Spontaneous Intracranial Hemorrhage

Brief HPI

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

Imaging

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

References

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

Portal Venous Gas

Brief HPI

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

Imaging

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

References

Rabou Ahmed A and Frank Gaillard. “Pneumobilia.” Radiopaedia. http://radiopaedia.org/articles/pneumobilia.
Morgan Matt A and Donna D’Souza. “Portal venous gas.” Radiopaedia. http://radiopaedia.org/articles/portal-venous-gas
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.
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

Assessment of Burn Depth

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

Estimating Burn Surface Area

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

References

Monafo WW. Initial management of burns. N Engl J Med. 1996;335(21):1581–1586. doi:10.1056/NEJM199611213352108.
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.
Singer AJ, Della-Giustina D. Thermal Burns: Rapid Assessment and Treatment. Emergency Medicine Practice; 2000.
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)
Gauglitz, GG. Overview of the management of the severely burned patient. In: UpToDate, Jeschke MG (Ed), UpToDate, Waltham, MA. (Accessed on March 29, 2016)

Epiglottitis

Brief H&P:

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

Labs

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

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

Spinal Epidural Abscess

Case Presentation

HPI:

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

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

Labs:

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

Radiology

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

MRI Lumbar Spine w/contrast

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

Assessment/Plan:

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

Hospital Course:

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

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

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

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

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

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

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

Spinal Epidural Abscess (SEA)¹

Risk factors:

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

Organism:

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

Staging:

Back pain at affected site
Nerve root pain from affected level
Weakness, sensory deficit, bladder/bowel dysfunction
Paralysis

Clinical features:

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

Diagnosis:

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

Prevalence of abnormal physical findings ²

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

Clinical Decision Guideline ³

Management:

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

References:

Darouiche RO. Spinal epidural abscess. N Engl J Med. 2006;355(19):2012–2020. doi:10.1056/NEJMra055111.
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.
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.
WikEM: Epidural abscess (spinal)

Back Pain

Causes of Back Pain

Key Historical Findings

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

Key Physical Findings

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

References

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

Aortic Dissection

Imaging

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

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

Sore Throat

Evaluation of Sore Throat

Physical Examination:

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

Centor Criteria (Modified)

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

Incidence of GABHS by Centor Criteria

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

References:

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.
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

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

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

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

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
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

Management of Seizures

Medications for Treatment of Seizures

Medication	Dose (adult)	Dose (peds)	Comment
1^st 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
2^nd Line
Fosphenytoin	20mg PE/kg IV
Phenytoin	20mg/kg IV		May cause hypotension
3^rd 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

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
WikEM: Seizure

Weakness

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

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

References

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

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

Terms Describing Eye Position

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

Algorithm for the Evaluation of Diplopia ²

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
INO	Limited adduction (exotropia)	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

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
Borooah, S., Wright, M., & Dhillon, B. (2011). Pocket Tutor Ophthalmology. JP Medical Limited. Retrieved from https://books.google.com/books?id=z\_CfWj8-ftoC
Dinkin, M. (2014). Diagnostic approach to diplopia. Continuum (Minneapolis, Minn.), 20(4 Neuro-ophthalmology), 942–965. doi:10.1212/01.CON.0000453310.52390.58
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
Friedman, D. I. (2010). Pearls: diplopia. Seminars in neurology, 30(1), 54–65. doi:10.1055/s-0029-1244995
Guluma, K. (2013). Diplopia. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 176-183). Elsevier Health Sciences.
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	Associated with trauma, coagulopathy, hypertension.	Unilateral, sharply circumscribed	Unaffected	None	Unaffected	Clear
Blepharitis	Acute/chronic inflammation of eyelid.	Diffuse	Unaffected	Foreign body sensation	Unaffected	Clear
Epislceritis	Recurrent, self-limited episodes, possible autoimmune association.	Engorged, radially-oriented vessels	Unaffected	Mild	Unaffected	Clear
Scleritis	Vascular or connective tissue disease.	Focal or diffuse, pink sclera	Unaffected	Moderate	Reduced	Clear
Acute angle-closure glaucoma	Mydriasis leading to decreased outflow of aqueous humor.	Circumcorneal injection	Semi-dilated	Severe	Reduced	Hazy
Acute anterior uveitis	Inflammation of iris or ciliary body.	Circumcorneal injection	Constricted	Moderate	Reduced	Hazy
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

References

Teoh, D. L., & Reynolds, S. (2003). Diagnosis and management of pediatric conjunctivitis. Pediatric emergency care, 19(1), 48–55.
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
Cronau, H., Kankanala, R. R., & Mauger, T. (2010). Diagnosis and management of red eye in primary care. American family physician, 81(2), 137–144.
Leibowitz, H. M. (2000). The red eye. New England Journal of Medicine, 343(5), 345–351. doi:10.1056/NEJM200008033430507
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
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

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 Injury^1,2

References

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
Stocchetti, N., & Maas, A. I. R. (2014). Traumatic intracranial hypertension. The New England journal of medicine, 370(22), 2121–2130. doi:10.1056/NEJMra1208708
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

Calf cellulitis and gas-producing cellulitis in the lateral foot and toes.
Thigh and inguinal lymphadenopathy.
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

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:

Morchi, R. (2/18/14). Emergency Medicine Procedures Cadaver Lab. Clinical Clerkship at UCLA. Los Angeles, CA.
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
Headley, A. J. (2003). Necrotizing soft tissue infections: a primary care review. American family physician, 68(2), 323–328.
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.
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)

- 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)

- 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)

- 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

HPI:

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

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 Factors^2,5,6

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 antagonist^10,11

References:

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
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
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.
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
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.
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
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
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.
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
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
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: 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

External Auditory Canal: in acute otitis externa, the canal will be narrowed, swollen and erythematous
Tympanic Membrane: use cone of light for orientation, identify malleus and move speculum to visualize all four quadrants

Differential Diagnosis of Hearing Loss⁴

Differential Diagnosis of Tinnitus⁵

References:

Tarlow, M. (1998). Otitis media: pathogenesis and medical sequelae. Ear, nose, & throat journal, 77(6 Suppl), 3–6.
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.
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.
Isaacson, J. E., & Vora, N. M. (2003). Differential diagnosis and treatment of hearing loss. American family physician, 68(6), 1125–1132.
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.

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:

Physiology of Voice Production: ¹

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

Adequate Air Stream
Smooth vocal fold edges
Vocal folds with normal vibratory properties
Appropriate vocal fold positioning

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

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:

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
Feierabend, R. H., & Shahram, M. N. (2009). Hoarseness in adults. American family physician, 80(4), 363–370.
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
Bruch, J.W., Kamani D.V. Diaphragmatic pacing. In: UpToDate, Basow, DS (Ed), UpToDate, Waltham, MA, 2013.
Rosen, C. A., Anderson, D., & Murry, T. (1998). Evaluating hoarseness: keeping your patient’s voice healthy. American family physician, 57(11), 2775–2782.

Brief HPI

Imaging

CT Head non-contrast

ED Course

Management of Supratherapeutic INR and Complications of Anti-Coagulation

References

Brief HPI

Imaging

CT Abdomen/Pelvis with Contrast

Differentiation between Portal Venous Gas and Pneumobilia

References

ED Presentation

Algorithm for the Management of Severe Burns

Assessment of Burn Depth

Estimating Burn Surface Area

Burn Transfer Criteria

See Also

References

Brief H&P:

Labs

CT Neck/Soft Tissue with Contrast

ED/Hospital Course

Evaluation of Sore Throat – Applied

Case Presentation

HPI:

Labs:

Radiology

MRI Lumbar Spine w/contrast

Assessment/Plan:

Hospital Course:

Spinal Epidural Abscess (SEA)1

Risk factors:

Organism:

Staging:

Clinical features:

Diagnosis:

Prevalence of abnormal physical findings 2

Clinical Decision Guideline 3

Management:

References:

Causes of Back Pain

Key Historical Findings

Key Physical Findings

References

Imaging

CT Angiography Aorta

Mediastinum Anatomy

Mediastinal Masses

References:

Evaluation of Sore Throat

Physical Examination:

Centor Criteria (Modified)

Incidence of GABHS by Centor Criteria

References:

Types of Dizziness

Distinguishing Central vs. Peripheral Vertigo

Causes of Vertigo

Characteristics of common causes of vertigo

History

Key Physical Examination Findings

Positional Testing

HINTS1

HINTS Gallery

Labs

Imaging

Management

References

Definition

Classification

Causes of Seizures

Management of Seizures

Medications for Treatment of Seizures

History

Key Physical Examination Findings

Labs

Indications for Imaging

References

Motor Neuron Signs

Causes of Weakness

Weakness Syndromes

Spinal Epidural Abscess (SEA)¹

Prevalence of abnormal physical findings ²

Clinical Decision Guideline ³

HINTS¹

Evaluation of Diplopia ¹

Algorithm for the Evaluation of Diplopia ²

Causes of Diplopia ^3,4,5,6

Differential diagnosis of Conjunctivitis ^1,2,3

Differential Diagnosis of Red Eye ^4,5

Algorithm for the Evaluation of the Red Eye ⁶

Algorithm for the Management of Severe Traumatic Brain Injury^1,2

Skin and soft-tissue layers and their infections: ¹

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

LRINEC score ⁵