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.



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


  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.



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


  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
Superficial partial-thickness Scald (splash)
Short flash
Blisters, moist, red
Painful to temperature/air
Deep partial-thickness Scald (spill)
Flame, oil, grease
Blisters, waxy dry, white/red
Full-thickness Scald (immersion)
Flame, steam, oil, grease, chemical, electrical
Waxy white, leathery grey, black
Deep pressure

Estimating Burn Surface Area


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


  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)


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.


  • CBC: 24.2/14.4/43.4/202
  • Wound culture: MSSA

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


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.


  • 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


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

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.


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


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


  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%)


  • 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


  • 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.


  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

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
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
Medications (particularly anti-coagulants)
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.


  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


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

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


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

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


  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:

Stiffness, limitation of extension suggestive of retropharyngeal abscess.
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.
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.
Presence of conjunctivitis (also rhinorrhea, exanthema) associated with viral pharyngitis.
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.
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%


  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
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
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


  • 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

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


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
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


  • Glucose
  • CBC/Chemistry
  • ECG


  • Warranted if findings concerning for central process
  • MRI preferred


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


  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.



Pathologic neuronal activation leading to abnormal function
Recurrent unprovoked seizures


  • 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


Points suggestive of seizure over alternative process
Abrupt onset
Duration < 120s
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

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)


  • 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


  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


View Algorithm
There is a ddxof algorithm for the evaluation of weakness. View it here.

Motor Neuron Signs

Upper Motor Neuron:
Pronator drift
Lower Motor Neuron:

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
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


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


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


  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


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


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


  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


  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


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.



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.

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


  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)


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.


  • Diabetes mellitus, diagnosed 8yrs ago


  • None


  • Non-contributory


  • 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.


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



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.


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


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.


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)


  • 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
Hb 11-13.5
Na <135 2
Creatinine >1.6 2
Glucose >180 1

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


  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


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.



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).


  • Parkinson Disease
  • HTN




No family history of angioedema


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


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



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


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


  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


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).








Worked in construction for 20yrs





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



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


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
Acute Otitis Media

Differential Diagnosis of Hearing Loss4

Differential Diagnosis of Hearing Loss

Differential Diagnosis of Tinnitus5

Differential Diagnosis of Tinnitus


  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


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.




Cesarean x2, L salpingoophorectomy




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





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.


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


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.


  • Hepatitis C
  • COPD


  • Hysterectomy




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


  • Methadone
  • Elavil
  • Multiple unknown inhaled medications


  • Naproxen (swelling)

Physical Exam:

Gen: WA, NAD
Head: NC/AT
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


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


  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.