Weakness

Motor Neuron Signs

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

Causes of Weakness

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

Weakness Syndromes

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

Review of Spinal Cord Anatomy

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

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

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

References

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

Fever

Causes of Fever

Causes of Fever

Key Features

  • Morbidity and mortality increase with age and comborbidities
  • Most common sources in elderly: respiratory, genitourinary, skin/soft-tissue
  • Atypical presentations: functional decline, altered mental status

Immediate Evaluation and Management

  • Critical Findings

    • Altered mental status
    • Respiratory distress
    • Hemodynamic instability
  • Critical Interventions

    • Airway management, supplemental O2
    • Cardiac monitoring
    • Fluid resuscitation
    • Empiric antibiotics
    • Cooling measures (T>41.0°C)

Pathophysiology of Fever

Production of endogenous or exogenous pyrogens
Increase temperature set point in hypothalamus
Patient experiences chills when core temperature < set point
Vasoconstriction, shivering causes fever
Patient experiences euthermia, though may feel malaise, fatigue
Resolution
Patient experiences sweats until core temperature returns to normal set point

References

  1. Blum, F., & Biros, M. (2013). Fever in the Adult Patient. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 119-123). Elsevier Health Sciences.

ECG Guide

The format of this article is atypical for the structure and concept of the website – but it’s always been about learning. Here is a simplified guide to ECG interpretation with a focus on the aspects I find more challenging to understand or recall.

Grid and Leads

The ECG grid
Limb leads
Precordial Leads

Axis

ECG axes

Atrial Enlargement

Atrial enlargement

Normal:
First portion of deflection is RA, second is LA
Right Atrial Enlargement:
P-wave amplitude > 2.5mm in inferior leads
Normal duration P-wave
Left Atrial Enlargement:
P-wave duration increased (terminal negative portion >0.04s)
Amplitude of terminal negative component >1mm below isoelectric line in V1

Ventricular Hypertrophy

Right Ventricular Hypertrophy:
Right axis deviation
Abnormal R-wave progression

  • Increased R-wave amplitude in leads overlying the right ventricle (V1)
  • Increased S-wave amplitude in leads overlying the left ventricle (V6)
Criteria

  • V1: R>S
  • V6: S>R
Left Ventricular Hypertrophy:
Left axis deviation
Increased R-wave amplitude in leads overlying the LV (I, aVL, V5, V6)
Increased S-wave amplitude in leads overlying the RV (V1)
Criteria:

  • Precordial Leads
    • R-wave in V5/V6 + S-wave in V1/V2 > 35mm
    • R-wave in V5 > 26mm
    • R-wave in V6 > 20mm
  • Limb Leads
    • R-wave in aVL > 11mm
    • R-wave in aVF > 20mm
  • Combined
    • R-wave in aVL + S-wave in V3 > 20mm (F), 28mm (M)

Secondary Repolarization Abnormalities

Secondary repolarization abnormality

  • Downsloping ST-segment depression
  • Asymmetric T-wave inversion

Bundle Branch Blocks

Left Bundle Branch Block

Left bundle branch block

  • QRS duration > 0.12s (3 boxes)
  • Broad or notched R-wave with prolonged upstroke in I, aVL, V5, V6
  • Associated ST-segment depression and T-wave inversion
  • Reciprocal changes in V1, V2 (deep S-wave)
  • Possible LAD

Right Bundle Branch Block

Right bundle branch block

  • QRS duration > 0.12s (3 boxes)
  • RSR’ in V1, V2
  • Reciprocal changes in I, aVL, V5, V6 (deep S-wave)

Hemiblocks

His-Purkinje system and hemiblocks (anterior fascicular block, posterior fascicular block)

Other Blocks

  • Non-specific intraventricular conduction delay: QRS >0.10s without BBB
  • Incomplete BBB: LBBB/RBBB pattern with non-prolonged QRS
  • Bifascicular block: RBBB + LAFB/LPFB (by axis deviation)

Ischemia and Infarction

ECG changes associated with ischemia and infarction

  1. Hyperacute T-waves
  2. T-wave inversion: Symmetric, compared to TWI associated with repolarization abnormalities
  3. ST-elevation: Unlike J-point elevation, ST-segment merges with T-wave
  4. Q-waves
    1. Duration > 0.04s
    2. Amplitude > 1/3 R-wave
    3. Normal in aVR

Coronary Artery Territories

Coronary artery territories

Distribution Coronary Artery Leads Reciprocal Changes
1. Inferior RCA, PDA II, III, aVF Anterior, Lateral
2. Lateral LCx I, aVL, V5, V6 Inferior
3. Anterior LAD V1-V6 Inferior
4. Posterior RCA Posterior Anterior (esp. V1)

External Links

Diplopia

History and Physical

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

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

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

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

Evaluation of Diplopia 1

History

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

Terms Describing Eye Position

Terms describing eye position

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

Algorithm for the Evaluation of Diplopia 2

Algorithm for the Evaluation of Diplopia

Causes of Diplopia 3,4,5,6

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

(esotropia)

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

(exotropia)

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

References

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

Anemia

HPI

70M with a history of dementia presenting with 3 days of fatigue. The patient was unable to provide detailed history, however family members reported worsening fatigue with the patient requiring assistance with ambulation for several days. The patient was referred from an outside clinic after point-of-care hemoglobin of 6.7. No reported history of anemia, and no history suggestive of obvious external bleeding.

Vital signs stable, tachycardia and tachypnea noted with minimal exertion but saturating well on ambient air and in no acute distress. Examination notable for conjunctival pallor without scleral icterus, systolic flow murmur, brown stool guaiac negative.

CBC with hemoglobin of 7.5 , MCV 80.3 , RDW 22.4 , no leukocytosis and normal platelets. Also noted was an alkaline phosphatase of 828 , normal total and direct bilirubin, and undetectable serum troponin. Chest x-ray showed a possible pleural-based mass.

The patient was transfused two units of PRBC’s and admitted for further evaluation. CT chest/abdomen/pelvis revealed sternal and rib-based pleural soft-tissue mass, prostate mass, pelvic and retroperitoneal lymphadenopathy as well as extensive bony metastatic disease consistent with primary prostate cancer with diffused metastasis. Serum PSA was 2,087 . Iron studies suggested anemia of chronic disease. Reticulocytes were not obtained but may have suggested inadequate production index given extensive bony metastases and possible associated myelosuppression. The patient was symptomatically improved after transfusion and discharged with outpatient follow-up for discussions regarding possible biopsy and treatment.

Images

Chest x-ray with pleural-based mass

Areas of pleural thickening. Possible pleural based mass in left mid lung.

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CT Chest: Lung Window

  • Rib-based pleural soft tissue masses.
  • Large 5.6 x 4.4cm anterior sternal soft-tissue mass.
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CT Body: Bone Window

  • Extensive bony metastatic disease.
  • Prostate mass, large pelvic and retroperitoneal lymphadenopathy.
  • Consistent with primary prostate cancer with diffuse metastasis.

Algorithm for the Evaluation of Anemia 1,2

Algorithm for the Evaluation of Anemia

References:

  1. Zaiden R, Rana F. Evaluation of Anemia. BMJ Best Practice. Oct 2014. http://us.bestpractice.bmj.com/best-practice/monograph/93/overview.html. Last accessed 15 May 2015.
  2. Janz, T. G., Johnson, R. L., & Rubenstein, S. D. (2013). Anemia in the emergency department: evaluation and treatment. Emergency medicine practice, 15(11), 1–15– quiz 15–6.
  3. WiKEM: Anemia

Conjunctivitis and the Red Eye

Differential diagnosis of Conjunctivitis 1,2,3

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

Differential Diagnosis of Red Eye 4,5

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

Algorithm for the Evaluation of the Red Eye 6

Algorithm for the Evaluation of the Red Eye

References

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

Severe Traumatic Brain Injury

HPI:

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

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

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

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

Images

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CT head without contrast one hour after presentation

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

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

Algorithm for the Management of Severe Traumatic Brain Injury1,2

Algorithm for the Management of Severe Traumatic Brain Injury

References

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

Lactic Acidosis

HPI:

59F with a reported history of congestive heart failure, presenting with intermittent chest discomfort for three days.

She characterized this discomfort as “heartburn”, describing a mid-epigastric burning sensation radiating up her neck, not associated with exertion, lasting 1-2 hours and resolving with antacids. The patient has poor exercise tolerance at baseline and for the past several years has been able to ambulate only short distances around her home, and states that these symptoms have been worsening in the past week. She denies chest pain on exertion, orthopnea or paroxysmal nocturnal dyspnea. She states that she was diagnosed with congestive heart failure five years ago, but was never prescribed medications.

On further questioning, the patient reports several weeks of mouth and lip pain which has limited oral intake, though no dysphagia to solids or liquids. She otherwise denies fevers/chills, abdominal pain, nausea/vomiting, cough, changes in urinary or bowel habits.

In the emergency department, the patient was noted to have an elevated serum troponin, though ECG showed no changes of acute ischemia/infarction.

PMH:

  • Congestive heart failure

PSH:

  • None

FH:

  • Mother with diabetes
  • Father with MI at age 65

SHx:

  • 4-5 drinks of alcohol/day
  • No tobacco or drug use

Meds:

  • None

Allergies:

NKDA

Physical Exam:

VS: T 37.4 HR 106 RR 18 BP 145/82 O2 100% RA
Gen: Morbidly obese female, lying in bed, in no acute respiratory distress, speaking in complete sentences.
HEENT: Dry, cracked lips, slightly erythematous, otherwise moist mucous membranes, poor dentition. Mild scleral icterus. No cervical lymphadenopathy.
CV: Rapid rate, regular rhythm, normal S1/S2, II/VI systolic ejection murmur at LUSB, no radiation appreciated. No jugular venous distension.
Lungs: Clear to auscultation in posterior lung fields bilaterally, no crackles appreciated.
Chest: Well-circumscribed erythematous patch in folds beneath left breast, no underlying fluctuance, no significant tenderness to palpation. On contralateral breast, some hyperpigmentation but no erythema.
Abdomen: Obese, non-tender, non-distended. Patch of erythema below pannus, mildly tender to palpation.
Ext: Bilateral lower extremities with marked edema and overlying scaly plaques, some slightly ulcerated weeping serous fluid. Peripheral pulses are difficult to palpate, capillary refill difficult to assess.

Labs/Studies:

  • CBC: 11.1/11.1/34.5/212 (MCV 114.2)
  • BMP: 140/4.5/97/20/10/1.14/64
  • Anion Gap: 23
  • LFT: AST: 73, ALT: 26, AP: 300, TB: 4.6, DB: 2.1, Alb: 3.0, INR 1.3
  • BNP: 158
  • Troponin: 1.284
Sinus tachycardia, LVH, secondary repolarization abnormalities

Sinus tachycardia, LVH, secondary repolarization abnormalities

Imaging:

CT Pulmonary Angiography:
No evidence of central pulmonary embolism, thoracic aortic dissection, or thoracic aortic aneurysm. Evaluation of the peripheral vessels is limited due to motion artifact. No focal consolidation or pneumothorax.

CT Abdomen/Pelvis non-contrast:
No evidence of intra-abdominal abscess or definite source of infection. Marked hepatic steatosis.

CT Lower Extremity non-contrast:
Diffuse circumferential subcutaneous edema involving both lower extremities from the level of the mid thighs distally through the feet. There are bilateral subcutaneous calcifications which are likely venous calcifications in the setting of chronic venous stasis disease. There is some overlying skin thickening.

TTE:
There is moderate concentric left ventricular hypertrophy with hyperdynamic LV wall motion. The Ejection Fraction estimate is >70%. Grade I/IV (mild) LV diastolic dysfunction. No hemodynamically significant valve abnormalities.

US Abdomen:
Hepatomegaly, echogenic liver suggesting fatty infiltration. Moderately blunted hepatic vein waveforms suggesting decreased hepatic parenchymal compliance.

Assessment/Plan:

The patient was admitted to the cardiology service for management of NSTEMI and evaluation of undiagnosed CHF. She was started on a heparin continuous infusion. In addition, a CT pulmonary angiogram was obtained to evaluate for pulmonary embolism as an explanation of her progressive dyspnea on exertion. No PE, consolidation or effusion was identified.

Despite the patient’s reported history of congestive heart failure, there was no evidence that her symptoms were a result of an acute exacerbation with only a mildly elevated BNP but no jugular venous distension or evidence of pulmonary edema. The patient’s significant lower extremity edema was more suggestive of chronic venous stasis.

One notable laboratory abnormality that was explored was her elevated anion gap metabolic acidosis. Studies submitted included serum lactate, salicylates, osmolarity, CK, and urinalysis for ketonuria. This evaluation was notable for an elevated serum lactate of 13.2mmol/L and an arterial blood gas that showed adequate respiratory compensation (and no A-a gradient). Given the patient’s modest leukocytosis (with neutrophil predominance), and tachycardia, the concern for sepsis was increased though the source remained unclear. Prominent possibilities included a skin and soft-tissue infection vs. less likely intra-abdominal source though the patient’s physical examination was not suggestive of a process that would produce such a substantial lactic acidosis. Blood cultures were drawn and the patient was started on empiric antibiotics for the suspected sources. In addition, the patient was cautiously volume resuscitated given her reported history of CHF while pending a transthoracic echocardiogram to evaluate cardiac function. Additional imaging including CT abdomen/pelvis and lower extremities was obtained (though without contrast due to the patient’s recent exposure), and no obvious source was identified.

Over the next two days, the patient’s serum lactate downtrended to normal range, as did the serum troponin. A transthoracic echocardiogram showed an LVEF >70% with mild concentric hypertrophy and diastolic dysfunction. Blood and urine cultures were without growth.

Additional issues managed during the hospitalization included elevated serum transaminases (AST > ALT), conjugated hyperbilirubinemia and evidence of decreased hepatic synthetic function with hypoalbuminemia and elevated INR. Given the patient’s history of EtOH use, as well as other corroborating findings including macrocytic anemia, hypomagnesemia, folate and B12 deficiency, this was attributed to alcoholic hepatitis (discriminant function <32). Infectious hepatitis serologies were negative. The patient was started on nutritional supplements. Finally, the patient persistently complained of lip and oral mucosal pain. Examination was without discrete lesions but some mucosal redness was identified. Despite poor dentition, there was no evidence of abscess and HSV/HIV testing was negative. This was thought to be stomatitis caused by her identified nutritional deficiencies.

Differential Diagnosis of Elevated Serum Lactate 1,2

Differential Diagnosis of Elevated Serum Lactate

Algorithm for Evaluation of Acidemia 3,4

Algorithm for Evaluation of Acidemia

Algorithm for Evaluation of Alkalemia 3,4

Algorithm for Evaluation of Alkalemia

References:

  1. Fall, P. J., & Szerlip, H. M. (2005). Lactic acidosis: from sour milk to septic shock. Journal of intensive care medicine, 20(5), 255–271. doi:10.1177/0885066605278644
  2. Luft, F. C. (2001). Lactic acidosis update for critical care clinicians. Journal of the American Society of Nephrology : JASN, 12 Suppl 17, S15–9.
  3. Ingelfinger, J. R., Berend, K., de Vries, A. P. J., & Gans, R. O. B. (2014). Physiological Approach to Assessment of Acid–Base Disturbances. The New England journal of medicine, 371(15), 1434–1445. doi:10.1056/NEJMra1003327
  4. Ingelfinger, J. R., & Seifter, J. L. (2014). Integration of Acid–Base and Electrolyte Disorders. The New England journal of medicine, 371(19), 1821–1831. doi:10.1056/NEJMra1215672

Pleural Effusion

HPI:

64F with a history of CAD, MI, CHF, CLL and rheumatoid arthritis who presented to the emergency department after transfer from a rehabilitation facility for respiratory distress. The patient reported several days of progressive shortness of breath with dyspnea on exertion. She also noted some associated orthopnea and lower extremity edema. The patient was recently hospitalized for similar symptoms and was diagnosed with CHF at the time. At the rehab facility, the patient became hypoxemic and hypertensive, reporting shortness of breath and chest pain prior to presentation.

Hospital Course:

The patient was initially managed with BiPAP and nitroglycerin continuous infusion, but was then stable on supplemental O2 via nasal cannula and was transitioned to long-acting nitrates and anti-hypertensives. The patient’s hypoxemic respiratory failure was initially attributed to acute exacerbation of left-ventricular heart failure, and the patient was managed with spot diuresis. However, there was no symptomatic improvement and the patient became hypernatremic so diuresis was held as alternative diagnoses were explored.

A transthoracic echocardiogram showed preserved LVEF (50-55%), but some diastolic dysfunction and elevated PAP/RAP. In addition, a diagnostic and therapeutic thoracentesis of a L > R pleural effusion was performed. Pleural fluid studies were suggestive of a transudative process, though with some abnormal characteristics (including lymphocyte predominance, as well as presence of signet cells).

Rheumatology and pulmonology services were consulted for input and recommendations for further evaluation were appreciated. Per rheumatology, the patient’s diagnosis of rheumatoid arthritis may not be consistent with her presentation or prior serologic studies. Her pleural fluid analysis was also not consistent with rheumatoid disease. According to pulmonary consult, the patient’s hypoxemia remains most consistent with left ventricular dysfunction though primary pulmonary processes cannot be excluded (and would warrant further evaluation with imaging and pulmonary function testing).

PMH:

  • CHF
  • CAD
  • CVA
  • Myocardial Infarction
  • HTN
  • Hypothyroidism
  • CLL
  • Anemia

PSH:

  • TAH-BSO

FH:

  • No family history of autoimmune disease.
  • Mother: DM

SHx:

  • Denies tobacco/EtOH/drug use
  • Lives at home, at SNF since discharge

Meds:

  • Furosemide 20mg p.o. daily
  • Gabapentin 300mg p.o. t.i.d.
  • Hydralazine 50mg p.o. t.i.d.
  • Hydrochlorothiazide 25mg p.o. b.i.d.
  • Hydroxychloroquine 200mg p.o. daily
  • Levothyroxine 25mcg p.o. daily
  • Minoxidil 2.5mg p.o. b.i.d.
  • Pantoprazole 40mg p.o. daily
  • Prednisone 15mg p.o. daily

Allergies:

  • Shellfish
  • Physical Exam:

    VS: T 37.2 HR 84 RR 15 BP 147/75 O2 97% 4LNC
    Gen: Elderly female, alert and oriented to self and place, responding appropriately to questions.
    HEENT: Mucous membranes moist, sclera anicteric, no cervical lymphadenopathy.
    CV: Regular rate and rhythm, normal S1/S2, no additional heart sounds. III/VI mid-systolic murmur heard best at LLSB with diastolic component, no radiation appreciated. Non-displaced PMI. JVP measured to 14cm.
    Lungs: Decreased breath sounds in left lung field to inferior 2/3 with crackles above, on right crackles to inferior 1/2 of lung fields posteriorly. Dullness to percussion of inferior left lung field posteriorly.
    Abdomen: Soft, non-tender, non-distended, no hepatosplenomegaly, no appreciable fluid wave.
    Ext: Bilateral lower extremities with 2+ pitting edema to knees, some hyperpigmentation to right lower extremity.

    Labs/Studies:

    • CBC: 11.2/10.2/32.7/179
    • BMP: 141/3.9/103/30/15/0.85/107
    • INR: 0.9
    • BNP: 1857
    • UA: WBC 4, RBC 29 , +Bacteria, UCr 90, UPr 14
    • Rheum: CCP <16, ANCA neg, RF 936
    • Pleural Fluid: LDH 98 (serum 237), Protein 2.8 (serum 6.0), Glucose 107
    • Cytology: Reactive mesothelial cells, histiocytes, lymphocytes, signet cells

    Imaging

    CXR

    CXR: Pleural Effusion

    There is a large left pleural effusion obscuring the lower half of the left hemi thorax. The cardiac silhouette is also obscured. There is pulmonary venous vascular congestion. There is also a right pleural effusion with fluid tracking into the minor fissure. Pulmonary interstitial edema is also noted.

    CT Chest (High-Resolution):

    • Bilateral, left greater than right, pleural effusions with adjacent atelectasis and collapse versus consolidation of the left lower lobe.
    • Prominent main pulmonary artery measuring 3.3 cm in diameter, which can be seen with pulmonary arterial hypertension.

    TTE:

    • LVEF is 50-55%.
    • Impaired left ventricular relaxation, which is associated with grade I/IV or mild diastolic dysfunction.
    • Moderate aortic stenosis with mild regurgitation (AVA 1.4 cm3, mean gradient 14mmHg, peak velocity 2.4 m/s).
    • Severe pulmonary hypertension (est PASP 52-62mmHg).
    • The inferior vena cava appeared dilated and decreased <50% with respiration (RAP 10-20 mmHg).
    • Minimal pericardial effusion without echocardiographic evidence of tamponade.

    Assessment/Plan:

    64F with history of CAD (prior MI), CHF, hypertension, CLL, hypothyroidism presented from a SNF with progressive shortness of breath, orthopnea and LE swelling, found to have bilateral (L>R) pleural effusion now s/p thoracentesis with transudative fluid.

    #Acute hypoxic respiratory failure: Large pleural effusions, s/p thoracentesis with pleural fluid suggestive of transudative process. Most likely secondary to left ventricular diastolic dysfunction. Improved after thoracentesis and diuresis. High-resolution CT chest performed without evidence of autoimmune-related pulmonary fibrosis or ILD (though persistent pleural effusions, pulmonary vascular congestion).

    #Pleural fluid signet cells: Identified on cytology, potentially related to history of untreated CLL or alternative primary malignancy.

    #Left ventricular diastolic dysfunction, decompensated: Associated with pleural effusions and hypoxemic respiratory failure. Management with diuresis.

    #Pulmonary Hypertension: Severe, noted on transthoracic echocardiography, may be secondary to hypoxemia associated with pleural effusions, consider repeat imaging once euvolemic or right-heart catheterization.

    #Microscopic Hematuria: No evidence of infection, no symptoms suggestive of nephrolithiasis. No casts identified or significant proteinuria. Plan for renal ultrasound.

    #Rheumatoid Arthritis: History of rheumatoid arthritis, on prednisone and hydroxychloroquine. Imaging without evidence of inflammatory arthropathy, RF elevated but CCP negative. Per rheumatology, the patient’s symptoms are not consistent with RA, continuing home medications while evaluation is ongoing. Pleural effusions unlikely associated with RA as transudative, and without monocyte predominance or low glucose.

    Case 2: Malignant Pleural Effusion

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    Within the lungs there are ground-glass opacities bilaterally, and a left pleural effusion with adjacent consolidation vs compressive atelectasis.
    • Protein: 2.6 (serum: 4.9)
    • LDH: 1275 (serum: 219)
    • Cytology: Malignant cells

    Case 3: Traumatic Thoracentesis

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    Moderate right pleural effusion, some fluid in non-dependent portions suggestive of loculation. Diffuse nodules and opacification in right lung with compressive atelectasis. Left pleural effusion with high density material at the posterior costophrenic angle. Left chest tube.
    • Protein: 2.7 (serum 6.4)
    • LDH: 344 (serum 236)
    • Cell count: 100,000 RBC

    Case 4: Pneumonia

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    Loculated right pleural effusion with foci of atelectasis and consolidative changes concerning for pneumonia. Minimal left-sided pleural effusion with consolidative changes. Enlarged mediastinal lymph nodes, possibly reactive.
    • Protein: 4.3 (serum 6.7)
    • LDH: 377 (serum 108)
    • pH: 7.46
    • Glucose: 153
    • Neutrophils: 84%

    Etiology of Pleural Effusions: 1

    Etiology Frequency (%)
    CHF 35
    Pneumonia 22
    Malignancy 15
    Pulmonary Embolism 11

    Clinical Features in the Diagnosis of Pleural Effusions and Identifying Etiology: 1,2

    Pleural effusions can be easily identified on chest radiography, physical examination findings include dullness to percussion, decreased tactile fremitus and decreased (or absent) breath sounds.

    • Hemoptysis: Malignancy, PE, TB
    • Weight Loss: Malignancy, TB
    • Ascites: Cirrhosis, ovarian cancer
    • Unilateral Leg Swelling: PE
    • Bilateral Leg Swelling: CHF, cirrhosis, nephrotic syndrome
    • Jugular Venous Distension: CHF

    Differential Diagnosis of Pleural Effusions: 1,2,3,4

    Differential Diagnosis of Pleural Effusions

    References:

    1. Light, R. W. (2002). Clinical practice. Pleural effusion. The New England journal of medicine, 346(25), 1971–1977. doi:10.1056/NEJMcp010731
    2. McGrath, E. E., & Anderson, P. B. (2011). Diagnosis of pleural effusion: a systematic approach. American journal of critical care : an official publication, American Association of Critical-Care Nurses, 20(2), 119–27– quiz 128. doi:10.4037/ajcc2011685
    3. Thomsen, T. W., DeLaPena, J., & Setnik, G. S. (2006). Videos in clinical medicine. Thoracentesis. The New England journal of medicine (Vol. 355, p. e16). doi:10.1056/NEJMvcm053812
    4. Wilcox, M. E., Chong, C. A. K. Y., Stanbrook, M. B., Tricco, A. C., Wong, C., & Straus, S. E. (2014). Does this patient have an exudative pleural effusion? The Rational Clinical Examination systematic review. JAMA : the journal of the American Medical Association, 311(23), 2422–2431. doi:10.1001/jama.2014.5552
    5. WikEM: Pleural effusion

    Pulmonary Embolism in Hospitalized Patients

    Brief Progress Note

    Notified by nursing of abnormal vital signs, SpO2 91%. Briefly, this patient is a 52 year-old G1P1 with no prior medical history who is post-operative day three status post total abdominal hysterectomy, bilateral salpingoophorectomy as well as tumor debulking and staging for suspected primary ovarian adenocarcinoma based on peritoneal fluid cyctology.

    On evaluation, the patient denied shortness of breath, chest pain, pleuritic chest pain, cough/hemoptysis, or calf/thigh pain. She states that she had been ambulating around the ward prior to having her vital signs assessed.

    Physical Exam:

    VS: T 98.9 HR 94 RR 18 BP 117/72 O2 91% RA
    Gen: No acute distress, speaking in full sentences.
    HEENT: No jugular venous distension.
    CV: RRR, normal S1/S2, no prominent P2, no additional heart sounds.
    Lungs: Decreased breath sounds at inferior 1/3 posterior lung fields bilaterally, faint crackles above, no wheezing. Dullness to percussion in inferior lung fields.
    Ext: Warm, well-perfused. Sequential compression devices on bilateral lower extremities, removed revealing trace pitting edema symmetric bilaterally, no tenderness to palpation of posterior leg, no pain with passive dorsiflexion.

    Medications:

    • Lovenox 40mg s.q. daily
    • Norco 5-325mg p.o. q.4.h. p.r.n. pain
    • Morphine 2mg i.v. q.3.h. p.r.n. breakthrough pain
    • Colace 100mg p.o. b.i.d. p.r.n. constipation
    • Zofran 4mg i.v. q.6.h. p.r.n. nausea/vomiting

    Imaging:

    CXR

    Bilateral pleural effusions with pleural fluid tracking along the minor fissure.

    CT Chest

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    No evidence of pulmonary embolism, study performed 5 days prior to onset of symptoms.

    CT Abdomen/Pelvis

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    Significant peritoneal carcinomatosis, ascites delineates peritoneal from retroperitoneal spaces.

    Assessment and Plan:

    52yo G1P1 with likely primary ovarian adenocarcinoma with extensive peritoneal involvement, complicated by malignant ascites and pleural effusions with hypoxemia. The primary concern in this post-operative patient with a history of malignancy is venous thromboembolism, particularly pulmonary embolism. Aside from hypoxemia, this patient had no symptoms suggestive of pulmonary embolism (denied dyspnea, chest pain, cough, or lower extremity pain). Her examination had some signs infrequently associated with pulmonary embolism which were otherwise adequately explained by known bilateral pleural effusions (including decreased breath sounds, rales, and tachypnea), she was not tachycardic, had no evidence of jugular venous distension, nor a prominent P2. In addition, she was receiving appropriate VTE prophylaxis (both pharmacological and mechanical). The application of the Modified Wells clinical decision rule suggests low likelihood of pulmonary embolism (with 2.5 points assigned for recent surgery and history of malignancy). The patient had a recent CT chest without evidence of pulmonary embolism, and given that an elevated D-dimer was virtually assured which would have necessitated repeat imaging (and the associated risks of radiation exposure and contrast injury), the episode was ascribed to ventilation/perfusion mismatch secondary to large pleural effusions. Hypoxemia resolved after several minutes at rest and no further testing was performed.

    Signs and Symptoms of Pulmonary Embolism1

    Signs Symptoms
    Tachypnea Dyspnea (rest/exertion)
    Tachycardia Pleurtic chest pain
    Rales Cough
    Decreased breath sounds Orthopnea
    Prominent P2 Calf/thigh pain or swelling
    JVD Wheezing

    Modified Wells Criteria1,2

    Feature Points
    Clinical symptoms of DVT (leg swelling, tenderness to palpation) 3.0
    Pulmonary embolism most likely diagnosis 3.0
    Tachycardia (HR >100) 1.5
    Immobilization >3d, surgery in prior 4 weeks 1.5
    Prior DVT/PE 1.5
    Hemoptysis 1.0
    Malignancy 1.0

    >4.0 Likely
    ≤4.0 Unlikely

    Algorithm for Evaluation of Suspected Pulmonary Embolism2

    Utility of D-Dimer:2
    Of limited utility in patients with high suspicion for pulmonary embolism
    Decreased specificity: malignancy, hospitalized patients, pregnancy, elderly
    Efficacy of DVT prophylaxis:3
    LMWH prevents approximately ½ of VTE events (including PE, symptomatic and asymptomatic DVT)

    References:

    • Kruip, M. J. H. A., Söhne, M., Nijkeuter, M., Kwakkel-Van Erp, H. M., Tick, L. W., Halkes, S. J. M., Prins, M. H., et al. (2006). A simple diagnostic strategy in hospitalized patients with clinically suspected pulmonary embolism. Journal of internal medicine, 260(5), 459–466. doi:10.1111/j.1365-2796.2006.01709.x
    • Tapson, V. F. (2008). Acute pulmonary embolism. The New England journal of medicine, 358(10), 1037–1052. doi:10.1056/NEJMra072753
    • Själander, A., Jansson, J.-H., Bergqvist, D., Eriksson, H., Carlberg, B., & Svensson, P. (2008). Efficacy and safety of anticoagulant prophylaxis to prevent venous thromboembolism in acutely ill medical inpatients: a meta-analysis. Journal of internal medicine, 263(1), 52–60. doi:10.1111/j.1365-2796.2007.01878.x

    Fever in Systemic Lupus Erythematosus

    HPI:

    48F with a history of SLE presenting with two weeks of fevers and joint pain. The patient reports progressive development of these symptoms associated with malaise and muscle aches. She also reports two days of cough productive of yellow sputum, but denies chest pain, shortness of breath or hemoptysis. She states that these symptoms are comparable to prior lupus flares but have persisted longer than usual. She has not travelled or been hospitalized recently and has no sick contacts.

    PMH:

    • SLE
    • AVN left hip

    PSH:

    • Total hip arthroplasty

    FH:

    Non-contributory

    SHx:

    • Denies tobacco, alcohol or drug use.
    • Works as an accountant.
    • No history of TB exposure.

    Meds:

    • Methotrexate 50mg p.o. weekly
    • Plaquenil 400mg p.o. daily
    • MVI

    Allergies:

    NKDA

    Physical Exam:

    VS: T 39.4 HR 138 RR 19 BP 97/61 O2 98% 2L NC
    Gen: Alert, responsive and in no acute distress.
    HEENT: PERRL, dry mucous membranes, no oropharyngeal lesions or erythema, TM intact bilaterally, no cervical lymphadenopathy, neck supple.
    CV: Tachycardia, regular rhythm without additional heart sounds.
    Lungs: Clear to auscultation bilaterally.
    Abd: +BS, soft, non-tender, non-distended, no rebound/guarding.
    Ext: No peripheral edema, extremities warm and well-perfused, diffuse tenderness to palpation and resisted range of motion of joints with particular involvement of bilateral shoulders, elbows, knees and ankles. No effusion noted, no erythema or warmth.
    Neuro: Alert, oriented to self, location and time. PERRL, EOMI, facial sensation intact, facial muscles symmetric, palate rises symmetrically, tongue protrudes midline without fasciculation, peripheral sensation and motor strength grossly intact with normal gait.

    Labs/Studies:

    • 0h:
    • CBC: 6.0/7.7/23.5/259
    • BMP: 138/2.8/116/18/12/0.66/71
    • Ca: 5.0 (corrected for hypoalbuminemia: 6.9)
    • Mg: 1.1
    • Lactate: 0.7
    • ESR: 81 (0-20)
    • CRP: 7.99 (0-0.74)
    • C3: 60 (79-152)
    • C4: 13 (16-38)
    • 12h:
    • BMP: 142/4.6/113/26/15/0.75/128
    • Ca: 7.8

    Imaging:

    • CXR: Negative for acute cardiopulmonary process.

    Assessment/Plan:

    48F with a history of SLE presenting with fever and polyarticular arthralgia.

    #SIRS: Fever and tachycardia in the setting of immunosuppression. The differential diagnosis includes pneumonia (bacterial, viral, less-likely fungal), which would be community-acquired. Association with polyarticular arthralgia suggests symptoms may represent lupus flare given no leukocytosis and elevated CRP.

    #Hypocalcemia: Asymptomatic, likely due to hypoalbuminemia and hypomagnesemia. Improved after IV fluids and correction of hypokalemia, hypomagnesemia.

    Hospital Course:

    The patient was admitted and completed a 7-day course of ceftriaxone and azithromycin. Rheumatology was consulted for management of lupus flare, which included resuming home medications and a prednisone taper upon discharge.
    The patient was admitted ten days later, presenting with fevers, productive cough and pleuritic chest pain. Found to have a left lower lobe sub-segmental pulmonary embolus and antiphospholipid syndrome. She was also treated empirically for healthcare-associated pneumonia with cefepime and vancomycin given fever and productive cough though there were no imaging findings suggestive of consolidation and sputum cultures were negative.

    Differential Diagnosis of Hypocalcemia: 1,2

    Differential Diagnosis of Hypocalcemia

    Laboratory Evaluation of Hypocalcemia: 1,2

    Laboratory Evaluation of Hypocalcemia

    Clinical Manifestations of Hypocalcemia: 1

    • Neuromuscular
      • Hyperexcitability
      • Perioral paresthesias
      • Muscle weakness, cramps, fasciulations, tetany
    • CNS
      • Depression
      • Irritability
      • Confusion
      • Seizure
    • Cardiac
      • Decreased contractility/conduction
      • QT prolongation

    Management of Symptomatic Hypocalcemia: 1

    • 10mL 10% Calcium Gluconate
    • Dilute in 100mL D5W

    Fever in SLE:

    It is important to differentiate whether fever in a patient with SLE is due to disease activity (flare) or active infection.

    Risk Factors for Infection:3

    • Neutropenia/Lymphopenia
    • Hypocomplementemia
    • Immunosuppressive therapy (especially Azathioprine4)

    Laboratory Studies:3

    • CRP: sensitivity 100%, specificity 90% >1.35mg/dL 5
    • PCT: sensitivity 75%, specificity 75% 6

    References:

    1. Cooper, M. S., & Gittoes, N. J. L. (2008). Diagnosis and management of hypocalcaemia. BMJ (Clinical research ed.), 336(7656), 1298–1302. doi:10.1136/bmj.39582.589433.BE
    2. Hannan, F. M., & Thakker, R. V. (2013). Investigating hypocalcaemia. BMJ (Clinical research ed.), 346(may09 1), f2213–f2213. doi:10.1136/bmj.f2213
    3. Cuchacovich, R., & Gedalia, A. (2009). Pathophysiology and clinical spectrum of infections in systemic lupus erythematosus. Rheumatic diseases clinics of North America, 35(1), 75–93. doi:10.1016/j.rdc.2009.03.003
    4. Zhou, W. J., & Yang, C.-D. (2009). The causes and clinical significance of fever in systemic lupus erythematosus: a retrospective study of 487 hospitalised patients. Lupus, 18(9), 807–812. doi:10.1177/0961203309103870
    5. Kim, H.-A., Jeon, J.-Y., An, J.-M., Koh, B.-R., & Suh, C.-H. (2012). C-reactive protein is a more sensitive and specific marker for diagnosing bacterial infections in systemic lupus erythematosus compared to S100A8/A9 and procalcitonin. The Journal of rheumatology, 39(4), 728–734. doi:10.3899/jrheum.111044
    6. Scirè, C. A., Cavagna, L., Perotti, C., Bruschi, E., Caporali, R., & Montecucco, C. (2006). Diagnostic value of procalcitonin measurement in febrile patients with systemic autoimmune diseases. Clinical and experimental rheumatology, 24(2), 123–128.

    Electrolyte Abnormalities

    Routine laboratory studies are common in the intensive care unit; abnormalities are even more common. Typically these studies include a chemistry panel (Chem 10). The differential diagnoses of the most frequent and clinically relevant electrolyte abnormalities are detailed below.

    Differential Diagnosis and Evaluation of Hyponatremia

    Differential Diagnosis and Evaluation of Hyponatremia

    Differential Diagnosis and Evaluation of Hypernatremia

    Differential Diagnosis and Evaluation of Hypernatremia

    Differential Diagnosis and Evaluation of Hypokalemia

    Differential Diagnosis and Evaluation of Hypokalemia

    Differential Diagnosis of Hyperkalemia

    Differential Diagnosis of Hyperkalemia

    Differential Diagnosis of Hypo and Hypercalcemia

    Differential Diagnosis of Hypo and Hypercalcemia

    Differential Diagnosis of Hypo and Hypermagnesemia

    Differential diagnosis of hypo and hypermagnesemia

    Differential Diagnosis of Hypo and Hyperphosphatemia

    Differential diagnosis of hypo and hyperphosphatemia

    References:

    1. Marino, P. (2014). Marino’s the ICU book. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.
    2. Fulop, M. (1998). Algorithms for diagnosing some electrolyte disorders. American Journal of Emergency Medicine, 16(1), 76–84.
    3. WikEM: Hypokalemia
    4. WikEM: Hyponatremia

    Biliary Duct Dilation

    A 45 year-old male presents with progressive jaundice over 1 month, he denies abdominal pain.

    Ultrasound

    Liver
    Common Bile Duct
    Gallbladder Wall

    CT Abdomen/Pelvis

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    • Markedly dilated intrahepatic biliary ducts, common bile duct and pancreatic duct.
    • Ill-defined fullness in the pancreatic head consistent with pancreatic adenocarcinoma vs. noncalcified obstructing biliary stone.

    Differential Diagnosis of Biliary Duct Dilation: 1,2,3

    Differential Diagnosis of Biliary Duct Dilation

    References:

    1. Kim, H. J., Lee, K. T., Kim, S. H., Lee, J. K., Lim, J. H., Paik, S. W., & Rhee, J. C. (2003). Differential diagnosis of intrahepatic bile duct dilatation without demonstrable mass on ultrasonography or CT: benign versus malignancy. Journal of gastroenterology and hepatology, 18(11), 1287–1292.
    2. Levy, A. D. (2009). Biliary Ducts – Pathology. The Radiology Assistant, 1–4. Retrieved from http://www.radiologyassistant.nl/en/p49e17de25294d/biliary-ducts-pathology.html
    3. Teefey, S. A., Baron, R. L., Schulte, S. J., Patten, R. M., & Molloy, M. H. (1992). Patterns of intrahepatic bile duct dilatation at CT: correlation with obstructive disease processes. Radiology, 182(1), 139–142. doi:10.1148/radiology.182.1.1727277

    Acute Kidney Injury

    Hospital Course:

    64 year-old female with a history of metastatic colonic adenocarcinoma was initially admitted for PO intolerance secondary to recurrent small bowel obstructions (associated with abdominal tumor burden). On hospital day six, the patient developed tachypnea, hypoxemia, hypotension and was intubated for respiratory distress. In the MICU, the patient was treated for acute hypoxic respiratory failure thought to be caused by aspiration (large volume bilious emesis prior to intubation despite NGT LCWS) vs. accumulating malignant pleural effusions vs. pulmonary embolism. Septic shock of a presumed pulmonary vs. intra-abdominal source was managed with vasopressors and broad-spectrum antimicrobials.

    On hospital day fourteen, an elevation in the serum creatinine was noted. Known nephrotoxic agents include iodinated contrast on hospital day five, and vancomycin. The patient’s vasopressor requirement had decreased to norepinephrine 6mcg/kg/min (previously requiring four vasopressors). Over the next six days, the serum creatinine continued to trend upwards associated with a decrease in urine output (0.3-0.5mL/kg/hour). Intravenous crystalloid and colloid administered liberally based on central venous pressure and ultrasound of the inferior vena cava did not impact urine output.

    Laboratory Studies

    Hospital day 19 18 17 16 15 14 3
    Creatinine 1.72 1.59 1.46 1.32 1.24 1.09 0.75
    Vancomycin 23.5 28.5 36.3 45.5 47.7 22.1

    Urine electrolytes:

    • Una: 10
    • Ucr: 180
    • Uk: 13
    • Ucl: 22
    • Uur: 265
    • FeNa: <1%

    UA: 3+LE, 1+ blood, 36WBC, 14RBC, 3+ bacteria, amorphous crystals

    Imaging:

    IM-0001-0054
    IM-0001-0054
    IM-0001-0056
    IM-0001-0056
    IM-0001-0058
    IM-0001-0058
    IM-0001-0060
    IM-0001-0060
    IM-0001-0062
    IM-0001-0062
    IM-0001-0064
    IM-0001-0064
    IM-0001-0066
    IM-0001-0066
    IM-0001-0068
    IM-0001-0068
    IM-0001-0070
    IM-0001-0070
    IM-0001-0072
    IM-0001-0072
    IM-0001-0074
    IM-0001-0074
    IM-0001-0076
    IM-0001-0076
    IM-0001-0078
    IM-0001-0078
    IM-0001-0080
    IM-0001-0080
    IM-0001-0082
    IM-0001-0082
    IM-0001-0084
    IM-0001-0084
    IM-0001-0086
    IM-0001-0086
    IM-0001-0088
    IM-0001-0088
    IM-0001-0090
    IM-0001-0090
    IM-0001-0092
    IM-0001-0092
    IM-0001-0094
    IM-0001-0094
    IM-0001-0096
    IM-0001-0096
    IM-0001-0098
    IM-0001-0098
    IM-0001-0100
    IM-0001-0100
    IM-0001-0102
    IM-0001-0102
    IM-0001-0104
    IM-0001-0104
    IM-0001-0106
    IM-0001-0106
    IM-0001-0108
    IM-0001-0108
    IM-0001-0110
    IM-0001-0110
    IM-0001-0112
    IM-0001-0112
    IM-0001-0114
    IM-0001-0114
    IM-0001-0116
    IM-0001-0116
    IM-0001-0118
    IM-0001-0118
    IM-0001-0120
    IM-0001-0120
    IM-0001-0122
    IM-0001-0122
    IM-0001-0124
    IM-0001-0124
    IM-0001-0126
    IM-0001-0126
    IM-0001-0128
    IM-0001-0128
    IM-0001-0130
    IM-0001-0130
    IM-0001-0132
    IM-0001-0132

    CT Abdomen/Pelvis with IV contrast

    • Within the retroperitoneum, the left kidney is small and atrophic and demonstrates limited peripheral enhancement. The left renal artery is also poorly visualized.
    • Severely dilated loops of small bowel, including a segment within the left lower quadrant that may represent a closed loop obstruction.
    • There is a large (16.4 cm in largest diameter) subphrenic fluid collection in the left upper quadrant. A second large (14.2 cm in largest diameter) intraabdominal fluid collection lies inferior and anteriorly.

    Assessment:

    Oliguric acute renal failure in the setting of convincingly pre-renal urine studies which was not responsive to adequate crystalloid and colloid volume resuscitation. The patient had a normal ejection fraction on a recent echocardiogram, and while the patient was hypoalbuminemic (presumably from poor nutritional status and PO intolerance), urine output was not even transiently responsive to colloid administration. While the patient had recent administration of intravenous contrast, the elevation in serum creatinine occurred more than one week later. Further, the elevated vancomycin trough was likely a consequence rather than the etiology of worsening renal failure. AKI was likely secondary to renal artery compression from mass effect associated with abdominal metastases. There was evidence of a similar process affecting the left kidney, which was severely atrophic. The patient declined further evaluation, which would have included a renal ultrasound.

    Definition of Acute Kidney Injury: 1

    • Elevation of serum creatinine > 0.3mg/dL in 48h
    • Elevation of serum creatinine > 1.5x baseline in 7d
    • Oliguria (UOP < 0.5mL/kg/hr) > 6h

    Staging of Acute Kidney Injury: 1

    Stage Creatinine UOP
    1 1.5-1.9x <0.5mL/kg/hr for 6-12h
    2 2.0-2.9x <0.5mL/kg/hr for >12h
    3 3.0x or RRT <0.3mL/kg/hr for > 24h

    Management of Contrast-induced AKI: 2

    • Administer lowest dose
    • Use iso-osmolar, or low-osmolar contrast
    • Volume expansion (NaCl, NaHCO3)
    • PO NAC questionable benefit but likely harmless

    Differential Diagnosis of Acute Kidney Injury: 3

    Algorithm for the Evaluation of Acute Kidney Injury

    NOTE: Algorithm revised in November, 2017. The prior version is no longer supported but remains available here.

    Evaluation of AKI: 4

    Condition Urinalysis Casts FeNa (%)
    Pre-renal Normal Hyaline <1
    Intra-renal
    ATN Mild proteinuria Pigmented granular >1
    AIN Mild proteinuria, Hb, WBC WBC casts, eosinophils >1
    GN Moderate/severe proteinuria, Hb RBC casts <1
    Post-renal Normal Crystals >1

    References:

    1. Kellum, J. A., Lameire, N., KDIGO AKI Guideline Work Group. (2013). Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1). Critical care (London, England), 17(1), 204. doi:10.1186/cc11454
    2. Lameire, N., Kellum, J. A., KDIGO AKI Guideline Work Group. (2013). Contrast-induced acute kidney injury and renal support for acute kidney injury: a KDIGO summary (Part 2). Critical care (London, England), 17(1), 205. doi:10.1186/cc11455
    3. Lameire, N., Van Biesen, W., & Vanholder, R. (2005). Acute renal failure. Lancet, 365(9457), 417–430. doi:10.1016/S0140-6736(05)17831-3
    4. Thadhani, R., Pascual, M., & Bonventre, J. V. (1996). Acute renal failure. New England Journal of Medicine, 334(22), 1448–1460. doi:10.1056/NEJM199605303342207
    5. WikEM: Acute kidney injury

    Ectopic Pregnancy

    HPI:

    32F G8P7A2 at 5 weeks by LMP presenting with abdominal pain. The patient reports acute onset of sharp left lower abdominal pain 1.5 hours prior to presentation. The pain has been constant since onset, 10/10 in severity, radiating to lower back and exacerbated with movement. She denies vaginal bleeding or discharge, passage of clots or other products. She also denies trauma, lightheadedness/dizziness/syncope, shortness of breath, nausea/vomiting or changes in bowel or urinary habits.
    Her pregnancy was detected 3 weeks ago with a home pregnancy test and was confirmed at her PCP one week later. She has not had an ultrasound during this pregnancy but has a history of uterine fibroids. She has no history of sexually transmitted infections, prior ectopic pregnancy, or use of assisted fertilization.

    PMH:

    • HTN
    • Uterine fibroids

    PSH:

    None

    FH:

    Non-contributory

    SHx:

    • Denies tobacco, alcohol or drug use.
    • Sexually active with husband only, no history of STI.

    Meds:

    None

    Allergies:

    NKDA

    Physical Exam:

    VS: T 37.4 HR 108 RR 36 BP 148/104 O2 99% RA
    Gen: Alert and oriented female, appears uncomfortable due to pain.
    HEENT: PERRL, EOMI, MMM.
    CV: Tachycardia, regular rhythm, no murmurs.
    Lungs: CTAB, no crackles.
    Abd: Normoactive bowel sounds, tenderness to palpation in LLQ and suprapubic area, with guarding but no rebound tenderness. No CVAT.
    GU: No external lesions. Closed cervical os, no blood or discharge, +CMT.
    Ext: Warm, well-perfused with strong peripheral pulses.

    Labs/Studies:

    • POC Hemoglobin: 11.8
    • POC ICON: positive

    Imaging:

    Bedside Ultrasound

    1. Transabdominal: Free fluid in hepatorenal and splenorenal recesses
    2. Transvaginal: Free fluid and debris in posterior cul-de-sac, likely pseudogestational sac in endometrial cavity, no IUP identified. Formal ultrasound revealed fetus with cardiac activity in left adnexa.
    Hepatorenal free fluid

    Hepatorenal free fluid

    Free fluid in the hepatorenal recess (Morison's Pouch)

    Splenorenal Free Fluid

    Splenorenal Free Fluid

    Free fluid in the splenorenal recess.

    Pelvic Free Fluid

    Pelvic Free Fluid

    Free fluid and debris in the posterior cul-de-sac.

    Pseudogestational Sac

    Pseudogestational Sac

    No obvious yolk sac or fetal pole.

    Assessment/Plan:

    32 year-old ICON positive female with acute-onset pelvic pain. The patient remained hemodynamically stable and absence of definitive IUP on bedside ultrasound was confirmed with presence of fetal cardiac activity in left adnexa indicative of ectopic pregnancy. OB-Gyn was consulted and the patient was taken emergently to the OR.

    Differential Diagnosis of First Trimester Abdominal Pain: 1

    Differential Diagnosis of 1st Trimester Abdominal Pain

    Initial Evaluation of First Trimester Abdominal Pain: 1

    • 2 large-bore IV’s, begin fluid resuscitation
    • POC testing: hemoglobin, urine pregnancy
    • CBC, type and cross (Rh), serum B-hCG
    • Emergent bedside ultrasound

    Features Associated with Ectopic Pregnancy: 1

  • History
    • PID
    • Tubal ligation
    • Prior ectopic
    • IUD
    • Assisted fertilization
  • Physical
    • CMT
    • Peritoneal irritation
  • Ultrasound
    • Empty uterus
    • Adnexal mass
    • Free fluid
  • Ultrasonographic Findings in the Evaluation of Ectopic Pregnancy: 2

    • Discriminatory hCG (1500-3000 mIU/mL): absence of IUP suggests ectopic or abnormal gestation
    • Normal IUP
      • 4-5wks: gestational sac (0.2-0.5cm)
      • 5wks: two echogenic rings
      • 5.5wks: yolk sac
      • 6wk: embryonic pole
      • 6.5wk: fetal cardiac activity
    • Abnormal IUP
      • >2cm gestational sac without fetal pole
      • CRL >0.5cm without cardiac activity
    • Ectopic
      • Extrauterine gestational sac with or without cardiac activity
      • Extrauterine ring sign
      • Non-homogenous adnexal mass

    Contraindications to Medical Management: 2,3

    • Absolute
      • Breast-feeding
      • Immunodeficiency
      • PUD
      • Pulmonary, hepatic or renal dysfunction
    • Relative
      • Ectopic mass > 3.5cm
      • Fetal cardiac activity

    References:

    1. Dart, R. (2003). First Trimester Emergencies A Practical Approach To Abdominal Pain And Vaginal Bleeding In Early Pregnancy. EB Medicine, 5(11), 1–20.
    2. Barnhart, K. T. (2009). Clinical practice. Ectopic pregnancy. The New England journal of medicine, 361(4), 379–387. doi:10.1056/NEJMcp0810384
    3. Jurkovic, D., & Wilkinson, H. (2011). Diagnosis and management of ectopic pregnancy. BMJ (Clinical research ed.), 342(jun10 1), d3397–d3397. doi:10.1136/bmj.d3397

    Ultrasound Gallery

    Appendicitis

    Appendicitis

    Non-compressible tubular structure in the RLQ of a patient with focal abdominal tenderness. >6mm in diameter.

    Common Bile Duct

    Common Bile Duct

    A tubular structure typically anterior to the portal vein without flow. Normally measures <4mm, increases by 1mm per decade after 40yrs.

    Cellulitis

    Cellulitis

    "Cobblestone" appearance of soft tissue suggesting infection/edema.

    Fetal Heart Rate

    Fetal Heart Rate

    Placing the M-Mode marker over the most visibly active portion of the fetal heart allows for measurement of the fetal heart rate.

    Free Fluid

    Free Fluid

    Free fluid in the hepatorenal recess.

    Hydronephrosis

    Hydronephrosis

    Severe hydronephrosis.

    Thoracic Aorta Aneurysm

    Thoracic Aorta Aneurysm

    Subxiphoid view of thoracic aorta, markedly dilated (>3cm) with thrombus.

    Pericardial Effusion

    Pericardial Effusion

    Mild pericardial effusion in a patient with pleuritic chest pain.

    Inferior Vena Cava

    Inferior Vena Cava

    IVC without significant respiratory variation.

    B-lines

    B-lines

    B-lines extending deep from pleura suggestive of interstitial fluid accumulation (pulmonary edema).

    "Shred" sign

    "Shred" sign

    Irregular, "shredded" pleural line suggestive of consolidation.

    Pneumothorax

    Pneumothorax

    Transition point with loss of lung sliding in a patient with a small spontaneous pneumothorax.

    Lower Extremity Edema

    HPI:

    51 year-old male with a history of HTN, DM and chronic alcohol abuse presenting with lower extremity swelling. He notes one month of progressive, bilateral lower extremity swelling, in the past two weeks associated with increasing pain and redness and is now no longer able to ambulate due to pain. He denies fevers/chills, chest pain or shortness of breath. He also denies orthopnea and paroxysmal nocturnal dyspnea. He states that he has not had these symptoms prior to one month ago. On review of systems he denies nausea/vomiting, abdominal pain, and changes in bowel or urinary habits. He has a history of GI bleeding (unknown treatment) but denies hematemesis, hematochezia or melena. He has previously experienced alcohol withdrawal, which manifested as tremors, but no hallucinations or seizures.

    PMH:

    • HTN
    • DM
    • Chronic EtOH abuse

    PSH:

    None

    FH:

    Unknown

    SHx:

    • Drinks 1-2 pints of alcohol daily, last drink this morning.
    • Denies current tobacco or drug abuse, no prior IVDA.

    Meds:

    None

    Allergies:

    NKDA

    Physical Exam:

    VS: T 37.6 HR 86 RR 16 BP 128/84 O2 99% RA
    Gen: Adult, non-obese male, lying in bed. Tremors noted in upper extremities.
    HEENT: PERRL, EOMI, no scleral icterus. Mucous membranes moist.
    CV: RRR, normal S1/S2, no additional heart sounds, JVP 3cm above sternal angle at 30°.
    Lungs: CTAB, no crackles.
    Abd: Soft, non-distended, with normoactive bowel sounds. Liver edge palpated 1cm below costal margin at mid-clavicular line, non-tender. No rebound/guarding.
    Ext: Warm, well-perfused with 2+ distal pulses (PT, DP). 3+ pitting edema symmetric in bilateral lower extremities to knee. Erythema and warmth bilaterally extending from ankles to mid-shin. Mild tenderness to palpation. No pain with passive dorsiflexion. 3x3cm shallow ulceration below medial malleolus on right lower extremity without underlying fluctuance or expression of purulent material. No venous varicosities noted. Decreased sensation to light touch below knee bilaterally.
    Rectal: Normal rectal tone, brown stool, guaiac negative.
    Neuro: Alert and oriented, CN II-XII intact, gait intact, normal FTN/RAM.

    Labs/Studies:

    • CBC: 7.4/13.1/39/180
    • Creatinine: 0.84
    • Albumin: 4.3
    • BNP: 28

    Imaging:

    Venous Lower Extremity Ultrasound

    1. No DVT.
    2. Pulsatile flow in bilateral EIV (external iliac veins) suggestive of elevated right heart pressure.

    Assessment/Plan:

    51M with HTN, DM, EtOH abuse presenting with lower extremity edema. Chronic bilateral lower extremity edema likely secondary to chronic venous insufficiency perhaps related to OSA given ultrasound findings of pulsatile flow in EIV’s. Doubt systemic cause: no evidence of heart failure on exam and normal BNP, no stigmata of cirrhosis and normal albumin, normal creatinine. Also, no evidence of DVT on ultrasound though bilateral DVT unlikely. Bilateral cellulitis also unlikely as the patient is afebrile without leukocytosis, however the patient was started on antibiotics including ceftriaxone and TMP/SMX given erythema, warmth and tenderness to palpation. The patient received benzodiazepines which eased withdrawal symptoms and he was admitted for continued treatment.

    Mechanisms of Lower Extremity Edema: 1

    Mechanisms of Lower Extremity Edema

    Differential Diagnosis of Lower Extremity Edema: 1,2

    Differential Diagnosis of Lower Extremity Edema

    Evaluation:

    History 1,2

    • Duration: acute (<72h) vs. chronic
    • Pain: DVT, CRPS, less severe in venous insufficiency
    • Systemic Disease
      • Cardiac: orthopnea, PND
      • Renal: proteinuria
      • Hepatic: jaundice, ascites
    • Malignancy: lymphedema
    • Improvement with elevation/recumbency: venous insufficiency
    • OSA: snoring, daytime somnolence
    • Medications: B-blocker, CCB, hormones, NSAID’s

    Physical Exam 1,2

    • Distribution: unilateral, bilateral, generalized
    • Quality: pitting, non-pitting
    • TTP: DVT, cellulitis
    • Varicose veins: venous insufficiency
    • Kaposi-Stemmer: inability to pinch dorsum of foot at base of 2nd toe (lymphedema)
    • Systemic Disease
      • Cardiac: JVD, crackles
      • Hepatic: ascites, scleral icterus, spider angiomas
    • Brawny, medial maleolar involvement: venous insufficiency

    Key Features Distinguishing Cellulitis: 3

    • Typically unilateral and acute
    • Often with systemic symptoms (fever, leukocytosis)
    • Risk Factors: immunosuppression, previous episodes, DM, PVD

    References:

    1. Trayes, K. P., Studdiford, J. S., Pickle, S., & Tully, A. S. (2013). Edema: diagnosis and management. American family physician, 88(2), 102–110.
    2. Ely, J. W., Osheroff, J. A., Chambliss, M. L., & Ebell, M. H. (2006). Approach to leg edema of unclear etiology. Journal of the American Board of Family Medicine : JABFM, 19(2), 148–160.
    3. Keller, E. C., Tomecki, K. J., & Alraies, M. C. (2012). Distinguishing cellulitis from its mimics. Cleveland Clinic journal of medicine, 79(8), 547–552. doi:10.3949/ccjm.79a.11121
    4. WikEM: Pedal edema

    Lymphadenopathy Applied: Lymphoma

    HPI:

    27 year-old female with no medical history presenting with neck swelling. She describes one month of progressive enlargement of a left-sided neck mass, and in the past two weeks has noted a new right-sided neck mass. This has been associated with worsening dysphagia to solids, describing a sensation of food lodging in the mid-chest and requiring liquids for passage – she attributes her recent 10lb weight loss to this. She also reports a non-productive cough for the past two weeks and generalized fatigue. She otherwise denies fevers, night sweats, chest pain, shortness of breath, nausea/vomiting, or changes in bowel/urinary habits. She has no known sick contacts or TB exposure risk factors. She has no medical history, no prior surgeries, does not take any medications and denies tobacco, alcohol or drug use.

    Physical Exam:

    VS: T 38.4 HR 98 RR 14 BP 108/68 O2 99% RA
    Gen: Well-appearing young female, in no acute distress.
    HEENT: PERRL, EOMI, MMM without lesions. There is a 2x3cm firm, non-tender, mobile left supraclavicular lymph node, as well as two 1x1cm firm, non-tender lymph nodes in the left and right anterior cervical chains.
    CV: RRR, normal S1/S2, no murmurs. No JVD.
    Lungs: Clear to auscultation bilaterally. There is a transition to bronchial breath sounds along the trachea inferior to the sternal angle with normal tracheal sounds superiorly.
    Abd: Soft, non-tender without organomegaly.
    Ext: Warm and well-perfused with normal peripheral pulses. No axillary or inguinal lymphadenopathy.
    Neuro: Alert and oriented, responding appropriately to questions. PERRL, EOMI, facial sensation symmetric, facial muscles symmetric, hearing grossly normal, palate rises symmetrically, tongue movements normal without fasciculation, SCM/trapezius normal. Normal FTN, RAM. Gait intact. Peripheral sensation and motor grossly normal.

    Imaging:

    CT Chest - Axial

    CT Chest - Axial

    Anterior mediastinal mass with a wide differential - likely represents lymphoma or germ cell tumor. Less likely thymic or thyroid origin.

    CT Chest - Sagittal

    CT Chest - Sagittal

    Anterior mediastinal mass with a wide differential - likely represents lymphoma or germ cell tumor. Less likely thymic or thyroid origin.

    Assessment/Plan:

    27F with no PMH presenting with progressive localized lymphadenopathy. Resultant dysphagia, cervical and supraclavicular distribution as well as abnormal tracheal sounds concerning for mediastinal involvement. The patient is currently stable without evidence of airway compromise. A CT of the chest was obtained to evaluate for thoracic malignancy, which showed a large anterior mediastinal mass concerning lymphoma or germ cell tumor. The location of the mass likely explains the patient’s dysphagia due to compression of the esophagus, as well as the abnormal pulmonary exam with compression potentially irritating the trachea and triggering her non-productive cough. The patient was admitted for further workup.

    Lymphadenopathy Applied – Lymphoma

    This case applies the differential diagnosis of lymphadenopathy. The most abnormal finding on examination was non-tender, left supraclavicular lymphadenopathy. The duration of symptoms and lack of tenderness is concerning for malignancy, and the left supraclavicular location suggests a thoracic or intra-abdominal source.

    Lymphadenopathy Applied - Lymphoma

    Necrotizing Soft-Tissue Infection (NSTI)

    HPI:

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

    PMH:

    • Diabetes mellitus, diagnosed 8yrs ago

    PSH:

    • None

    FH:

    • Non-contributory

    SHx:

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

    Meds:

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

    Allergies:

    NKDA

    Physical Exam:

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

    Labs/Studies:

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

    Imaging:

    CT Lower Extremity

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

    Assessment/Plan:

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

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

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

    Skin and soft-tissue layers and their infections: 1

    Skin and soft-tissue layers and their infections

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

    Risk Factors

    • IVDA
    • Comorbid conditions
      • DM
      • Obesity
      • Immunosuppression

    Physical Exam

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

    Treatment

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

    LRINEC score 5

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

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

    References:

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

    Acute Respiratory Distress Syndrome

    HPI:

    25M with a history of mild asthma transferred from an outside hospital after 10 days in the intensive care unit for continued management of ARDS.

    The patient was well until one week prior to admission when he developed intermittent subjective fevers and general malaise associated with a non-productive cough and nausea/vomiting. He presented to the emergency department of an outside hospital with difficulty breathing and was noted to have respiratory distress and was subsequently admitted. Initial CT at the outside hospital revealed pneumomediastinum but no evidence of pulmonary embolism. Results from the outside hospital reveal a wide array of bacterial/fungal cultures and viral serologies including bronchoscopy but no obvious infectious source. The patient was treated with broad spectrum antibiotics for several days but his condition worsened requiring intubation, mechanical ventilation and transfer to the ICU. Further imaging was suggestive of ARDS, and the patient was transferred for additional management.

    The patient was well until one week prior to admission when he reported development of malaise and fatigue. On the day of hospitalization, the patient presented to primary care doctor with complaint of cough and shortness of breath and was found to be in respiratory distress and was admitted. The patient received IV antibiotics (cefepime, vancomycin) and was intubated when respiratory distress worsened. Found to have evidence of ARDS on CXR.

    PMH:

    • Mild asthma, not requiring medication
    • MRSA skin abscess

    PSH:

    • None

    FH:

    • Non-contributory.

    SHx:

    • Lives with family and works at a local supermarket. Rare alcohol use and no prior tobacco or drug use.
    • No recent travel or sick contacts.

    Meds:

    • ciprofloxacin 400mg i.v. q12h
    • linezolid 600mg i.v. q12h
    • meropenem 1g i.v. q8h
    • heparin 5000units s.q. q8h
    • cisatracurium 1.48mcg/kg/min
    • fentanyl 125mcg/hr
    • midazolam 10mg/hr
    • propofol 20mcg/kg/min

    Allergies:

    NKDA

    Physical Exam:

    VS: T 97.8 HR 120 RR 35 BP 123/68 O2 96%
    Vent: PRVC, VT 320, RR 35, PEEP 6, FiO2 95%
    Gen: Young male, thin-appearing, intubated and sedated and not responding to verbal commands
    HEENT: PERRL, unable to assess EOM, ET tube in place
    CV: RRR, normal S1/S2, no murmurs
    Lungs: Coarse breath sounds bilaterally
    Abd: Normoactive bowel sounds, soft, non-distended, no hepatosplenomegaly
    Ext: No clubbing, cyanosis, edema
    Neuro: Unable to assess

    Labs/Studies:

    • CBC: 25.06/7.0/21.3/426
    • BMP: 132/3.3/88/32/18/1.1/103
    • ABG: 7.30/97/76/18
    • Blood/sputum/urine cultures: Negative
    • Aspergillus, crypto, cocci: Negative
    • EBV, HIV, influenza, RSV: Negative

    Imaging


    CT Chest: Evidence of pneumomediastinum and pneumopericardium. Bilateral pulmonary infiltrates, but no pulmonary embolism.

    Assessment/Plan:

    25M with ARDS transferred from outside hospital for further management.
    # ARDS: Severe (P/F ratio <100). Etiology unclear, thorough infectious workup without obvious source. Consider autoimmune or allergic cause.

    • Ventilator: PRVC lung-protective ventilation
    • Consider NMB for dyssynchrony despite sedation
    • Monitor strict I/O, maintain net negative fluid balance.

    # Sepsis: Leukocytosis, tachycardia. Continue broad-spectrum antibiotics and monitor cultures.
    # Acidosis: Largely respiratory, place dialysis catheter if acute need arises.
    # Pneumomediastinum: Possible Boerhaave syndrome given reports of nausea/vomiting.

    Pathophysiology of Acute Respiratory Distress Syndrome (ARDS):1

    ARDS represents a stereotyped response to multiple insults. It is characterized by damaged capillary endothelium and alveolar epithelium resulting in increased permeability and the accumulation of fluid in the alveolar space. This causes diffuse alveolar damage and triggers the release of various cytokines (TNF, IL-1, IL-6) which recruit and activate neutrophils causing oxidative cell damage.

    Definition of ARDS (Berlin):2,3

    Timing Acute in onset (<1 week)
    Chest imaging Bilateral opacities
    Origin of pulmonary edema Not explained by heart failure or fluid overload (assessed with echocardiography)
    Oxygenation (PaO2/FiO2)
    1. Mild: 200-300
    2. Moderate: 100-200
    3. Severe: <100

    Causes of ARDS:2,4

    Causes of ARDS


    An Introduction to Mechanical Ventilation:5,6,7

    This is a simplification of the general principles underlying the most common ventilator modes. For more detail, see the articles cited in the references.
    An Introduction to Mechanical Ventilation

    Breath Sequences:

    Continuous Mandatory Ventilation (CMV)

    Continuous Mandatory Ventilation (CMV)

    All breaths controlled by ventilator, no triggered breaths.

    Assist-Control Ventilation (AC)

    Assist-Control Ventilation (AC)

    Every patient-triggered breath is fully supported, a backup rate is set. In the absence of patient-triggered breaths, AC acts like CMV.

    Synchronized Intermittent Mandatory Ventilation (SIMV)

    Synchronized Intermittent Mandatory Ventilation (SIMV)

    Preset minimum mandatory breaths are “synchronized” to patient’s efforts. The patient is allowed to breathe spontaneously between supported breaths.

    Pressure Support (PS)

    Pressure Support (PS)

    All breaths are triggered by the patient and each is supported by preset pressure.

    Continuous Positive Airway Pressure (CPAP)

    Continuous Positive Airway Pressure (CPAP)

    Spontaneous breathing at elevated baseline pressure.

    Control Variables:

    Volume Control (VC)
    Volume Control (VC)

    Volume Control (VC)

    Volume is set, pressure is variable. With a drop in compliance, the preset minimum volume is maintained with an increase in pressure.

    Pressure Control (PC)
    Pressure Control (PC)

    Pressure Control (PC)

    Pressure is set, volume is variable. With a drop in compliance, a smaller volume is delivered to maintain pressures at the preset limit.

    Pressure-Regulated Volume Control (PRVC)
    Pressure-Regulated Volume Control (PRVC)

    Pressure-Regulated Volume Control (PRVC)

    Pressure is targeted with a set minimum volume. The ventilator makes breath-to-breath adjustments of pressure to maintain minimum volumes. Breath mechanics are therefore comparable to pressure-control as a defined pressure is delivered based on prior breath’s respiratory mechanics (note pressure and flow tracings for PRVC/PC vs. VC)

    References:

    1. Pierrakos C, Karanikolas M, Scolletta S, Karamouzos V, Velissaris D. Acute respiratory distress syndrome: pathophysiology and therapeutic options. J Clin Med Res. 2012;4(1):7–16. doi:10.4021/jocmr761w.
    2. Fanelli V, Vlachou A, Ghannadian S, Simonetti U, Slutsky AS, Zhang H. Acute respiratory distress syndrome: new definition, current and future therapeutic options. J Thorac Dis. 2013;5(3):326–334. doi:10.3978/j.issn.2072-1439.2013.04.05.
    3. ARDS Definition Task Force, Ranieri VM, Rubenfeld GD, et al. Acute respiratory distress syndrome: the Berlin Definition. In: Vol 307. 2012:2526–2533. doi:10.1001/jama.2012.5669.
    4. Ware LB, Matthay MA. The acute respiratory distress syndrome. N. Engl. J. Med. 2000;342(18):1334–1349. doi:10.1056/NEJM200005043421806.
    5. Deng, J. (10/20/13). Principles of Mechanical Ventilation. Medical Intensive Care Unit Lecture. Los Angeles, CA.
    6. Singer BD, Corbridge TC. Basic invasive mechanical ventilation. South. Med. J. 2009;102(12):1238–1245. doi:10.1097/SMJ.0b013e3181bfac4f.
    7. Hamed HMF, Ibrahim HG, Khater YH, Aziz ES. Ventilation and ventilators in the ICU: What every intensivist must know. Current Anaesthesia & Critical Care. 2006;17(1-2):77–83. doi:10.1016/j.cacc.2006.07.008.