A 33 year-old female with a history of idiopathic intracranial hypertension and ventriculoperitoneal shunt placement presents with headache and confusion. She denies fever, trauma, neck pain or stiffness. She has not had symptoms like this since her shunt was placed 2 years ago. Imaging was obtained which showed ventriculomegaly and a fracture of the shunt at the level of the cervical spine. Neurosurgery was consulted and the patient was admitted for shunt repair.

• CT Head
• XR Shunt Series

CT Head

Ventriculomegaly with dilatation of the temporal horns in particular. Right parietal approach ventricular drain. Case courtesy of Dr. Henry Knipe, Radiopaedia.org, rID: 39615

XR Shunt Series

Shunt tubing fractured at the level of the upper cervical spine

An Algorithm for CSF Shunt Complications

References:

1. Madsen MA. Emergency department management of ventriculoperitoneal cerebrospinal fluid shunts. Ann Emerg Med. 1986;15(11):1330-1343.
2. Ferras M, McCauley N, Stead T, Ganti L, Desai B. Ventriculoperitoneal shunts in the emergency department: a review. Cureus. 2020;12(2):e6857.
3. Paff M, Alexandru-Abrams D, Muhonen M, Loudon W. Ventriculoperitoneal shunt complications: A review. Interdisciplinary Neurosurgery. 2018;13:66-70.
4. Pitetti R. Emergency department evaluation of ventricular shunt malfunction: is the shunt series really necessary? Pediatr Emerg Care. 2007;23(3):137-141.
5. Fowler JB, De Jesus O, Mesfin FB. Ventriculoperitoneal Shunt. [Updated 2021 Feb 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK459351/
6. Broggi M, Zattra CM, Schiariti M, et al. Diagnosis of ventriculoperitoneal shunt malfunction: a practical algorithm. World Neurosurg. 2020;137:e479-e486.

The post CSF Shunt Complications appeared first on Differential Diagnosis of.

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.

Assessment/Plan:

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

Hospital Course:

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

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

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

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

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

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

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

Spinal Epidural Abscess (SEA)¹

Risk factors:

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

Organism:

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

Staging:

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

Clinical features:

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

Diagnosis:

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

Prevalence of abnormal physical findings ²

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:

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)

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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

History

Points suggestive of seizure over alternative process

Abrupt onset

Duration < 120s

LOC

Purposeless activity: automatisms, tonic-clonic

Provocation: fever in children, substance withdrawal

Postictal state

Retrograde amnesia

Incontinence, oral trauma (buccal maceration, tongue laceration)

Rapidly resolving lactic acidosis

Important historical points for patients with seizure history

Recent illness

Medications (adherence, changes, interactions)

Substance use

Ictogenic factors

Recent/remote head trauma

Developmental abnormalities

Substance use

Sleep deprivation

Pregnancy

Key Physical Examination Findings

• Vital sign abnormalities persisting beyond immediate postictal state (may suggest drug/toxin exposure, CNS lesion)
• Nuchal rigidity
• Signs of IVDA
• Sequela
  • Head trauma
  • Tongue laceration
  • Shoulder dislocation (posterior)
• Neurological exam
  • Stroke
  • Elevated ICP
  • Failure to note improvement in postictal confusion (encephalopathy, subclinical seizures)

Labs

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

Indications for Imaging

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

References

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

The post Seizure appeared first on Differential Diagnosis of.

Motor Neuron Signs

Upper Motor Neuron:

Spasticity

Hyperreflexia

Pronator drift

Babinski

Lower Motor Neuron:

Flaccidity

Hyporeflexia

Fasciculation

Atrophy

Causes of Weakness

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

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

The post Weakness appeared first on Differential Diagnosis of.

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

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

References

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

The post Severe Traumatic Brain Injury appeared first on Differential Diagnosis of.

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.

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

HPI:

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

PE:

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

Assessment & Plan:

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

Types of Skull Fractures:

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