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

Volvulus


Swirling mesenteric vessels in mid-pelvis associated with narrowed segments of small bowel and fluid-filled proximal small bowel raises concern for volvulus and small bowel obstruction.

Head Trauma: Radiographic Evolution

CT Head (Initial)

CT Head (Initial)

- Noncontrast axial images through the head demonstrate no evidence of skull fracture.
- Large lentiform-shaped mixed density extra-axial acute epidural hematoma in the right parietal occipital
- Associated subdural hematoma tracking along right convexity toward the right temporal lobe.
- There is no evidence of midline shift.

CT Head (+8h)

CT Head (+8h)

- Significant interval increase in the size of the right hemispheric subdural hematoma
- There is now midline shift from right to left at the level of the septum pellucidum measuring 10 mm, partial effacement of the right lateral ventricle and subfalcial herniation.
- Scattered subarachnoid blood is redemonstrated.
- Comminuted fractures of the nasal bone are present and there is overlying and associated periorbital soft tissue swelling.

CT Head (+16h, s/p SDH evacuation)

CT Head (+16h, s/p SDH evacuation)

- Interval gross total evacuation of right hemispheric subdural hematoma.
- Moderate anterior bifrontal subdural and right epidural air is present.
- Small scattered subarachnoid and intraventricular blood is redemonstrated.

Angioedema

AngioedemaHPI:

63-year old African American male with a history of HTN presenting with lip swelling x1 day. The patient states he was well until this morning when he noticed progressive swelling of his lips. The swelling is not associated with any difficulty speaking, swallowing or breathing and is not painful.

He denies new rashes or itching, and has no history of such swelling. He also denies any exposure to known allergens, recent insect bites or travel. He has been taking lisinopril for his blood pressure regularly for the past several months and denies any prior adverse effects (cough, rash).

PMH:

  • Parkinson Disease
  • HTN

PSH:

None

FH:

No family history of angioedema

SHx:

  • No t/e/d use
  • Lives at home with caretaker

Meds:

  • Lisinopril 20mg p.o. daily
  • Carbidopa/levodopa 50mg p.o. t.i.d.

Allergies:

NKDA

Physical Exam:

VS: T 37.8 HR 84 RR 14 BP 146/98 O2 99% RA
Gen: Well-appearing, no respiratory distress, speaking comfortably
HEENT: PERRL, significant external upper/lower lips swelling extending to lateral cheeks, non-tender, no fluctuance or overlying skin changes. No visible tongue swelling, floor of mouth swelling/tenderness, uvular/palatal deviation.
CV: RRR, no M/R/G
Lungs: CTAB, no crackles/wheezing, good air movement b/l
Abd: +BS, soft, NT/ND, no rebound/guarding
Ext: Warm, well-perfused, 2+ peripheral pulses
Skin: No visible skin lesions/rashes
Neuro: AAOx4, CN II-XII intact

Assessment/Plan:

63M with acute onset, progressive facial swelling. Currently restricted to external lips, with no evidence of airway compromise. Likely ACE inhibitor-induced angioedema given patient is on lisinopril and has no history of hereditary angioedema. Doubt anaphylaxis given no allergies, suspicious exposures or history of pruritus. Doubt infection given afebrile and painless swelling without e/o erythema.

Pathophysiology of ACE inhibitor-induced angioedema1

Pathophysiology of ACE-inhibitor induced angioedema

Angioedema is a vascular reaction associated with tissue (subcutaneous, submucosal) edema resulting from increased activity of vasoactive substances. The vasoactive substances in ACE inhibitor-induced angioedema are bradykinin and substance P. In the presence of ACE inhibition, these enzymes are inactivated through alternative pathways which, if disturbed, lead to angioedema.

Epidemiology of ACE inhibitor-induced angioedema

Angioedema occurs in 0.1-0.7% of patients taking ACE inhibitors, and 60% of cases occur within the first week of starting an ACE inhibitor (though it can occur as much as years later).2,3 ACE inhibitors are implicated as the cause of 20-40% of all ED visits for angioedema.4

Risk Factors2,5,6

  • Female
  • Age > 65yo
  • African American
  • Prior angioedema
  • Smoking
  • ACE inhibitor-associated cough

Clinical Features of ACE inhibitor-induced angioedema

Affected Sites:

  • Mucous membranes of the head and neck
    • Face
    • Tongue
    • Lips
    • Pharynx
    • Larynx
  • GI tract
    • Diffuse abdominal pain
    • Nausea/vomiting/diarrhea

Signs/Symptoms at initial presentation:4

  • SOB (89%)
  • Lip swelling (70%)
  • Tongue swelling (52%)
  • Voice change/hoarseness (29%)
  • Stridor (11%)

Key Clinical Features:

  • Onset in minutes with resolution in 24-72 hours
  • Absence of itching/urticaria7

Staging and Disposition:8

Stage Affected Site Outpatient (%) Floor (%) ICU (%) Intervention (%)
I Face, lip 48 52 0 0
II Soft palate 60 40 0 0
III Tongue 26 7 67 7
IV Larynx 0 0 100 24

Management of ACE inhibitor-induced angioedema

  • Proven benefit
    • Airway management
    • Withdrawal of ACE inhibitor
  • Unclear benefit
    • Epinephrine 0.3mg IM q15min
    • Diphenhydramine 50mg IV
    • Famotidine 20mg IV
    • Solumedrol 125mg IV
  • Future treatment options
    • FFP: contains ACE9
    • Icatibant: bradykinin B2 receptor antagonist10,11

References:

  1. Vleeming, W., van Amsterdam, J. G., Stricker, B. H. C., & de Wildt, D. J. (1998). ACE inhibitor-induced angioedema. Drug Safety, 18(3), 171–188. doi:10.2165/00002018-199818030-00003
  2. Grant, N. N., Deeb, Z. E., & Chia, S. H. (2007). Clinical experience with angiotensin-converting enzyme inhibitor-induced angioedema. Otolaryngology – head and neck surgery, 137(6), 931–935. doi:10.1016/j.otohns.2007.08.012
  3. Slater, E. E., Merrill, D. D., Guess, H. A., Roylance, P. J., Cooper, W. D., Inman, W. H., & Ewan, P. W. (1988). Clinical profile of angioedema associated with angiotensin converting-enzyme inhibition. JAMA : the journal of the American Medical Association, 260(7), 967–970.
  4. Banerji, A., Clark, S., Blanda, M., LoVecchio, F., Snyder, B., & Camargo, C. A. (2008). Multicenter study of patients with angiotensin-converting enzyme inhibitor-induced angioedema who present to the emergency department. Annals of allergy, asthma & immunology, 100(4), 327–332. doi:10.1016/S1081-1206(10)60594-7
  5. Gibbs, C. R., Lip, G. Y., & Beevers, D. G. (1999). Angioedema due to ACE inhibitors: increased risk in patients of African origin. British journal of clinical pharmacology, 48(6), 861–865.
  6. Morimoto, T., Gandhi, T. K., Fiskio, J. M., Seger, A. C., So, J. W., Cook, E. F., Fukui, T., et al. (2004). An evaluation of risk factors for adverse drug events associated with angiotensin-converting enzyme inhibitors. Journal of evaluation in clinical practice, 10(4), 499–509. doi:10.1111/j.1365-2753.2003.00484.x
  7. Kanani, A., Schellenberg, R., & Warrington, R. (2011). Urticaria and angioedema. Allergy, Asthma & Clinical Immunology, 7(Suppl 1), S9. doi:10.1186/1710-1492-7-S1-S9
  8. Ishoo, E., Shah, U. K., Grillone, G. A., Stram, J. R., & Fuleihan, N. S. (1999). Predicting airway risk in angioedema: staging system based on presentation. Otolaryngology – head and neck surgery, 121(3), 263–268.
  9. Hassen, G. W., Kalantari, H., Parraga, M., Chirurgi, R., Meletiche, C., Chan, C., Ciarlo, J., et al. (2013). Fresh frozen plasma for progressive and refractory angiotensin-converting enzyme inhibitor-induced angioedema. The Journal of emergency medicine, 44(4), 764–772. doi:10.1016/j.jemermed.2012.07.055
  10. Bas, M., Greve, J., Stelter, K., Bier, H., Stark, T., Hoffmann, T. K., & Kojda, G. (2010). Therapeutic Efficacy of Icatibant in Angioedema Induced by Angiotensin-Converting Enzyme Inhibitors: A Case Series. Annals of emergency medicine, 56(3), 278–282. doi:10.1016/j.annemergmed.2010.03.032
  11. MD, M. G., & MD, M. A. (2012). Icatibant: a novel approach to the treatment of angioedema related to the use of angiotensin-converting enzyme inhibitors. American Journal of Emergency Medicine, 30(8), 1664.e1–1664.e2. doi:10.1016/j.ajem.2011.09.014

Hearing loss and Tinnitus

HPI:

42 year-old male with no significant medical history presenting to ENT clinic after referral from PMD for perforated TM. The patient last had normal hearing approximately 1yr ago when he noted acute onset of right ear pain, discharge, hearing loss and ringing in the setting of fever and a productive cough. He does not recall an inciting event (trauma, swimming) to this initial episode, and had no previous history of ear infections. He saw his PMD several days later, was told he had a perforated ear drum and was treated with antibiotics.

Since then, the patient has not had any further ear pain or discharge but is left with persistent and constant hearing loss and ringing (high-pitched, non-pulsatile).

PMH:

None

PSH:

None

FH:

Non-contributory

SHx:

Worked in construction for 20yrs

Meds:

None

Allergies:

NKDA

Physical Exam:

Gen: Well-appearing, no acute distress
Head: NC/AT
Eyes: PERRL (4-2mm), disc margins sharp
Ears: Weber lateralizes to left, AC > BC b/l
AD: Decreased acuity to finger rub, EAC with some cerumen, cleared to reveal central perforation in posterior-superior quadrant of tympanic membrane.
AS: EAC clear, TMI
Nose: Nasal mucosa pink, septum midline
Mouth: MMM, no lesions, good dentition, no pharyngeal erythema/exudates
Neck: Trachea midline, supple, no cervical lymphadenopathy, no thyroid enlargement

Studies

Audiogram

Audiogram: Severe low-mid frequency progressing to profound high frequency mixed hearing loss

Assessment/Plan:

42M, no significant PMH, with perforated TM and audiogram showing mixed hearing deficit. The patient describes a history suggestive of acute otitis media complicated by TM perforation. Persistent perforation seen on examination today can result in the tinnitus and hearing loss the patient complains of. However the marked sensorineural component remains unexplained, particularly given the patient reported previously normal hearing. While there is some evidence that acute otitis media can lead to sensorineural hearing loss, it is typically only mild and only in high-frequency ranges.1,2  Plan for further evaluation with repeat audiogram and MRI IAC, RTC when studies completed.


Examination of the Ear3

  1. External Auditory Canal: in acute otitis externa, the canal will be narrowed, swollen and erythematous
  2. Tympanic Membrane: use cone of light for orientation, identify malleus and move speculum to visualize all four quadrants
Tympanic Membrane
Ear Anatomy
Normal
Perforation
Tympanosclerosis
Acute Otitis Media

Differential Diagnosis of Hearing Loss4

Differential Diagnosis of Hearing Loss

Differential Diagnosis of Tinnitus5

Differential Diagnosis of Tinnitus

References:

  1. Tarlow, M. (1998). Otitis media: pathogenesis and medical sequelae. Ear, nose, & throat journal, 77(6 Suppl), 3–6.
  2. Tsuprun, V., Cureoglu, S., Schachern, P. A., Ferrieri, P., Briles, D. E., Paparella, M. M., & Juhn, S. K. (2008). Role of pneumococcal proteins in sensorineural hearing loss due to otitis media. Otology & neurotology, 29(8), 1056–1060.
  3. Bickley, Lynn S., Peter G. Szilagyi, and Barbara Bates. Bates’ guide to physical examination and history taking. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins, 2009. Print.
  4. Isaacson, J. E., & Vora, N. M. (2003). Differential diagnosis and treatment of hearing loss. American family physician, 68(6), 1125–1132.
  5. Crummer, R. W., & Hassan, G. A. (2004). Diagnostic approach to tinnitus. American family physician, 69(1), 120–126.

Dysphonia (Hoarseness)

Case 1

HPI:

36 year-old female with no significant medical history who presents after referral for voice hoarseness. According to the patient, she underwent a C-section 3 months ago (at an outside hospital) complicated by bleeding requiring a second operation (L salpingoophorectomy); however, neither procedure required emergent intubation. She reports that she had some vomiting associated with anesthesia which ultimately required intubation and admission to the MICU for 5-6d. She was discharged 10 days after the initial operation, and both she and her baby were in good health. Two weeks after discharge, she began experiencing throat irritation and 1 month after discharge she noticed voice hoarseness which has been persistent. Today, she denies difficulty swallowing or breathing, F/C, N/V, abdominal pain.

PMH:

None

PSH:

Cesarean x2, L salpingoophorectomy

FH:

Non-contributory

SHx:

Lives at home taking care of 3 children, denies t/e/d

Meds:

None

Allergies:

NKDA

Physical Exam:

Gen: WA, NAD
Head: NC/AT
OC: MMM, no lesions, no pharyngeal erythema/exudates, hoarse voice
Ears: EAC clear, TMI b/l
Flex: Posterior commissure edema, cobblestoning, b/l TVC with shiny white masses
Flexible nasolaryngoscopy image showing trauma granulomata.

Flexible nasolaryngoscopy image showing trauma granulomata.

Assessment/Plan:

36F, no significant PMH, recent Cesarean and L salpingoophorectomy c/b likely aspiration requiring intubation and mechanical ventilation for several days with onset of progressive voice hoarseness 1mo later. History and flexible nasolaryngoscopy consistent with trauma granulomata, as well as laryngopharyngeal reflux.

  • Discussed treatment options with patient, recommend voice rest x2mo and continued monitoring
  • Laryngopharyngeal reflux, given dietary/lifestyle education, start omeprazole 20mg p.o. b.i.d.
  • RTC 1mo

Case 2

HPI:

51 year-old female with a history of Hepatitis C, COPD and an 80 pack-year smoking history presents with concern about progressive voice hoarseness x2mo. She reports quitting smoking two months ago and is not sure if the hoarseness preceded or followed quitting. She has occasional throat discomfort which is mild. She otherwise denies difficulty or pain with swallowing, worsening shortness of breath, unintentional weight loss.

She also reports a new mass on her neck which she first noticed yesterday. Denies associated pain, or surrounding skin changes.

PMH:

  • Hepatitis C
  • COPD

PSH:

  • Hysterectomy

FH:

Non-contributory

SHx:

80 pack-year smoking history, no current EtOH, drug use (previously used heroin and opiates)

Meds:

  • Methadone
  • Elavil
  • Multiple unknown inhaled medications

Allergies:

  • Naproxen (swelling)

Physical Exam:

Gen: WA, NAD
Head: NC/AT
Eyes: PERRL, EOMI
Ears: b/l EAC erythema, TMI, no lesions/exudates
OC: MMM, no lesions
Neck: Supple, no thyroid enlargement, no cervical lymphadenopathy, 5x6cm soft, round, mobile, non-tender mass on left lateral neck w/o overlying skin changes
Flex: Diffuse laryngeal damage, thickened posterior commissure, right TVC with area of leukoplakia, left TVC appears irregular

Assessment/Plan:

51F hx HepC, COPD, 80py smoking, presenting with voice hoarseness x2mo. History concerning for malignancy, exam today shows significant laryngeal damage and vocal cord irregularities warranting further evaluation. Possible component of fungal infection 2/2 inhaled steroid use for COPD, plan to reduce potentially aggravating factors (treat fungal infection, voice rest) and repeat evaluation. Neck mass possibly lipoma however will evaluate further given concern for malignancy.

  • Start fluconazole 100mg two tables p.o. on day1, 100mg p.o. daily x7d
  • Start nystatin 100,000 units/mL 10mL gargle and swallow t.i.d. x2wks
  • Advised voice rest
  • RTC in 3wks
  • CT neck/soft tissue w/wo IV contrast to evaluate neck mass

Anatomy of the Pharynx/Larynx:

Vocal cord anatomy
Pharyngeal wall anatomy
Structure of the pharynx

Physiology of Voice Production: 1

Voice is produced through the passive vibration of vocal folds in an air stream and requires:

  1. Adequate Air Stream
  2. Smooth vocal fold edges
  3. Vocal folds with normal vibratory properties
  4. Appropriate vocal fold positioning

Differential diagnosis of dysphonia (hoarseness): 1,2,3

 Differential Diagnosis of Dysphonia (hoarseness)

Characteristics of Hoarse Voice: 5

Characteristic Likely cause
Breathy Vocal cord paralysis
Hoarse Vocal cord lesion, LPR
Low-pitched Reinke’s edema, vocal abuse, LPR

References:

  1. Mau, T. (2010). Diagnostic Evaluation and Management of Hoarseness. Medical Clinics of North America, 94(5), 945–960. doi:10.1016/j.mcna.2010.05.010
  2. Feierabend, R. H., & Shahram, M. N. (2009). Hoarseness in adults. American family physician, 80(4), 363–370.
  3. Schwartz, S. R., Cohen, S. M., Dailey, S. H., Rosenfeld, R. M., Deutsch, E. S., Gillespie, M. B., Granieri, E., et al. (2009, September). Clinical practice guideline: hoarseness (dysphonia). Otolaryngology. doi:10.1016/j.otohns.2009.06.744
  4. Bruch, J.W., Kamani D.V. Diaphragmatic pacing. In: UpToDate, Basow, DS (Ed), UpToDate, Waltham, MA, 2013.
  5. Rosen, C. A., Anderson, D., & Murry, T. (1998). Evaluating hoarseness: keeping your patient’s voice healthy. American family physician, 57(11), 2775–2782.

Macroscopic Hematuria

CC:

Macroscopic hematuria

HPI:

85yo male with a history of prostate cancer s/p radiation and androgen deprivation therapy four years ago complicated by urethral strictures requiring chronic indwelling catheter who presented to the ED yesterday with 3 days of red urine followed by no output from catheter and abdominal pain. In the ED, the patient was found to have stable hemoglobin and creatinine and was discharged with urology follow-up after symptom resolution with catheter irrigation.

Today, the patient reports no new issues, denies abdominal/flank pain, further catheter obstruction, fevers/chills. He states that his urine has been light pink in color, without clots, and significantly more clear than the prior 3 days. He has had intermittent episodes of blood in his urine in the past, but never causing obstruction. His catheter is managed at home with regular (q3wk) changes and no recent traumatic catheterizations.

He denies any new back/bone pain or unintentional weight loss.

PMH:

  • Prostate CA
  • HTN
  • DM
  • CKD
  • CAD

PSH:

  • None

FH:

  • Non-contributory

SHx:

  • No current or previous t/e/d use
  • Lives with wife

Meds:

  • lisinopril 20mg p.o. daily
  • glyburide/metformin 1.25/250mg p.o. b.i.d.
  • atorvastatin 20mg p.o. daily
  • ASA 81mg p.o. daily

Allergies:

  • NKDA

Physical Exam:

VS: T 98.4 HR 64 RR 13 BP 136/94 O2 99% RA
Gen: Well-appearing, pleasant man in no acute distress.
Abd: +BS, soft, NT/ND, no suprapubic tenderness, no CVAT
GU: Foley catheter in place draining clear-pink fluid to leg bag, no clots. No evidence of trauma to urethra, no visible skin lesions. Testes descended bilaterally, no inguinal lymphadenopathy.

Assessment/Plan:

85M hx CaP (2009) s/p radiation and androgen deprivation therapy with urethral strictures requiring chronic indwelling catheter presenting with macroscopic hematuria. Given patient’s history, radiation cystitis is a likely cause of his symptoms. However, given the long-standing catheter, other considerations include trauma and infection. Also, recurrence or new malignancy must be considered. Will obtain UA, UCx, and schedule patient for cystoscopy with bilateral retrograde pyelogram. Also, educated patient on how to irrigate catheter if needed and provided ED precautions should obstruction persist despite irrigation attempts. Patient’s last surveillance PSA undetectable, continue routine follow-up.

Differential Diagnosis of Macroscopic Hematuria

Differential Diagnosis of Macroscopic Hematuria

Important Historical Elements:

  • Painless: suggests malignancy
  • Painful: suggests calculi/infection
  • Urinalysis: presence of dysmorphic RBC’s, RBC/WBC casts, proteinuria suggest intrinsic renal disease
  • Timing: early (distal urethra), throughout (upper urinary tract), terminal (bladder neck, prostatic)

Guided Lecture

EM Ed
Watch “Gross Hematuria: Just a Bit of Kool-Aid” from EM Ed. In this lecture Dr. Basrai reviews the differential diagnosis and management of macroscopic hematuria in the emergency department.

References:

  1. Hicks, D., & Li, C.-Y. (2007). Management of macroscopic haematuria in the emergency department. Emergency medicine journal : EMJ, 24(6), 385–390. doi:10.1136/emj.2006.042457
  2. Mazhari, R., & Kimmel, P. L. (2002). Hematuria: an algorithmic approach to finding the cause. Cleveland Clinic journal of medicine, 69(11), 870–872–4– 876.
  3. Howes DS, Bogner MP. Chapter 94. Urinary Tract Infections and Hematuria. In: Tintinalli JE, Stapczynski JS, Cline DM, Ma OJ, Cydulka RK, Meckler GD, eds.Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York: McGraw-Hill; 2011. http://www.accessmedicine.com/content.aspx?aID=6362340. Accessed June 14, 2013.
  4. Sutton, J. M. (1990). Evaluation of hematuria in adults. JAMA : the journal of the American Medical Association, 263(18), 2475–2480.

Small Bowel Obstruction

Dilated loops of small bowelCC:

Consultation for bowel obstruction

HPI:

The patient is a 40yo male with a history of alcohol abuse, and seizure disorder secondary to traumatic brain injury who was admitted to this hospital 4d ago after an altercation with law enforcement officials. On arrival, the patient was reported to be acutely intoxicated with ecchymosis and bleeding from left lateral/posterior head and ear. No other significant injuries were found and the patient underwent CT imaging of head and c-spine, with notable findings of left occipital epidural hematoma, subarachnoid hemorrhage, but no significant midline shift. Neurosurgery was consulted and no emergent surgical intervention was required, the patient underwent serial imaging to monitor the bleed which was found to be stable and the patient slowly returned to baseline mental status.

On HOD4, the patient developed nausea/vomiting and abdominal pain, a nasogastric tube was placed with feculent output. CT abdomen/pelvis showed high grade SBO and possible mesenteric ischemia/infarct, and general surgery was consulted for further evaluation. The patient reported experiencing some abdominal pain since the altercation, but could not recall if he was hit in the abdomen.

PMH:

  • Alcohol abuse
  • Seizure disorder

PSH:

  • Tibia fracture
  • No prior abdominal surgery

FH:

  • Non-contributory

SHx:

  • Current alcohol, marijuana use, no tobacco use
  • History of homelessness

Medications:

  • Norco PRN
  • Ativan PRN
  • LISS, SQH, Thiamine
  • NKDA

Physical Exam:

  • VS:  T 99.5°F    HR 108    RR 16    BP 128/82    O2 99% RA
  • Gen: NAD
  • HEENT: PERRL, EOMI, sclera clear, anicteric
  • CV: RRR, normal S1/S2
  • Lungs: CTAB
  • Abd: Distended, diffuse tenderness to palpation, no rebound tenderness, no ecchymoses or signs of trauma
  • Ext: Warm, well-perfused
  • Neuro: AAOx4, appropriate

Assessment/Plan:

40M w/hx alcohol abuse, TBI and seizure disorder, presented initially with evidence of head trauma which was stabilized. However, the development of abdominal pain, N/V, and finding of distension on exam associated with copious output of feculent material from NGT suggests bowel obstruction. This patient has no history of abdominal surgeries to suggest adhesions as a possible cause. Though the patient cannot recall any abdominal trauma, and there was no e/o trauma on exam, findings on CT abdomen/pelvis are suggestive of traumatic cause (hematoma causing obstruction or ischemia resulting from mesenteric injury). The patient was monitored for several days, continuing NGT to suction and with serial abdominal films. However, abdominal pain persisted, abdominal radiographs showed worsening obstruction and the patient developed leukocytosis and on HOD7 the patient was taken to the OR for exploratory laparotomy. Upon entering the peritoneal cavity, there was obvious blood and very distended small bowel which was run distally with finding of a mesenteric laceration in the distal ileum which was walled off by omentum. Additionally, a grade 2 splenic laceration was found. Ultimately, a small bowel resection with primary anastomosis along with a repair of the splenic laceration was performed.

Imaging:

CT abdomen/pelvis

CT abdomen/pelvis

Moderate abdominal and pelvic ascites which has Hounsfield unit attenuation is greater than simple fluid suggestive of blood products.

CT abdomen/pelvis

CT abdomen/pelvis

Fluid dilated small bowel

CT abdomen/pelvis

CT abdomen/pelvis

Complex transition point in the central mid abdomen.
Segment of bowel at the transition point has circumferential mural thickening and surrounding complex attenuation mesenteric fluid and mesenteric stranding.

Abdominal X-Ray

Abdominal X-Ray

Small bowel distention
Nasogastric tube is seen coiled in the gastric fundus

CT Head

CT Head

Left occipital extracranial soft tissue hematoma
Left occipital epidural hematoma subjacent to the fracture site in addition to subarachnoid hemorrhage within the sulci of the left temporal lobe and interpeduncular cistern
Extra-axial fluid collection along the right frontal convexity, tracking down the anterior falx, compatible with a subdural hematoma

Differential Diagnosis for bowel obstruction: 1, 2, 3

A System for Bowel Obstruction

Types of Abdominal Pain: 4

Types of Abdominal Pain

References:

  1. Kulaylat MN, Doerr RJ. Small bowel obstruction. In: Holzheimer RG, Mannick JA, editors. Surgical Treatment: Evidence-Based and Problem-Oriented. Munich: Zuckschwerdt; 2001. Available from: http://www.ncbi.nlm.nih.gov/books/NBK6873/
  2. Jackson, P. G., & Raiji, M. T. (2011). Evaluation and management of intestinal obstruction. American family physician, 83(2), 159–165.
  3. Maung, A. A., Johnson, D. C., Piper, G. L., Barbosa, R. R., Rowell, S. E., Bokhari, F., Collins, J. N., et al. (2012). Evaluation and management of small-bowel obstruction. Journal of Trauma and Acute Care Surgery, 73, S362–S369. doi:10.1097/TA.0b013e31827019de
  4. Stabile, Bruce. “The Acute Abdomen.” Chairman’s Hour. Harbor UCLA Department of Surgery Student Lecture Series. 5/17/13. Lecture.

Abdominal Wall Hernias

Inguinal hernia CTHPI:

23M w/no known medical history presenting with abdominal “ball” x10d. Patient denies pain, and is tolerating regular diet w/o N/V. Reports lifting weights.

PMH/PSH/FHx/SHx:

None, non-contributory, no t/e/d.

Meds:

Acetaminophen, NKDA

PE:

  • VS:     T N/A      HR 86     RR 18       BP 116/64      O2 N/A
  • Gen: Well-appearing young male, no acute distress
  • HEENT: PERRL, MMM no lesions
  • CV: RRR, normal S1/S2, no murmurs
  • Lungs: CTAB, no crackles/wheezes
  • Abd: +BS, soft, NT/ND, 3cm bulge in right inguinal region with valsalva, above inguinal ligament, ~7cm lateral to symphysis, non-tender, reduces spontaneously after valsalva GU: uncircumcised penis, testes descended b/l, normal size, non-tender, no herniation through inguinal canal palpated with valsalva
  • Ext: Warm, well-perfused, 2+ peripheral pulses
  • Neuro: Alert and oriented, appropriate

Assessment/Plan:

23M ċ inguinal hernia, currently asymptomatic with no evidence of incarceration/strangulation. Recommend follow-up at city hospital for evaluation and possible surgical repair. Advised to refrain from strenuous activity, heavy lifting.

Physical Examination Techniques: 1

Physical Examination Techniques

  • Observation: Best performed with patient standing and physician seated on a stool facing the patient
  • Palpation: place hand over patient’s groin (see figure), with two fingers each superior and inferior to the inguinal ligament. Have the patient cough and feel for a palpable bulge or impulse.
  • GU: With a finger in the inguinal canal, bulges felt against the side of the examining finger are direct hernias, while those felt at the tip of the finger are indirect.

Types of Abdominal Wall Hernias: 2

Types of abdominal wall hernias

Name Location Etiology/Epidemiology
1. Umbilical Linea alba through weakened umbilical ring.Paraumbilical hernias through linea alba in the region of the umbilicus. Congenital or acquired due to increased intra-abdominal pressure (obesity, pregnancy, ascites, PD)
2. Epigastric Linea alba between umbilicus and xiphoid process Congenital weakness of linea alba (lack of decussating fibers)
3. Spigelian Semilunar line: along the lateral borders of rectus abdominus. Herniation typically occurs caudally (below arcuate line) due to absence of posterior rectus sheath.
4. Incisional Site of prior incision Poor fascial healing possibly due to: infection (increased risk in wound dehiscence), obesity, smoking, immunosuppression excess wound tension, CT disorders.
5. Inguinal Indirect: internal (deep) inguinal ring, lateral to inferior epigastric vessels.Direct: external (superficial) inguinal ring, medial to inferior epigastric vessels. Indirect > direct.
6. Femoral Inferior to the inguinal ligament, through empty space medial to femoral sheath. F > M, increased likelihood of incarceration/strangulation (40%)
7. Lumbar 3 Arise in two anatomical triangles:Superior lumbar triangle – lateral border internal oblique, medial border erector spinae, superior border 12thrib.Inferior lumbar triangle – lateral border external oblique, medial border latissimus dorsi, inferior border iliac crest. (See figure) Associated with surgery (incisional), typically urologic.
8. Obturator Protrusion of peritoneal sac through obturator foramen. Rare, occur primarily in elderly women (high predisposition for incarceration).

Locations of Abdominal Wall Hernias:

Locations of abdominal wall hernias

Layers of the Anterior Abdominal Wall:

abdominal_wall

Differential diagnosis for groin masses: 4

Category Inguinal 5 Scrotal 6 Vulvar 7 Perineal 8
Vascular Varicocele extension Varicocele Vulvar varicocity

Hemangioma
Infectious, Inflammatory Lymphadenopathy
Abscess
Inflammatory joint process (hip, related bursae)
Thrombophlebitis
Epididymitis
Epididymo-orchitis
Condyloma
Molluscum
Bartholin’s cyst
Neoplastic Benign (lipoma)
Lymph node metastatsis
Testicular malignancy Malignant skin lesions Soft-tissue malignancy
Anal SCC
Rectal GIST
Metastasis (commonly anorectal, prostatic)
Congenital, Anatomic Hernia
Testis (undescended, retracted)
Epididymal cyst
Spermatocele
Hydrocele
Embryological remnants (mucocele)
Traumatic Hematoma
Aneurysm (complication of catheterization)
Hematoma Hematoma

Locations of Groin Masses: 9

Locations of groin masses

References:

  1. Amerson JR. Inguinal Canal and Hernia Examination. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 96. Available from: http://www.ncbi.nlm.nih.gov/books/NBK423/
  2. Aguirre, D. A., Casola, G., & Sirlin, C. (2004). Abdominal Wall Hernias: MDCT Findings. American Journal of Roentgenology, 183(3), 681–690. doi:10.2214/ajr.183.3.1830681
  3. Guillem, P., Czarnecki, E., Duval, G., Bounoua, F., & Fontaine, C. (2002). Lumbar hernia: anatomical route assessed by computed tomography. Surgical and radiologic anatomy : SRA, 24(1), 53–56.
  4. Roberts, J. R., & Hedges, J. R. (2010). Clinical procedures in emergency medicine. (5th ed., Vol. section 7, p. Ch. 44). W B Saunders Co. Retrieved from http://www.mdconsult.com/books/page.do?eid=4-u1.0-B978-1-4160-3623-4.00044-4
  5. Shadbolt, C. L., Heinze, S. B., & Dietrich, R. B. (2001). Imaging of groin masses: inguinal anatomy and pathologic conditions revisited. Radiographics : a review publication of the Radiological Society of North America, Inc, 21 Spec No, S261–71.
  6. Eyre, RC. Evaluation of nonacute scrotal pathology in adult men. In: UpToDate, Rose, BD (Ed), UpToDate, Waltham, MA, 2013.
  7. Foster, D. C. (2002). Vulvar disease. Obstetrics and gynecology, 100(1), 145–163.
  8. Tappouni, R. F., Sarwani, N. I., Tice, J. G., & Chamarthi, S. (2011). Imaging of unusual perineal masses. American Journal of Roentgenology, 196(4), W412–20. doi:10.2214/AJR.10.4728
  9. Collins, R. (2008). Differential diagnosis in primary care. Philadelphia: Lippincott Williams & Wilkins.

Skull Fracture

Frontal bone fractureID:

14 year-old female, previously healthy, brought in by ambulance s/p auto vs. pedestrian.

HPI:

Incident unwitnessed, paramedics report no LOC with GCS 15 at scene. GCS 10 upon arrival to ED, with 2min GTC seizure. Patient intubated for airway protection and CT head showed non-displaced frontal bone fracture and small frontal SAH. Patient self-extubated, returned to baseline mental status and was transferred to PICU.

PE:

  • VS: 128/76mmHg, 120bpm, 22 R/min, 100% RA, 37.6°C
  • General: Alert and responsive young female with multiple bandages on extremities
  • HEENT: Right frontal hematoma, no bony defect palpated, multiple facial abrasions, no otorrhea, no rhinorrhea, TM clear b/l, no other ecchymosis.
  • CV: RRR, normal S1/S2, no M/R/G
  • Lungs: CTAB
  • Abdomen: +BS, soft, NT/ND, no rebound/guarding, no flank ecchymoses
  • Neuro: AAOx3, CN II-XII intact, sensation/motor/reflexes symmetric and intact.
  • Extremities: Well-perfused with good pulses, no focal bony tenderness, no joint effusions, multiple abrasions on extensor surfaces of all four extremities.

Assessment & Plan:

14yo female, previously healthy, s/p auto vs. peds followed by GTC seizure and CT head showing small SAH and non-displaced frontal bone skull fracture. No evidence of basilar skull fracture on examination or imaging. Seizure likely 2/2 irritation from SAH. Patient was followed closely in PICU with q1h neuro checks with low threshold for repeat CT if change in mental status or more seizures occurred. The patient was eventually transferred to the general ward and was discharged with neurology follow-up and Keppra for seizure prophylaxis for 6mo.

Types of Skull Fractures:

A system for skull fractures

Sore Throat

Oropharynx AnatomyID:

17 year-old female presenting to the pediatric ED with sore throat for 2 days.

HPI:

The patient reports steadily worsening sore throat over the past 2 days, associated with a sensation of swelling. The pain is described as sharp, 4/10 in severity, located on the left side of her throat, and worsened with swallowing. She denies inability to swallow or difficulty breathing, she also denies fever, cough, new skin rashes or genital lesions.

She has no PMH/PSH, takes no medications, denies t/e/d use and is not currently sexually active.

PE:

  • VS: 111/65mmHg, 80bpm, 97.8°, 16/min, 100% RA
  • Gen: Well-appearing, NAD
  • HEENT: PERRL, no conjunctival injection, TM clear b/l, minimal pharyngeal erythema on left with 6mm white circular lesion on left tonsil, no tonsillar enlargement, no uvular deviation, no cervical LAD, neck supple no masses, normal neck ROM
  • CV: RRR, no M/R/G, Lungs: CTAB
  • Abdomen: +BS, soft, NT/ND
  • Ext: Warm, well-perfused, normal peripheral pulses

Assessment & Plan:

17yo female with no significant PMH with acute pharyngitis for 2 days. The most likely cause of the patient’s symptoms is viral pharyngitis, potentially herpangina (given the appearance of the tonsillar lesion). A more serious viral/bacterial pharyngitis is less likely given the absence of fever or significant erythema/exudate. There was no uvular deviation to suggest peritonsillar abscess and no evidence of airway obstruction to suggest other acute processes (epiglottitis, retropharyngeal abscess). The plan is to recommend supportive care and ibuprofen for symptomatic relief. The patient will be discharged home in good condition with precautions to return if symptoms worsen or she begins to have difficulty swallowing/breathing.

Differential Diagnosis of Acute Pharyngitis:

Acute Pharyngitis

 

Evaluation (history):

  • Respiratory distress: epiglottitis, retropharyngeal abscess, peritonsillar abscess, EBV (obstruction in or near pharynx)
  • Fatigue: infectious mononucleuosis
  • Abrupt onset: epiglottitis

Evaluation (physical examination):

  • Vesicles anterior: herpetic stomatitis, SJS, Behcet
  • Vesicles posterior: herpangina (± involvement of extremities)
  • Asymmetry: peritonsillar abscess
  • Stridor, drooling, respiratory distress: airway obstruction
  • Generalized inflammation: Kawasaki