odontoid view may reveal bilateral offset distance of >7mm between lateral masses of C1/C2.
  • Stability: Unstable

Cervical Spine Imaging Decision Rule (Canadian)

Algorithm for the Evaluation of Cervical Spine Trauma (Canadian)

References:

  1. MD RK, MD BED, CAQ-SM KHM, MD WF. Emergency Department Evaluation and Treatment of Cervical Spine Injuries. Emergency Medicine Clinics of NA. 2015;33(2):241-282. doi:10.1016/j.emc.2014.12.002.
  2. Denis F. Spinal instability as defined by the three-column spine concept in acute spinal trauma. Clin Orthop Relat Res. 1984;(189):65-76.
  3. Munera F, Rivas LA, Nunez DB, Quencer RM. Imaging evaluation of adult spinal injuries: emphasis on multidetector CT in cervical spine trauma. Radiology. 2012;263(3):645-660. doi:10.1148/radiol.12110526.

Pediatric Head Trauma

Brief H&P:

A young child, otherwise healthy, is brought to the pediatric emergency department after a fall. The parents report a fall from approximately 2 feet after which the patient cried immediately and without apparent loss of consciousness. Over the course of the day, the patient developed an enlarging area of swelling over the left head. The parents were concerned about a progressive decrease in activity and interest in oral intake by the child, and they were brought to the emergency department for evaluation. Examination demonstrated a well-appearing and interactive child – appropriate for age. Head examination was notable for a 5x5cm hematoma over the left temporoparietal skull with an underlying palpable skull irregularity not present on the contralateral side. Non-contrast head computed tomography was obtained.

Imaging

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CT Head

Fracture of the left temporal and parietal bone with overlying scalp hematoma.

Algorithm for the Evaluation of Pediatric Head Trauma (PECARN)1,2,3

Algorithm for the evaluation of pediatric head trauma

References

  1. Kuppermann N, Holmes JF, Dayan PS, et al. Identification of children at very low risk of clinically-important brain injuries after head trauma: a prospective cohort study. Lancet. 2009;374(9696):1160-1170. doi:10.1016/S0140-6736(09)61558-0.
  2. Brenner D, Elliston C, Hall E, Berdon W. Estimated risks of radiation-induced fatal cancer from pediatric CT. American Journal of Roentgenology. 2001;176(2):289-296. doi:10.2214/ajr.176.2.1760289.
  3. Schonfeld D, Bressan S, Da Dalt L, Henien MN, Winnett JA, Nigrovic LE. Pediatric Emergency Care Applied Research Network head injury clinical prediction rules are reliable in practice. Archives of Disease in Childhood. 2014;99(5):427-431. doi:10.1136/archdischild-2013-305004.

Acute Urinary Retention

Brief H&P:

A 62 year-old male with no significant medical history, presented to the emergency department with several days of vomiting. Examination showed suprapubic fullness with tenderness to palpation and a bedside ultrasound was performed:

RUQ
RUQ

RUQ

Right upper quadrant ultrasound with moderate hydronephrosis.

LUQ
LUQ

LUQ

Left upper quadrant ultrasound with moderate hydronephrosis.

Bladder
Bladder

Bladder

Relatively non-distended bladder.

Bladder Volume
Bladder Volume

Bladder Volume

Post-void bladder volume.

Ultrasound revealed moderate bilateral hydronephrosis with a relatively non-distended bladder. Labs were notable for new renal failure and the patient was admitted for continued evaluation. He was ultimately diagnosed with idiopathic retroperitoneal fibrosis with bilateral distal ureteral obstruction requiring stenting.

Anatomy of Acute Urinary Retention:

Differential Diagnosis of Acute Urinary Retention:1,2,3

Algorithm for the Evaluation of Acute Urinary Retention

 

Spontaneous Intracranial Hemorrhage

Brief HPI

An approximately 40 year-old male with a history of aortic stenosis s/p mechanical aortic valve replacement (on Coumadin) as well as hypertension presented to the emergency department with a chief complaint of severe headache. The patient was in severe distress on arrival and was unable to provide detailed history, he complained of two days of severe left-sided headache while clutching his head and groaning. Examination was notable for sensory localization with directed movements of right hemibody, and no apparent response on the left. He was taken to emergently for CT head non-contrast.

Imaging

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CT Head non-contrast

57 mm right posterior parenchymal hemorrhage with intraventricular component. Moderate edema, mass effect and 9 mm of midline shift.

ED Course

Admission INR was 2.9, the patient received 25 units/kg of PCC as well as vitamin K 10mg IV x1. Neurosurgery was consulted and the patient was taken to the operating room for management.

Management of Supratherapeutic INR and Complications of Anti-Coagulation

Management of Supratherapeutic INR

References

  1. Ansell J, Hirsh J, Hylek E, et al. Pharmacology and management of the vitamin K antagonists: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest 2008; (6 Suppl):160s

Portal Venous Gas

Brief HPI

Young male with no significant medical history presenting with progressively worsening right lower quadrant abdominal pain with marked tenderness to palpation and involuntary guarding.

Imaging

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CT Abdomen/Pelvis with Contrast

Inflammatory changes in the right lower quadrant concerning for ruptured appendicitis with approximately 9 cm abscess.
Gas in the liver likely representing portal venous gas which can be seen in the setting of appendicitis vs less likely secondary to bowel ischemia.

Differentiation between Portal Venous Gas and Pneumobilia

Portal venous gas vs. Pneumobilia

References

  1. Rabou Ahmed A and Frank Gaillard. “Pneumobilia.” Radiopaedia. http://radiopaedia.org/articles/pneumobilia.
  2. Morgan Matt A and Donna D’Souza. “Portal venous gas.” Radiopaedia. http://radiopaedia.org/articles/portal-venous-gas
  3. Sebastià C, Quiroga S, Espin E, Boyé R, Alvarez-Castells A, Armengol M. Portomesenteric vein gas: pathologic mechanisms, CT findings, and prognosis. Radiographics. 2000;20(5):1213–24–discussion1224–6. doi:10.1148/radiographics.20.5.g00se011213.
  4. Sherman SC, Tran H. Pneumobilia: benign or life-threatening. J Emerg Med. 2006;30(2):147-153. doi:10.1016/j.jemermed.2005.05.016.

Severe Burns

ED Presentation

34F with no reported medical history BIBA with severe burns after house fire with estimated 70% TBSA involvement. On arrival, the patient was hypoxic, striderous, and unable to provide history. She was intubated for airway protection with some difficulty. Examination revealed deep partial and full-thickness burns to 70% of total body surface area including circumferential burns to bilateral upper extremities and extensive neck and anterior chest involvement. Initial fluid resuscitation and warming measures were instituted. Emergent bedside bronchoscopy revealed copious carbonaceous material throughout with attempts at lavage. Urine output was minimal despite aggressive resuscitation. Critical care transport to local burn facility was arranged where the patient ultimately expired.

Algorithm for the Management of Severe Burns

Algorithm for the Management of Severe Burns

Assessment of Burn Depth

Depth Cause Appearance Sensation
Superficial UV exposure Dry, red
Blanching
Painful
Superficial partial-thickness Scald (splash)
Short flash
Blisters, moist, red
Blanching
Painful to temperature/air
Deep partial-thickness Scald (spill)
Flame, oil, grease
Blisters, waxy dry, white/red
Non-blanching
Pressure
Full-thickness Scald (immersion)
Flame, steam, oil, grease, chemical, electrical
Waxy white, leathery grey, black
Non-blanching
Deep pressure

Estimating Burn Surface Area

Burn TBSA

Image from UWHealth.org

  • Trunk: 18% anterior, 18% posterior
  • Lower extremity (each): 9% anterior, 9% posterior
  • Upper extremity (each): 9%
  • Head/neck: 9%
  • Perineum: 1%

Burn Transfer Criteria

  • Partial thickness > 20% TBSA
  • Partial thickness > 10% TBSA for extremes of age (<10 or >50 years-old)
  • Any full-thickness
  • Burns involving face, hands, feet, genitalia, major joints
  • Electrical/chemical
  • Inhalation injury
  • Medical comorbidities impacting management/healing

See Also

References

  1. Monafo WW. Initial management of burns. N Engl J Med. 1996;335(21):1581–1586. doi:10.1056/NEJM199611213352108.
  2. Hettiaratchy S, Papini R. Initial management of a major burn: I–overview. BMJ. 2004;328(7455):1555–1557. doi:10.1136/bmj.328.7455.1555.
  3. Singer AJ, Della-Giustina D. Thermal Burns: Rapid Assessment and Treatment. Emergency Medicine Practice; 2000.
  4. Rice, PL. Emergency care of moderate and severe thermal burns in adults. In: UpToDate, Moreira ME (Ed), UpToDate, Waltham, MA. (Accessed on March 29, 2016)
  5. Gauglitz, GG. Overview of the management of the severely burned patient. In: UpToDate, Jeschke MG (Ed), UpToDate, Waltham, MA. (Accessed on March 29, 2016)

Epiglottitis

Brief H&P:

30 year-old male with no significant medical history presenting with 24 hours of progressively worsening throat pain, difficulty swallowing and voice hoarseness. He reports subjective fevers and chills.
Vital signs notable for Tmax 38.4°C. On physical examination, the patient was sitting upright, unable to swallow secretions with faint inspiratory stridor and dysphonia (though he was able to speak in full sentences and without apparent respiratory distress). Oropharyngeal examination showed minimal right parapharyngeal edema without uvular or palatal deviation and there was exquisite right lateral neck tenderness to palpation.

Labs

  • CBC: 24.2/14.4/43.4/202
  • Wound culture: MSSA
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CT Neck/Soft Tissue with Contrast

Edema of the oropharynx/hypopharynx, consistent with epiglottitis and early abscess formation.

ED/Hospital Course

The patient acutely decompensated prior to fiberoptic laryngoscopy and proceeded emergently to the operating room for controlled intubation. The operative report described the following findings: “The patient had diffuse edema of the posterior oropharyngeal wall. The epiglottis was severely thickened, Omega shaped, soft to palpation and with moderate pressure, it appeared to come to a head and pus was expressed from the lingual side of the epiglottis.” The patient was extubated on hospital day three and discharged soon thereafter, he was doing well on follow-up.

Evaluation of Sore Throat – Applied

Evaluation of Sore Throat - Applied

Spinal Epidural Abscess

Case Presentation

HPI:

34M with no PMH presenting with joint pain and rash. The patient was in his usual state of good health until 1 week prior to presentation, noting bilateral shoulder pain. Diagnosed with musculoskeletal process at outside hospital and discharged with analgesics. Presented with partner due to worsening pain involving multiple joints, a non-painful, non-pruritic rash on bilateral lower extremities, and apparent confusion/hallucinations. Social history was non-contributory, no recent procedures or instrumentation.

Objectively, vital signs were notable for tachycardia and elevated core temperature. The patient was ill-appearing, disoriented and unable to provide detailed history. Skin examination was notable for non-blanching petechial rash with areas of confluence most dense in anterior distal lower extremities, rarer proximally, and otherwise without palm/sole involvement. Mucous membranes were dry, neck was supple. There was tenderness to palpation and manipulation of bilateral shoulders. No back tenderness to palpation or percussion was identified. Neurological examination notable for disorientation, intact cranial nerve function, pain-limited weakness in bilateral upper extremities particularly shoulder abduction, and 4/5 hip flexion, knee flexion/extension in bilateral lower extremities.

Labs:

  • CBC: 34.0/11.8/35.7/216
  • Differential: 31 bands
  • INR: 1.94
  • BMP: 131/5.3/102/17/88/2.55/215
  • LFT: AST 93, ALT 57, AP 237, TB 2.9, DB 1.9, Alb 1.4
  • Lactate: 3.3
  • UA: 47WBC, 5RBC
  • Utox: Negative
  • ESR: 83, CRP: 11.9
  • HIV: Nonreactive

Radiology

  • CT head: Negative
  • CXR: Negative
  • XR Shoulder: Negative
  • CT Chest/Abdomen/Pelvis non-contrast: Mild bilateral hydrouereter/hyndronephrosis, L4-L5 grade 2 anterolisthesis.
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MRI Lumbar Spine w/contrast

Diffuse epidural enhancement posterior to the L4 and L5 vertebral bodies compressing the thecal sac and resulting in moderate severe spinal canal stenosis. Rim enhancement of the 1.5 cm left paraspinal fluid that may be within the L4 tendon sheath or simply paraspinal abscess.

Assessment/Plan:

Severe sepsis with end-organ dysfunction, unclear source (urinary tract involvement unlikely to account for severity of illness). Covered empirically with broad-spectrum anti-microbials including CNS infection given component of encephalitis. Admitted to the intensive care unit.

Hospital Course:

On hospital day 1, the patient underwent non-contrast MRI of the entire neuraxis with findings concerning for L4-L5 and L5-S1 epidural and paraspinal infection resulting in moderate-severe spinal canal stenosis. Blood and urine cultures grew gram-positive cocci in clusters.

On hospital day 2, the patient became increasingly somnolent. Repeat examination by consulting neurology service was concerning for evidence of meningeal irritation. Cultures speciated as methicillin-sensitive staphylococcus aureus and oxacillin was added. MRI was repeated with gadolinium, findings concerning for L4 epidural vs. paraspinal abscess.

On hospital day 3, the patient’s mental status continued to worsen and he was intubated for airway protection. Neurosurgical intervention was deferred due to deteriorating clinical status. Shoulder synovial fluid aspirate culture positive for MSSA, orthopedic surgery consulted for washout/serial arthrocentesis. TTE performed without evidence of valvular vegetation.

On hospital day 4, additional warm joints were aspirated by orthopedic surgery including knee, bilateral ankles, and shoulder each of which ultimately grew MSSA.

On hospital day 6, the patient underwent OR washout of affected joints with intraoperative findings of purulent fluid. TEE performed without evidence of valvular vegetation. The following day, underwent fluoroscopically-guided lumbar puncture, CSF studies inconclusive. Rifampin added for high-grade bacteremia with multiple seeded sites.

The patient was extubated on hospital day 9 and transferred out of the intensive care unit. The following day, he became increasingly tachypneic with evidence of volume overload on examination and was intubated and returned to the intensive care unit. Sustained PEA arrest post-intubation with ROSC, possibly secondary to pneumothorax vs. hypoxia from extensive mucous plugging. Required increasing vasopressor support over the subsequent 12 hours, emergent CVVHD for worsening academia and hypervolemia. The patient sustained another arrest and ultimately expired.

The final impression was that of high-grade bacteremia from unclear source (vague history of proximate hand laceration/infection) with resultant seeding of epidural/paraspinal space, urinary tract, multiple joints, and likely CNS/meninges. Review of abdominal ultrasonography with evidence of cirrhosis, suggesting that some component of initial hepatic synthetic dysfunction may have been chronic and this may have increased the patient’s risk for disseminated infection and SEA. Neurosurgical intervention was not pursued due to unstable clinical status and as the patient’s neurological findings were not consistent with the location of the identified lesion.

Spinal Epidural Abscess (SEA)1

Risk factors:

  • Immunocompromise: diabetes, cirrhosis, CKD, HIV/AIDS
  • Anatomic: DJD, trauma, prior surgery
  • Introduction: IVDA, epidural anesthesia, tattoo

Organism:

  • S. aureus, 2/3
  • S. epidermidis (associated with device, instrumentation)
  • E. coli (urine spread)
  • P. aeruginosa (IVDA)
  • Rare: anaerobes, mycobacteria, fungi

Staging:

  1. Back pain at affected site
  2. Nerve root pain from affected level
  3. Weakness, sensory deficit, bladder/bowel dysfunction
  4. Paralysis

Clinical features:

  • Back pain (75%)
  • Fever (50%)
  • Neuro deficit (33%)

Diagnosis:

  • Labs: Leukocytosis, ESR/CRP, blood cultures
  • Imaging: MRI with gadolinium, 90% sensitivity
  • Clinical findings and laboratory studies are insensitive and non-specific, in one study, approximately ½ of patients had >2 visits.

Prevalence of abnormal physical findings 2

Finding Prevalence
Fever (T>38°C) 19-32%
Focal spinal TTP 52-62%
Diffuse spinal TTP 63-65%
Positive SLR 11-13%
Abnormal sensation 17-27%
Weakness 29-40%
Abnormal reflexes 8-17%
Abnormal rectal tone 5-10%
Saddle anesthesia 2%

Clinical Decision Guideline 3

Spinal Epidural Abscess Clinical Decision Guideline

Management:

  • Neurosurgical evacuation/fusion
  • Antibiotics (vancomycin, oxacillin, cefepime)
  • Neurosurgical intervention may not result in neurological recovery if symptoms present for > 24-36 hours and may be impractical in the setting of panspinal infection.

References:

  1. Darouiche RO. Spinal epidural abscess. N Engl J Med. 2006;355(19):2012–2020. doi:10.1056/NEJMra055111.
  2. Davis DP, Wold RM, Patel RJ, et al. The clinical presentation and impact of diagnostic delays on emergency department patients with spinal epidural abscess. J Emerg Med. 2004;26(3):285–291. doi:10.1016/j.jemermed.2003.11.013.
  3. Davis DP, Salazar A, Chan TC, Vilke GM. Prospective evaluation of a clinical decision guideline to diagnose spinal epidural abscess in patients who present to the emergency department with spine pain. J Neurosurg Spine. 2011;14(6):765–770. doi:10.3171/2011.1.SPINE1091.
  4. WikEM: Epidural abscess (spinal)

Back Pain

Causes of Back Pain

Causes of Back Pain

Key Historical Findings

Onset
Acute onset with associated activity suggests mechanical process
Acute onset without trigger, particularly if severe pain may suggest vascular process
Progressive onset without trigger suggests non-mechanical process (i.e. malignancy)
Aggravating/Alleviating Factors
Worsening with cough/valsalva suggests herniated disk
Relief with flexion associated with spinal stenosis
Location/Radiation
Radicular pain typically extends below knee, associated with nerve root involvement
Radiation to/from chest or abdomen suggests visceral source
Flank location suggests retroperitoneal source
History/Associated Symptoms
Fever
Medications (particularly anti-coagulants)
Hematuria
Malignancy
IVDA
Vascular disease

Key Physical Findings

  • Abnormal vital signs

    • Fever: abscess, osteomyelitis, discitis
    • Hypertension: dissection
    • Shock: AAA
  • Localize point of greatest tenderness
  • Examine abdomen for pulsatile mass
  • Perform thorough neurological examination including rectal tone and perianal sensation
  • Positive straight leg raise associated with sciatic nerve root irritation and is sensitive (but not specific) for disk disease.

References

  1. Mahoney, B. (2013). Back Pain. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 278-284). Elsevier Health Sciences.
  2. WikEM: Lower back pain

Aortic Dissection

Imaging

Prominent cardiomediastinal silhouette, which may be due to patient position.

Prominent cardiomediastinal silhouette, which may be due to patient position.

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CT Angiography Aorta

Highly complex type B aortic dissection originating at the distal arch (just distal to the left subclavian artery) and terminating at the level of diaphragm. The dissection contains multiple false lumens containing blood products of differing ages (thrombus and contrast-opacified blood). No apparent involvement of the left common carotid or left subclavian artery.

Mediastinum Anatomy

Mediastinal Masses

Anterior
Retrosternal goiter
Thymoma
Germ-cell tumor
Lymphadenopathy (lymphoma)
Middle
Aortic arch aneurysm
Dilated pulmonary artery
Tracheal lesion
Posterior
Esophageal lesions
Hiatal hernia
Descending aortic aneurysm
Paraspinal abscess

References:

  1. Faiz, O., & Moffat, D. (2002). Anatomy at a glance. Malden, MA: Blackwell Science.
  2. Whitten CR, Khan S, Munneke GJ, Grubnic S. A diagnostic approach to mediastinal abnormalities. Radiographics. 2007;27(3):657–671. doi:10.1148/rg.273065136.
  3. WikEM: Widened mediastinum

Sore Throat

Evaluation of Sore Throat

Evaluation of Sore Throat

Physical Examination:

Neck
Stiffness, limitation of extension suggestive of retropharyngeal abscess.
Jaw
Trismus associated with peritonsillar cellulitis or abscess.
Oral Cavity
Dry mucous membranes suggest dehydration (from odynophagia) and indicates severity of symptoms.
Tongue elevation, sublingual/submental induration, poor dentition (particularly of mandibular molars) associated with Ludwig Angina.
Unilateral tonsillar enlargement with contralateral uvular deviation suggests peritonisllar abscess. Fluctuance may be palpated.
Tonsilar exudates suggest infectious pharyngitis (non-specific).
Palatal petechiae suggest bacterial pharyngitis.
Ulcerations of the anterior oral cavity are associated with herpes infection, lesions on the soft palate are suggestive of coxsackievirus infection.
Rarely, a grey membrane in the posterior pharynx will suggest diphtheria.
Lymphadenopathy
Tender anterior cervical lymphadenopathy may suggest bacterial pharyngitis.
Posterior cervical lymphadenopathy is associated with infectious mononucleosis.
Large, firm, non-mobile lymph nodes may suggest malignancy.
Eyes
Presence of conjunctivitis (also rhinorrhea, exanthema) associated with viral pharyngitis.
Skin
Ulcers involving the hands, feet, in addition to pharyngeal lesions suggest coxsackievirus infection.
Scarlatiniform rash associated with pharyngitis (particularly in school-age children) suggests streptococcal pharyngitis.
Abdomen
Splenomegaly is associated with infectious mononucleosis.

Centor Criteria (Modified)

  • +1: Fever
  • +1: Tonsillar Exudate
  • +1: Tender anterior cervical lymphadenopathy
  • +1: Absence of cough
  • -1: Age >45yo

Incidence of GABHS by Centor Criteria

  • 0, -1: 1%
  • 1: 10%
  • 2: 17%
  • 3: 35%
  • 4: 51%

References:

  1. Newman, D., & Shreves, A. (2013). Sore Throat. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 198-202). Elsevier Health Sciences.
  2. King, B. R., & Charles, R. A. (2004). Pharyngitis In The ED Diagnostic Challenges And Management Dilemmas. Emergency medicine practice, 6(5), 1–24.

Dizziness and Vertigo

Types of Dizziness

Types of Dizziness

Distinguishing Central vs. Peripheral Vertigo

Characteristic Peripheral Central
Onset Sudden Gradual
Intensity Severe Mild
Duration Minutes Weeks
Timing Intermittent Continuous
Nystagmus Horizontal Vertical, bidirectional
Exacerbation with head movement +
Auditory symptoms +
Neurological findings +

Causes of Vertigo

Causes of Vertigo

Characteristics of common causes of vertigo

Cause Mechanism Onset Symptoms Findings
Peripheral
BPPV Otolith Brief, positional episodes Nausea, vomiting, absent auditory symptoms. Dix-Hallpike positive
Vestibular neuronitis Viral, post-viral inflammation of vestibular portion of CNVIII Acute and severe, subsiding over days. Nausea, vomiting, absent auditory symptoms. Head thrust abnormal
Meniere Endolymphatic hydrops Recurrent, lasting hours Tinnitus, hearing loss. SNHL
Central
Vertebrobasilar insufficiency Atherosclerosis (vascular risk factors) Acute onset, recurrent episodes if TIA Headache, gait impairment, diplopia, absent auditory symptoms. Neurologic deficits
Cerebellar stroke Atherosclerosis (vascular risk factors) Acute and severe Headache, dysphagia, gait impairment Dysmetria, dysdiadochokinesia, ataxia, CN palsy
Brainstem stroke Atherosclerosis (vascular risk factors), dissection Acute and severe Dysphagia, dysphonia, gait impairment, sensory disturbances Loss of pain/temperature on ipsilateral face, contralateral body, palatal/pharyngeal paralysis
MS Demyelination Subacute onset History of other, variable symptoms INO

History

  • Onset, duration, timing, severity, exacerbating factors
  • Vascular risk factors: age, male, HTN, CAD, DM, atrial fibrillation
  • Vestibulotoxic medications: aminoglycosides, AED

Key Physical Examination Findings

  • VS: Presence of hypotension suggests presyncope
  • Head: Examine for evidence of trauma
  • Neck: Auscultate for carotid bruit
  • Ear: Effusion or perforation suggests peripheral process (possible perilymphatic fistula)
  • Eye: Examine for pupillary defects (CNIII), papilledema, extraoccular muscles
  • Neuro: Cerebellar testing

Positional Testing

Dix-Hallpike
Turn head 45°
Upright sitting → supine (head overhanging bed)
Positive: nystagmus + symptoms on one side
Roll
Supine
Turn head 90°
Positive: nystagmus + symptoms on both sides, more severe on affected

HINTS1

Normal head impulse, direction-changing nystagmus, or skew deviation suggests stroke.

Head impulse
Focus on examiner’s nose
Rapidly turn head 10° in horizontal plan
Presence of corrective saccade suggests defect of peripheral vestibular nerve
Nystagmus
Peripheral: Horizontal, unidirectional. Increases on gaze in direction of fast phase (decreases or resolves opposite)
Central: Direction changing
Skew deviation
Cross cover
Presence of vertical disconjugate gaze suggests brainstem dysfunction

HINTS Gallery

Positive Head Impulse Test
Central Changing Nystagmus
Skew Deviation

Labs

  • Glucose
  • CBC/Chemistry
  • ECG

Imaging

  • Warranted if findings concerning for central process
  • MRI preferred

Management

Specific etiologies
Vestibular neuronitis: steroids
Meniere: dietary changes
BPPV: canalith repositioning
Symptomatic relief
Promethazine (Phenergan) 12.5-25mg PO
Ondansetron (Zofran) 4mg IV
Lorazepam (Ativan) 1-2mg PO/IV
Meclizine (Antivert) 25mg PO q6-8h PRN

References

  1. Kattah, J. C., Talkad, A. V., Wang, D. Z., Hsieh, Y.-H., & Newman-Toker, D. E. (2009). HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke; a journal of cerebral circulation, 40(11), 3504–3510. doi:10.1161/STROKEAHA.109.551234
  2. Chang, A., & Olshaker, J. (2013). Dizziness and Vertigo. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 162-169). Elsevier Health Sciences.

Seizure

Definition

Seizure
Pathologic neuronal activation leading to abnormal function
Epilepsy
Recurrent unprovoked seizures

Classification

  • Cause
    • Primary: Unprovoked
    • Secondary: Provoked, caused by trauma, illness, intoxication, metabolic disturbances, etc.
  • Effect on mentation
    • Generalized: involvement of both hemispheres with associated loss of consciousness (tonic-clonic, absence, atonic, myoclonic)
    • Focal: Involving single hemisphere with preserved level of consciousness
  • Status epilepticus
    • Witnessed convulsions lasting >5min
    • Recurrent seizure without recovery from postictal period

Causes of Seizures

Causes of Seizures

Management of Seizures

Management of Seizures

Medications for Treatment of Seizures

Medication Dose (adult) Dose (peds) Comment
1st Line
Lorazepam 4mg IV <13kg: 0.1mg/kg (max 2mg)
13-39kg: 2mg

>39kg: 4mg
Repeat in 10min
Midazolam 10mg IM 0.2mg/kg IM (max 5mg) Repeat in 10min
Midazolam 10mg buccal 0.5mg/kg buccal (max 5mg) Repeat in 10min
2nd Line
Fosphenytoin 20mg PE/kg IV    
Phenytoin 20mg/kg IV   May cause hypotension
3rd Line
Midazolam 0.05-2mg/kg/hr    
Propofol 1-2mg/kg bolus then 20-200mcg/kg/min    
Pentobarbital 5-15mg/kg bolus then 0.5-5mg/kg/hr    
Special Conditions
Glucose 50mL D50/W   Hypoglycemia
MgSO4 6g IV over 15min   Eclampsia (20wks gestation to 6wks post-partum)
Pyridoxine 0.5g/min until seizures stop, max 5g   INH ingestion
3% saline 100-200mL over 1-2h   Confirmed hyponatremia

History

Points suggestive of seizure over alternative process
Abrupt onset
Duration < 120s
LOC
Purposeless activity: automatisms, tonic-clonic
Provocation: fever in children, substance withdrawal
Postictal state
Retrograde amnesia
Incontinence, oral trauma (buccal maceration, tongue laceration)
Rapidly resolving lactic acidosis
Important historical points for patients with seizure history
Recent illness
Medications (adherence, changes, interactions)
Substance use
Ictogenic factors
Recent/remote head trauma
Developmental abnormalities
Substance use
Sleep deprivation
Pregnancy

Key Physical Examination Findings

  • Vital sign abnormalities persisting beyond immediate postictal state (may suggest drug/toxin exposure, CNS lesion)
  • Nuchal rigidity
  • Signs of IVDA
  • Sequela

    • Head trauma
    • Tongue laceration
    • Shoulder dislocation (posterior)
  • Neurological exam

    • Stroke
    • Elevated ICP
    • Failure to note improvement in postictal confusion (encephalopathy, subclinical seizures)

Labs

  • Glucose
  • BMP (Na, Ca, Mg)
  • AED levels
  • CBC (leukocytosis and bandemia common post-seizure)
  • CSF
  • B-hCG
  • LFT (hepatic dysfunction, alcoholic hepatitis)
  • Lactate (rapidly resolves on repeat)

Indications for Imaging

  • New seizures
  • History of trauma
  • History of malignancy
  • Immunocompromised
  • Headache
  • Anti-coagulation
  • Focal neurological exam
  • Persistent AMS

References

  1. McMullan, J., Davitt, A., & Pollack, C. (2013). Seizures. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 156-161). Elsevier Health Sciences
  2. WikEM: Seizure

Weakness

Motor Neuron Signs

Upper Motor Neuron:
Spasticity
Hyperreflexia
Pronator drift
Babinski
Lower Motor Neuron:
Flaccidity
Hyporeflexia
Fasciculation
Atrophy

Causes of Weakness

Lesion Critical Emergent
Non-neurological Shock (VS, clinical assessment)
Hypoglycemia (POC glucose)
Electrolyte derangement (BMP)
Anemia (POC Hb, CBC)
MI (ECG, troponin)
CNS depression (Utox, EtOH)
 
Cortex Stroke Tumor
Abscess
Demyelination
Brainstem Stroke Demyelination
Spinal Cord Ischemia
Compression (disk, abscess, hematoma)
Demyelination (transverse myelitis)
Peripheral Acute demyelination (GBS) Compressive plexopathy
Muscle Rhabdomyolysis Inflammatory myositis

Weakness Syndromes

Unilateral weakness, ipsilateral face
Lesion: Contralateral cortex, internal capsule
Causes: Stroke (sudden onset), demyelination/mass (gradual onset)
Symptoms: Neglect, visual field cut, aphasia
Findings: UMN signs
Key features: Association with headache suggests hemorrhage or mass
Unilateral weakness, contralateral face
Lesion: Brainstem
Causes: Vertebrobasilar insufficiency, demyelination
Symptoms: Dysphagia, dysarthria, diplopia, vertigo, nausea/vomiting
Findings: CN involvement, cerebellar abnormalities
Unilateral weakness, no facial involvement
Lesion: Contralateral medial cerebral cortex, discrete internal capsule
Causes: Stroke
Rare Cause: Brown-Sequard if contralateral hemibody pain and temperature sensory disturbance
Unilateral weakness single limb (monoparesis/plegia)
Lesion: Spinal cord, peripheral nerve, NMJ
UMN signs: Brown-Sequard if contralateral pain and temperature sensory disturbance
LMN signs: Radiculopathy if associated sensory disturbance
Normal reflexes, normal sensation: Consider NMJ disorder
Bilateral weakness of lower extremities (paraparesis/plegia)
Lesion: Spinal cord, peripheral nerve
UMN signs: Anterior cord syndrome (compression, ischemia, demyelination) if contralateral pain and temperature sensory disturbance
Cauda equina: Loss of perianal sensation, loss of rectal tone, or urinary retention
GBS: If no signs of cauda equina and sensory disturbances paralleling ascending weakness (with hyporeflexia)
Bilateral weakness of upper extremities
Lesion: Central cord syndrome
Causes: Syringomyelia, hyperextension injury
Findings: Pain and temperature sensory disturbances in upper extremities (intact proprioception)
Bilateral weakness of all four extremities (quadriparesis/plegia)
Lesion: Cervical spinal cord
Findings: UMN signs below level of injury, strength/sensory testing identifies level
Bilateral weakness, proximal groups
Lesion: Muscle
Causes: Rhabdomyolysis, polymyositis, dermatomyositis, myopathies
Findings: Muscle tenderness to palpation, no UMN signs, no sensory disturbances
Facial weakness, upper and lower face
Lesion: CNVII
Causes: Bell’s palsy, mastoiditis, parotitis
Other CN involvement suggests brainstem lesion, multiple cranial neuropathies, or NMJ

Review of Spinal Cord Anatomy

  • Dorsal Column – Medial Lemniscus (fine touch, proprioception)
    1. Afferent sensory fibers with cell body in DRG
    2. Ascend in ipsilateral posterior column
    3. Synapse in medulla, decussate, ascend in contralateral medial lemniscus
    4. Synapse in thalamus (VPL)
    5. Synapse in sensory strip of post-central gyrus
  • Spinothalamic Tract (pain, temperature)

    1. Afferent sensory fibers with cell body in DRG
    2. Ascends 1-2 levels
    3. Synapse in ipsilateral spinal cord, decussate, ascend in contralateral lateral spinothalamic tract
    4. Synapse in thalamus (VPL)
    5. Synapse in sensory strip of post-central gyrus
  • Lateral Corticospinal Tract (motor)

    1. Efferent cell body in motor strip of pre-central gyrus
    2. Descends through internal capsule
    3. Decussates in pyramid of medulla, descends in contralateral lateral corticospinal tract
    4. Synapse in anterior horn, lower motor neuron to muscle fiber
Spinal Cord Syndromes
Spinothalamic Tract
Dorsal Column / Medial Lemniscus
Lateral Corticospinal Tract

References

  1. Morchi, R. (2013). Weakness. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 124-128). Elsevier Health Sciences.

Diplopia

History and Physical

38F with no medical history, presenting with double vision. The patient reported six weeks of intermittent diplopia for which she had presented to this hospital previously. She was briefly admitted for evaluation of possible cranial nerve IV palsy. Extensive imaging was unremarkable, without mass lesion, infarction, vascular malformation, or meningeal enhancement. She was discharged with outpatient follow-up including ophthalmology clinic and further imaging.

The patient represented due to persistent diplopia that is worse with right gaze. The diplopia is predominantly vertical, alleviated by head tilt. Now associated with three days of right ptosis as well as two weeks of progressive weakness and fatigue – most notable when climbing stairs.

Examination notable for right hypertropia increased on right or downward gaze suggestive of isolated inferior rectus weakness. Pupils were equal and reactive. There was marked fatigable ptosis with 2mm right palpebral fissure compared to 10mm on contralateral side. Symmetrical muscle weakness was noted, 4/5 neck flexion, elbow extension, wrist flexion/extension, shoulder abduction, hip flexion. Gait was wide-based. Application of ice for 5 minutes improved right palpebral fissure opening to >7mm.

Further evaluation included CXR and CT chest with intravenous contrast which did not identify a mediastinal mass. The patient’s respiratory status remained stable throughout hospitalization as assessed by measurements of forced vital capacity. On hospital day one, an edrophonium test was performed which was positive. The patient was started on pyridostigmine, completed a course of IVIG and was discharged with outpatient neurology follow-up.

Evaluation of Diplopia 1

History

  1. Onset/cadence
  2. Direction of gaze with worst diplopia
  3. Orientation (vertical/horizontal)
  4. Associated symptoms (headache, vertigo, dysarthria, eye pain)

Terms Describing Eye Position

Terms describing eye position

Tropias are always present, phorias are identified by cross-cover testing (break fusion)

Algorithm for the Evaluation of Diplopia 2

Algorithm for the Evaluation of Diplopia

Causes of Diplopia 3,4,5,6

Finding EOM Causes Features
Mechanical orbitopathy Variable. Abrupt restriction of movement Orbital cellulitis Pain, erythema
Orbital pseudotumor Autoimmune
Trauma History
Thyroid eye disease Bilateral
Isolated CN III Limited adduction/upgaze/downgaze Microvascular ischemia Pain, risk factors, pupil-sparing
Aneurysm Pupil involvement
Demyelination MRI
Isolated CN IV Limited downgaze (hypertropia) Trauma May be mild
Microvascular ischemia Less common than CN III
ICP Fundoscopy, imaging
Demyelination MRI
Isolated CN VI Limited abduction

(esotropia)

ICP Fundoscopy, imaging
Demyelination MRI
Microvascular ischemia Less common than CN III
INO Limited adduction

(exotropia)

Demyelination MRI
Stroke Dysarthria, ataxia, facial weakness
Multiple CN involvement (III, IV, VI) Variable Cavernous sinus process Retroorbital pain, conjunctival injection or chemosis
Brainstem deficits Variable Brainstem stroke Weakness, dysmetria, tremor
Basilar artery occlusion Vertigo, slurred speech
Wernicke AMS, ataxia, nystagmus
Basilar meningitis Fever, photophobia, meningismus
Miller-Fisher Ataxia, areflexia
Neuromuscular process Variable Myasthenia gravis Fatigability, ice test

References

  1. Alves, M., Miranda, A., Narciso, M. R., Mieiro, L., & Fonseca, T. (2015). Diplopia: a diagnostic challenge with common and rare etiologies. The American journal of case reports, 16, 220–223. doi:10.12659/AJCR.893134
  2. Borooah, S., Wright, M., & Dhillon, B. (2011). Pocket Tutor Ophthalmology. JP Medical Limited. Retrieved from https://books.google.com/books?id=z\_CfWj8-ftoC
  3. Dinkin, M. (2014). Diagnostic approach to diplopia. Continuum (Minneapolis, Minn.), 20(4 Neuro-ophthalmology), 942–965. doi:10.1212/01.CON.0000453310.52390.58
  4. Rucker, J. C., & Tomsak, R. L. (2005). Binocular diplopia. A practical approach. The neurologist, 11(2), 98–110. doi:10.1097/01.nrl.0000156318.80903.b1
  5. Friedman, D. I. (2010). Pearls: diplopia. Seminars in neurology, 30(1), 54–65. doi:10.1055/s-0029-1244995
  6. Guluma, K. (2013). Diplopia. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 176-183). Elsevier Health Sciences.
  7. WikEM: Diplopia

Conjunctivitis and the Red Eye

Differential diagnosis of Conjunctivitis 1,2,3

Condition Pain Visual Acuity Photophobia Discharge Conjunctiva Lymphadenopathy Laterality Associated Features
Viral conjunctivitis None Unaffected None + watery ++ follicular pattern Pre-auricular Unilateral, spreads bilateral Viral URI
Bacterial conjunctivitis None Unaffected None ++ purulent +++ papillary pattern Occasional Unilateral, spreads bilateral Otitis media
Allergic conjunctivitis None Unaffected None + mucoid + None Bilateral Atopy

Differential Diagnosis of Red Eye 4,5

Condition Comment Hyperemia Pupil Pain Visual Acuity Cornea
Subconjuntival hemorrhage Subconjunctival Hemorrhage Associated with trauma, coagulopathy, hypertension. Unilateral, sharply circumscribed Unaffected None Unaffected Clear
Blepharitis Blepharitis Acute/chronic inflammation of eyelid. Diffuse Unaffected Foreign body sensation Unaffected Clear
Epislceritis Episcleritis Recurrent, self-limited episodes, possible autoimmune association. Engorged, radially-oriented vessels Unaffected Mild Unaffected Clear
Scleritis Scleritis Vascular or connective tissue disease. Focal or diffuse, pink sclera Unaffected Moderate Reduced Clear
Acute angle-closure glaucoma Acute Angle-Closure Glaucoma Mydriasis leading to decreased outflow of aqueous humor. Circumcorneal injection Semi-dilated Severe Reduced Hazy
Acute anterior uveitis Uveitis Inflammation of iris or ciliary body. Circumcorneal injection Constricted Moderate Reduced Hazy
Keratitis Keratitis Inflammation of corneal epithelium. Caused by infection, contact lenses, UV exposure. Multiple punctate erosions, stain with fluorescein Unaffected Moderate Reduced Hazy

Algorithm for the Evaluation of the Red Eye 6

Algorithm for the Evaluation of the Red Eye

References

  1. Teoh, D. L., & Reynolds, S. (2003). Diagnosis and management of pediatric conjunctivitis. Pediatric emergency care, 19(1), 48–55.
  2. Azari, A. A., & Barney, N. P. (2013). Conjunctivitis. JAMA: the journal of the American Medical Association, 310(16), 1721. doi:10.1001/jama.2013.280318
  3. Cronau, H., Kankanala, R. R., & Mauger, T. (2010). Diagnosis and management of red eye in primary care. American family physician, 81(2), 137–144.
  4. Leibowitz, H. M. (2000). The red eye. New England Journal of Medicine, 343(5), 345–351. doi:10.1056/NEJM200008033430507
  5. Richards, A., & Guzman-Cottrill, J. A. (2010). Conjunctivitis. Pediatrics in review / American Academy of Pediatrics, 31(5), 196–208. doi:10.1542/pir.31-5-196
  6. Borooah, S., Wright, M., & Dhillon, B. (2011). Ophthalmology. JP Medical Limited.

Severe Traumatic Brain Injury

HPI:

34 year-old male brought in by ambulance s/p assault. Field GCS reportedly 7, in trauma bay assessed as E2-V4-M6. Witnessed seizure in CT scanner, resolved with lorazepam. Intubated for airway protection, underwent external ventricular drain placement and transferred to surgical ICU.

Initial imaging revealed bifrontal subdural hematomas and right temporal hemorrhagic contusion with generalized edema. Repeat imaging one hour later showed interval development of large extra-axial hemorrhage overlying the right occipital and parietal lobes (2.2cm), representing subdural or epidural hematoma.

The patient’s ICU course was complicated by continued seizures and refractory elevation in intracranial pressure. A pentobarbital infusion was started and titrated to adequate burst suppression and hyperosmolar therapy with both mannitol and hypertonic saline continued. Additional imaging revealed stable hemorrhage but continued diffuse cerebral edema evidenced by sulcal effacement.

On hospital day 5, examination revealed bilateral fixed and dilated pupils. Imaging revealed effacement of basilar cisterns, pre-pontine cistern, and cisterna magna suggestive of impending/ongoing transtentorial and tonsillar herniation. Pentobarbital was weaned and conventional cerebral angiography as well as cerebral perfusion studies were consistent with brain death.

Images

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CT head without contrast one hour after presentation

  • Large extra-axial posterior hemorrhages. Hemorrhagic contusions in the right frontal and temporal lobes.
  • The cerebral sulci appear effaced – findings suggest diffuse cerebral edema.
  • S/p EVD using a right frontal approach.
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CT head without contrast on hospital day 5

  • Interval evidence of global hypoxic/ischemic injury to the brain.
  • Interval apparent effacement of the basilar cisterns, pre-pontine cistern, and cisterna magna suggesting impending/ongoing downward transtentorial herniation and tonsillar herniation.
  • Stable supra/infratentorial subdural/epidural hematoma.

Algorithm for the Management of Severe Traumatic Brain Injury1,2

Algorithm for the Management of Severe Traumatic Brain Injury

References

  1. Brain Trauma Foundation, American Association of Neurological Surgeons, Congress of Neurological Surgeons, Joint Section on Neurotrauma and Critical Care, AANS/CNS, Carney, N. A., & Ghajar, J. (2007). Guidelines for the management of severe traumatic brain injury. Introduction. Journal of neurotrauma, 24 Suppl 1, S1–2. doi:10.1089/neu.2007.9997
  2. Stocchetti, N., & Maas, A. I. R. (2014). Traumatic intracranial hypertension. The New England journal of medicine, 370(22), 2121–2130. doi:10.1056/NEJMra1208708
  3. WikEM: Severe traumatic brain injury

Necrotizing Soft-Tissue Infection (NSTI)

HPI:

40 year-old male with a history of diabetes presents with right foot pain and swelling. His symptoms began 3 days ago with pain on the lateral surface of his right foot, described as aching, non-radiating and exacerbated with walking. Yesterday, he noted more prominent swelling and redness involving 4th and 5th toes. He denies trauma, fevers, and discharge.

PMH:

  • Diabetes mellitus, diagnosed 8yrs ago

PSH:

  • None

FH:

  • Non-contributory

SHx:

  • Lives with wife and 2 children and works an office job.
  • Ten year history of tobacco use, quit 3 years ago.
  • No EtOH or drug abuse.

Meds:

  • Metformin 500mg p.o. b.i.d.
  • Ibuprofen p.r.n. joint pain

Allergies:

NKDA

Physical Exam:

VS: T 101.2 HR 88 RR 14 BP 147/71 O2 100% RA
Gen: Obese male, pleasant and in no acute distress, lying in bed with right foot raised.
HEENT: PERRL, EOMI, dry mucous membranes.
CV: RRR, normal S1/S2, no extra heart sounds, no murmurs.
Lungs: CTAB
Abd: +BS, non-tender.
Ext: Right lower extremity with 8x8cm area of erythema predominantly involving lateral aspect of foot, dorsum of foot and 3-5th digits. There is a shallow, 1x1cm ulcer on the plantar surface of foot near 5th MTP. Area is also notable for ecchymosis and palpable crepitus. There is minimal tenderness to palpation or with active/passive range of motion.
Skin: The remainder of the skin exam is unremarkable.
Neuro: AAOx3.

Labs/Studies:

  • BMP: 134/4.3/104/26/18/1.4/206
  • WBC: 27.3/13.1/40/189 (90% neutrophils)
  • Lactate: 1.2
  • CRP: [pending]

Imaging:

CT Lower Extremity

  1. Calf cellulitis and gas-producing cellulitis in the lateral foot and toes.
  2. Thigh and inguinal lymphadenopathy.
  3. Although gas is seen down to the level of the bone, no definite bony changes are identified to establish a diagnosis of osteomyelitis. Please note that MRI is more sensitive for detection of early osteomyelitis.

Assessment/Plan:

40M with DM and diabetic foot ulcer resulting in a necrotizing soft tissue infection as evidenced by gas on imaging. Recommended surgical debridement and started on broad-spectrum antibiotics including:

  • vancomycin 1g i.v. q.12.h.
  • cefepime 2g i.v. q.8.h.
  • metronidazole 500mg i.v. q.8.h.

The patient underwent amputation of 3-5th digits with good surgical margins and was discharged on post-operative day three in good condition.

Skin and soft-tissue layers and their infections: 1

Skin and soft-tissue layers and their infections

Necrotizing Soft-Tissue Infections (NSTI):2,3,4

Risk Factors

  • IVDA
  • Comorbid conditions
    • DM
    • Obesity
    • Immunosuppression

Physical Exam

  • Early (non-specific)
    • Swelling
    • Erythema
    • Pain
  • Late (non-sensitive)
    • Tense edema outside affected skin perimeter
    • Disproportionate pain
    • Ecchymosis
    • Bullae
    • Crepitus
    • Systemic signs (fever, tachycardia, hypotension)

Treatment

  • Surgical debridement
  • Antimicrobials
    • Carbapenem, combination B-lactam B-lactamase
    • Vancomycin, linezolid (MRSA coverage)
    • Clindamycin (inhibit protein synthesis)
  • Supportive therapy

LRINEC score 5

Name Value Score
CRP ≥150 4
WBC 15-25
>25
1
2
Hb 11-13.5
<11
1
2
Na <135 2
Creatinine >1.6 2
Glucose >180 1

<5 Low risk, 6-7 Intermediate risk, >8 High risk

References:

  1. Morchi, R. (2/18/14). Emergency Medicine Procedures Cadaver Lab. Clinical Clerkship at UCLA. Los Angeles, CA.
  2. Goldstein, E. J. C., Anaya, D. A., & Dellinger, E. P. (2007). Necrotizing Soft-Tissue Infection: Diagnosis and Management. Clinical infectious diseases, 44(5), 705–710. doi:10.1086/511638
  3. Headley, A. J. (2003). Necrotizing soft tissue infections: a primary care review. American family physician, 68(2), 323–328.
  4. McHenry, C. R., Piotrowski, J. J., Petrinic, D., & Malangoni, M. A. (1995). Determinants of mortality for necrotizing soft-tissue infections. Annals of surgery, 221(5), 558–63.
  5. Wong, C.-H., Khin, L.-W., Heng, K.-S., Tan, K.-C., & Low, C.-O. (2004). The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score: A tool for distinguishing necrotizing fasciitis from other soft tissue infections. Critical Care Medicine, 32(7), 1535–1541. doi:10.1097/01.CCM.0000129486.35458.7D