there s always a first time
play

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


  1. 10/26/2015 There’s Always a First Time A Clinical Problem Solving Case Gurpreet Dhaliwal, MD Professor of Medicine University of California, San Francisco 1

  2. 10/26/2015 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 2

  3. 10/26/2015 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. 3

  4. 10/26/2015 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 observation 4

  5. 10/26/2015 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 5

  6. 10/26/2015 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 6

  7. 10/26/2015 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 7

  8. 10/26/2015 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 8

  9. 10/26/2015 9

  10. 10/26/2015 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 10

  11. 10/26/2015 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 11

  12. 10/26/2015 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 Meds on transfer: Fluconazole Home Meds: Budesonide nebs Coumadin Furosemide Carvedilol Aspart insulin SS Lisinopril Levothyroxine Furosemide Famotidine Simvastatin Docusate Levothyroxine Senna Omeprazole Polyethylene glycol Vitamin D Ferrous sulfate 12

  13. 10/26/2015 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 CRP 112 Plt: 411 ABG: 7.44/41/382 (60% FiO2) Na: 129 Lactate 0.8 K: 4.4 Cl: 95 Blood, urine cultures sent CO2: 25 BUN: 7 EKG: LVH with repolarization Cr: 0.5 abnormality Glucose 126 Ca: 9.2 PTT 37.4, INR 1.9 13

  14. 10/26/2015 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. 14

  15. 10/26/2015 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. 15

  16. 10/26/2015 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) 16

  17. 10/26/2015 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 17

  18. 10/26/2015 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 18

  19. 10/26/2015 Low lung volumes; diffuse ground glass opacities, some ill defined nodules. 19

  20. 10/26/2015 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 20

Download Presentation
Download Policy: The content available on the website is offered to you 'AS IS' for your personal information and use only. It cannot be commercialized, licensed, or distributed on other websites without prior consent from the author. To download a presentation, simply click this link. If you encounter any difficulties during the download process, it's possible that the publisher has removed the file from their server.

Recommend


More recommend