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Theres Always a First Time A Clinical Problem Solving Case Gurpreet - - PDF document

10/26/2015 Theres Always a First Time A Clinical Problem Solving Case Gurpreet Dhaliwal, MD Professor of Medicine University of California, San Francisco 1 10/26/2015 Ground Rules for CPS Exercise Goop has never heard these cases


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10/26/2015 1

There’s Always a First Time

A Clinical Problem Solving Case

Gurpreet Dhaliwal, MD Professor of Medicine University of California, San Francisco

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Ground Rules for CPS Exercise

 Goop has never heard these cases

 Not a trivial undertaking

 Goal is to make the thought process of a master

clinician transparent  It’s not magic  You don’t have to “know everything”

 “Getting it right” is cool, but relatively

unimportant in the grand scheme

 Enjoy – this is the fun part of medicine

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Ockham’s Razor vs. Hickam’s Dictum

 “Entities must not be multiplied beyond necessity.”

  • - William of Ockham

 “Patients can have as many diseases as they

damn well please.”

  • - John Hickam

History

 A 73-year-old man with a history of COPD and a

mechanical MVR/porcine AVR (on coumadin) was admitted to an outside hospital for several acute episodes of dyspnea over the prior month.

 He denied cough, CP, palpitations, orthopnea, or

  • fever. He did endorse mild abdominal distension.

 He had no prior history of PE, pneumonia, or

heart failure. He had never been hospitalized for

  • COPD. His valve surgery was 5 years earlier. He

claimed to be taking his coumadin. No travel history documented.

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ED Assessment and Exam

 The patient was noted to be wheezing and in mild

respiratory distress

 Afebrile, RR 20, O2 97% RA, BP 85/57, which

responded to fluids

 Initial ABG: 7.46/42/63 (RA)  WBC 9.7, diff normal  CXR unremarkable  A CT scan was neg for PE and volume overload; it

showed only mild bibasilar atelectasis

ED Management

 The patient was treated for a COPD

exacerbation

 He received a steroid burst, duonebs, and

azithromycin

 He improved over the first 6-12 hours but

was admitted for further treatment and

  • bservation
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What do you think is going on?

  • 1. Sounds like a routine case of COPD exacerbation. Is

Bob trying to fool Goop by giving him a bread and butter VA case?

  • 2. Must have something to do with the valves
  • 3. I remember one of my profs from med school saying

something like, “All that wheezes isn’t asthma,” but I can’t remember what it is

  • 4. Did he say “no travel history documented”?
  • 5. Did he also say “the patient claimed to be taking his

coumadin”?

Goop’s Initial Thoughts

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Hospital Course

 The patient’s abdominal distension (a mild complaint on

admission, not confirmed on exam) worsened over the first 2-3 days of hospitalization

 A KUB on hospital day 4 showed dilated bowel loops

consistent with ileus

 An abdominal CT was obtained: no evidence of ileus or

bowel abnormalities (his symptoms had improved)

 On hospital day 6, his breathing took a marked turn for the

worse – with severe dyspnea and tachypnea

 A diagnosis of respiratory failure was made  The patient was taken to the ICU and intubated

Now I’m worried about…

  • 1. Bowel ischemia
  • 2. Churg-Strauss vasculitis
  • 3. Inflammatory bowel disease
  • 4. Lupus
  • 5. Sepsis and ARDS
  • 6. A hypercoagulable state and in-situ thromboses
  • 7. That Donald Trump could really be our next

president

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ICU Course

 Repeat CXR unchanged from admission  TTE showed no evidence of heart failure, valvular

dysfunction, or vegetations

 Antibiotics were broadened to vanco and tigecycline  Blood cultures from the time of the deterioration grew

enterococcus faecalis

 Vanco was changed to linezolid  UA was negative  PICC line felt likeliest source of bacteremia and d/ced  Aggressive COPD rx led to improvement, extubated on

hospital day 14

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Post-Intubation Course

 The patient complained, for the first time, of back

pain and lower extremity weakness

 On further questioning, he noted that he had had

progressive leg weakness for several weeks

 Spinal imaging showed a T5-6 burst fracture with

retropulsion and mild central canal narrowing, along with soft tissue fullness around the spine, c/w necrotic mass or abscess

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Wow, that’s not good. Now I’m worried about…

  • 1. Syphilis
  • 2. Tuberculosis
  • 3. Lymphoma
  • 4. Cocci
  • 5. Endocarditis
  • 6. MRSA
  • 7. Sorry, I’m still worried about Donald Trump
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Post-Intubation Course

 Cocci serum titers sent and returned weakly

positive

 Started on fluconazole  Soon, cocci immunodiffusion and comp fix

returned negative, so fluconazole d/c’ed

 Patient transferred from community hospital

to UCSF neurosurgery service

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10/26/2015 12 Past Medical History (obtained at UCSF admission)

 COPD (no prior PFTs, hospitalizations)  HTN  Bioprosthetic AVR & Mechanical MVR (both placed 2

yrs earlier)

 Knee osteoarthritis, treated with NSAIDs, injections  Hypothyroidism

SH: Originally from Guatemala, with frequent trips back. Single, lives with son. 20 pack year tobacco hx, quit in

  • 1992. 2 cans of beer/wk. No elicits. Used to work in a

warehouse; now retired. FH: Son with pulmonary TB rxed for at least 6 months (more than 20 years ago). No other history of cardiac, pulmonary, infectious, rheum, heme, bone disorders. NKDA Home Meds: Coumadin Carvedilol Lisinopril Furosemide Simvastatin Levothyroxine Omeprazole Vitamin D Meds on transfer: Fluconazole Budesonide nebs Furosemide Aspart insulin SS Levothyroxine Famotidine Docusate Senna Polyethylene glycol Ferrous sulfate

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Physical Exam After Transfer

VITALS: 36.9 °C, 98, 159/43, 20, 95 % RA GENERAL: Deeply sedated. HEENT: NC/AT. Neck supple. No JVD. CVR: RRR. Mechanical second heart sound. No m/r/g. PULM: Clear to ascultation bilaterally. ABD: Soft, non-tender. Distended and tympanitic. MSK: No edema. Warm distally. NEURO:

After lightening sedation, the patient was A+O x 2.

PERRL, EOMI.

5/5 strength in face and BUE with no pronator drift. No movement in LE’s. Absent rectal tone.

Nl sensation to light touch and pain in bilat UEs. Sensory level at T3~T4.

0+ reflexes in patella/ankles bilaterally; UE reflexes normal.

Labs

WBC: 16.6 Hgb: 13.1 Plt: 411 Na: 129 K: 4.4 Cl: 95 CO2: 25 BUN: 7 Cr: 0.5 Glucose 126 Ca: 9.2 PTT 37.4, INR 1.9 CRP 112 ABG: 7.44/41/382 (60% FiO2) Lactate 0.8 Blood, urine cultures sent EKG: LVH with repolarization abnormality

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CXR at time of transfer

Low lung volumes. RLL patchy consolidation. Diffuse indistinct pulmonary vascularity.

Studies

KUB: Nonspecific bowel gas pattern. TTE:

  • 1. Normal ventricular size and EF.
  • 2. Severe concentric LVH. Paradoxical septal motion.
  • 3. Mod LAE. Nl right atrium.
  • 4. Mechanical mitral prosthesis normal. Bioprosthetic

aortic valve normal.

  • 5. Mitral prosthesis precludes the accurate

evaluation of diastolic function.

  • 6. PASP estimated 12-16 mmHg.
  • 7. No pericardial effusion.
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MRI Spine – T2 MRI Spine – T2

Vertebral collapse at T5, 50% height loss at T6. Retropulsion at T5 leading to canal stenosis. Abnormal cord signal T7 on up, with moderate cord compression at T5-

  • 6. Pre-syrinx (fluid

filled cavity within cord) formation.

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Neurosurgery Management

 While the neurosurgeons felt there was little hope for LE

recovery, the pre-syrinx formation risked moving upwards, potentially compromising UE function

 Recommended decompressive laminectomy  A few days after transfer, pt had posterior spinal fusion  Finding: epidural phlegmon,T5 fracture with cord infarct,

spinal stenosis—fused.

 Fluid from phlegmon, tissue from ligament sent for culture

and path

 Path: hypercellular, esp. plasma cells, but not clonal  C/w chronic inflammation  Micro: gram stain, culture, AFB, special stains all negative

Post-op Labs

Day 30 (2 days post-neurosurgery) labs: WBC 16.9, with 6.51K eos (39%) Looking back: Admission to outside hospital: WBC 9.7, 194 eos (2%) Day 16: 270 eos (3%) Day 26: (day prior to transfer, 2 days pre-op) 3.6K eos (40%) (This bump in eos was not previously recognized)

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  • Huh. Eos. Wow. Now…

1.

Could this be a really nasty case of asthma?

2.

Could this be whatever they call Wegener’s now?

3.

Can TB do this?

4.

Can cocci do this?

5.

Could this all be a worm?

6.

Could this be another sign of thromboembolism?

7.

Pulmonary infiltrates and eos… I think that’s a syndrome

8.

Gotta be from one of his drugs

Goop’s Riff on the Eos

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Hospital Course

 Because eos developed in-house, suspicion for drug

reaction

 Antibiotics changed to aztreonam, dapto

 Stool O&P and strongyloides antibody sent, along

with IgE, ANCA, SPEP, UPEP

 Cosyntropin test sent to r/o adrenal insufficiency  Eos continued to rise, peaking at 9.8K  Patient continued to have episodes of respiratory

distress and wheezing

 A chest CT was performed to further assess lungs

and eosinophilia

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10/26/2015 19 Low lung volumes; diffuse ground glass

  • pacities,

some ill defined nodules.

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Bronchoscopy

 Differential: 88% monos, 5% lymphs and 7% eos  Gram stain & culture: Mod mixed gram positive flora  CMV culture: positive  Pneumocystis: negative  KOH stain and fungal culture: negative  No strongyloides on parasite wet mount  AFB smears: negative  Respiratory virus panel PCR and Ag testing: negative

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Recurrent respiratory distress

 On hospital day 40, the patient woke from a nap with

severe respiratory distress  Exam, Diffuse expiratory wheezing, RR 20  30

 92% on 2L  87% on 2L  ABG 7.30/58/107  CXR unchanged  Continuous nebs, tx to ICU for bipap, trial of diuresis  VBG 7.32/53  A diagnostic test returned

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Goop, Time to Take a Shot Gurpreet Dhaliwal, is that your… final answer?

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A diagnostic test returned…

 Strongyloides antibody: 3.76, 4.94 on repeat  Stool O&P: Strongyloides stercoralis rhabditiform

larvae

 ANCA neg  SPEP, UPEP unremarkable  HIV neg  Cort stim 6  15

Treatment

 The diagnosis of strongyloides hyperinfection was

made, involving lungs, GI tract, and possibly vertebrae

 Started treatment with ivermectin, 15 mg/d  Steroids weaned and then held  Patient placed on bipap along with COPD meds  Over next few days, rapid improvement in respiratory

condition

 Discharged back to outside hospital for PT for

paraplegia, with markedly improved pulmonary status

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Final Diagnosis

 Strongyloides stercoralis hyperinfection with  Pulmonary infiltrates and recurrent wheezing  Eosinophilia  Gram-negative bacteremia  Spinal osteomyelitis with cord compression  Strongyloides vs. enterococcus faecalis

Special thanks to Kara Bischoff for preparing the case

Ddx of Profound Eosinophilia

 ID: Parasitic infections, certain fungi (cocci, ABPA),

infestations (scabies)

 Allergic or atopic diseases  Heme-Malignant: hypereosinophic syndromes, some

leukemias & lymphomas, other tumors (particularly lung, bladder), systemic mastocytosis

 Immunologic: HyperIgE syndrome, GVH disease  Endocrine: hypoadrenalism  Other: radiation, atheroembolic, sarcoid

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Doesn’t anybody take histories anymore?

DDx of Eosinophilic Lung Diseases

Primary

Simple pulmonary eosinophilia

Chronic eosinophilic pneumonia

Acute eosinophilic pneumonia

Churg-Strauss vasculitis

Idiopathic hypereosinophilic syndrome

ABPA

Bronchocentric granulomatosis

Secondary

Drug-induced

Parasite-induced

Fungal-induced

Diseases Assoc w/ Eos

Asthma

Ideopathic pulmonary fibrosis

Sarcoidosis

Hypersensitivity pneumonitis

Malignancy

Langerhans cell granulomatosis

Cryptogenic organizing pneumonia

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Strongyloides Hyperinfection Syndrome

 Parasite endemic in tropical, subtropical regions

 Including SE United States

 Normal life cycle: skin->lungs->GI tract  Autoinfection cycle: may lay dormant for decades, or

cause indolent disease w/ GI symptoms and eosinophilia

 With immunosuppression, massive growth in disease

burden, disseminated disease  Lungs, GI tract (enteric bacteremia), skin, CNS  No cases of strongyloides osteomyelitis reported, but

there is one case of entercoccus faecalis involving CNS in setting of hyperinfection

Rhabditiform larvae of strongyloides found in stool specimen

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There’s Always a First Time

A Clinical Problem Solving Case

Gurpreet Dhaliwal, MD Professor of Medicine University of California, San Francisco

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