Regional Pericarditis: an unusual diagnosis Nitin Gupta DO, Juan - - PowerPoint PPT Presentation

regional pericarditis an unusual diagnosis
SMART_READER_LITE
LIVE PREVIEW

Regional Pericarditis: an unusual diagnosis Nitin Gupta DO, Juan - - PowerPoint PPT Presentation

Regional Pericarditis: an unusual diagnosis Nitin Gupta DO, Juan Pablo Rodriguez-Escudero MD, Rehan Ansari MD, Roger Chaffee MD, Otto Costantini MD Overview Review Case Differential Diagnosis Disease Pathogenesis Patient Update


slide-1
SLIDE 1

Regional Pericarditis: an unusual diagnosis

Nitin Gupta DO, Juan Pablo Rodriguez-Escudero MD, Rehan Ansari MD, Roger Chaffee MD, Otto Costantini MD

slide-2
SLIDE 2

Overview

▪ Review Case ▪ Differential Diagnosis ▪ Disease Pathogenesis ▪ Patient Update

slide-3
SLIDE 3

HPI

74 yo CM presents to ED with left sided chest pain. Started 45 minutes after trimming rose bushes. Pleuritic in nature, radiating across chest, associated with SOB. Took ASA. Pain eased to dull sensation with nitro.

slide-4
SLIDE 4

Medical Hx

▪ PMHx: OSA (compliant with CPAP), HLD, RLS ▪ PSHx: R Knee arthroplasty 3/2017, Lumbar fusion 1/2018 ▪ FamHx: n/a ▪ Social Hx: Former Smoker (quit in 1974), social drinker (once every couple of months), denies illicit drugs

slide-5
SLIDE 5

Physical Exam

▪ Vitals: BP 133/78 | Pulse 72 | Temp 97.8 °F (36.6 °C) (Oral) | Resp 18 | SpO2 97% ▪ General appearance: alert, appears stated age and cooperative ▪ Skin: Skin color, texture, turgor normal. No rashes or lesions ▪ HEENT: Head: Normocephalic, no lesions, without obvious abnormality. ▪ Neck: no adenopathy, no carotid bruit, no JVD, supple, symmetrical, trachea midline and thyroid not enlarged, symmetric, no tenderness/mass/nodules ▪ Lungs: clear to auscultation bilaterally ▪ Chest Wall: No TTP ▪ Heart: regular rate and rhythm, S1, S2 normal, no murmur, click, rub or gallop ▪ Abdomen: obese, non-tender; bowel sounds normal; no masses, no organomegaly ▪ Extremities: extremities normal, atraumatic, no cyanosis, +2 BLE nonpitting( pt states chronic) ▪ Neurologic: Mental status: Alert, oriented, thought content appropriate

slide-6
SLIDE 6

Labs

HbA1c 5.4%

slide-7
SLIDE 7

Imaging

▪ CXR: No acute pulmonary process ▪ CTA Chest: No acute process, coronary calcifications

slide-8
SLIDE 8
slide-9
SLIDE 9

Hospital Course

▪ Repeat troponins: 2.140, 4.520 ng/ml ▪ Patient treated medically for NSTEMI ▪ LHC done next day showed multivessel disease:

– 1. LVEF 70-75% no RWMA

  • 2. Left main: Distal vessel lesion: There is a 70% stenosis.
  • 3. LAD: Mid-vessel lesion: There is a 70% stenosis.
  • 4. Right coronary: Proximal vessel lesion: There is an 80% stenosis. Distal

vessel lesion: There is an 80% stenosis.

  • 5. IVUS of LAD-LM shows discrete lesion in the LAD after the DIAG-1

▪ Two days later patient underwent CABG (LIMA to LAD, SVG to PDA, ramus marginalis and posterior lateral branch of circumflex)

slide-10
SLIDE 10

Hospital Course Cont’d

▪ Extubated same day, began having pleuritic chest pain the next day ▪ PE unremarkable, troponins down trending

slide-11
SLIDE 11
slide-12
SLIDE 12

Differential Diagnosis

▪ Unusual localized pericarditis ▪ LIMA to LAD occlusion ▪ Spasm

slide-13
SLIDE 13

Hospital Course Cont’d

▪ No acute intervention was done as patient’s symptoms and EKG were not concerning enough that aggressive measures needed to be taken, and patient showed resolution in symptoms and EKG changes quickly ▪ Patient was discharged to cardiac rehab a few days later with following EKG

slide-14
SLIDE 14
slide-15
SLIDE 15

Regional Pericarditis

▪ Pericarditis is the most common cause of chest pain following and acute MI ▪ Typically occurs 1-2 months post cardiac injury (i.e. MI or CABG), referred to as Drexler Syndrome ▪ Hypothesized to be an autoimmune response ▪ Localized irritation of pericardium can produce focal ST-segment elevations and can be misdiagnosed as an acute STEMI ▪ No set criteria to diagnose

– Diffuse PR segment depressions with PR segment elevation in aVR

▪ Pericardial effusions may be seen in 85% of patient following CABG, friction rub much less common with an incidence of 13%

– Can be confused with mediastinal rub (surgical emphysema) frequently seen after cardiac surgery

slide-16
SLIDE 16

Patient Update

▪ Recent office visit to cardiologist, no recurrence in symptoms and doing well

slide-17
SLIDE 17

References

▪ UpToDate, Post-Cardiac Injury Syndromes ▪ Journal Article, The postcardiac injury syndrome: case report and review of the literature (2006) ▪ Journal Article, Post-cardiac injury syndromes. An emerging cause of pericardial diseases (2013)

slide-18
SLIDE 18

Propofol Embolism via previously unknown Atrial Septal Defect resulting in Opisthotonos and Chemical Meningitis

Davis S. Mann

slide-19
SLIDE 19

Medical History

  • PMH: Sigmoid Stricture, HTN, HLD, DMT2, Colovaginal fistula, Colon Cancer
  • Surgical Hx: Colonoscopy, C-section, Sigmoidectomy, EGD

○ Colonoscopy 03/2014: Proximal sigmoid stricture ○ Colonoscopy 06/2017: Pancolonic Diverticulosis, colon polyp, rectal anastomosis

  • Family Hx: HTN, DM
  • Social Hx: Occasional Alcohol consumption
slide-20
SLIDE 20

Recent Admission

  • 05/2019: Increasing dysphagia to solid foods, weight loss > 60 lbs

○ Dysphagia since 2016 (s/p intubations) ○ GI Consulted ■ Barium Swallow Study ■ EGD

slide-21
SLIDE 21

Impression: Smooth long segment moderate stricture of the mid and distal esophagus

slide-22
SLIDE 22

EGD

  • “Esophagus appears normal for about 5cm, however beginning at 20cm it severely narrows.”
  • “... complete circumferential ulceration/exudate with some areas beneath the exudate showing a bluish discoloration, possibly

ischemic all the way down the EGJ…”

  • Biopsies taken: ulceration and inflammation consistent with acute esophagitis
  • CT Surgery consulted secondary to risk of perforation, EGD with dilation
  • Discharged, return in 2 weeks for repeat
slide-23
SLIDE 23

Repeat EGD

  • EGD, prior to dilation, while advancing scope had disruption of mucosa, procedure aborted and transferred to main OR for

removable, completely covered esophageal stent placement

○ VS: BP 140s/80s, HR 100s, SpO2 96% on RA, RR 20

  • Patient stented
  • Patient would not awaken after first EGD, thought to be secondary to persistent anesthetic effect
  • Patient kept intubated, biting ETT, resedated (Propofol), noted rigidity, muscle fasciculations, diaphoresis
  • Transfer to HLU
slide-24
SLIDE 24

Stroke Team

  • Vitals: HR 110, BP 140s/70s, RR 18, SpO2 95% on RA
  • PE: Intubated, dilated pupils, increased jaw jerk with anti bite, rigidity in all extremities LE>UE, posturing extension
  • Neurologic Examination: Obtunded/Lethargic, reacted to voice?
  • CT Head non contrast, CT Brain Perfusion, CTA Head/Neck, CT Chest non contrast
  • STAT EEG, Keppra Loaded 1g BID, Versed gtt
slide-25
SLIDE 25

There are low density lesions scattered in the cerebral hemisphere and right cerebellum consistent with lipomas

slide-26
SLIDE 26

Hospital Course

  • CTA: Patent vertebrals, 50% stenosis of the LICA
  • CT Chest: Well positioned stent, no effusion, no mediastinal air, no mass
  • EEG 06/07: No clear seizures or epileptiform activity seen, abnormal consistent with severe generalized nonspecific cerebral

dysfunction

  • EEG 06/08: Exactly the same
slide-27
SLIDE 27

Hospital Course

  • MRI Brain: Diffuse leptomeningeal enhancement throughout both cerebral and cerebellar hemispheres, concern for meningitis

vs leptomeningeal spread, no acute ischemic injury

  • MRI Cervical Spine: multilevel cervical spondylosis
  • Empiric abx and antiviral therapy initiated
  • Discontinued Keppra
  • Discontinued Versed gtt
  • Repeat CT Head:

○ “The scattered, small, fat density parenchymal foci present on the CT head examination previously are no longer on the current study” ○ Mild Cerebral Edema

slide-28
SLIDE 28

Hospital Course

  • Lumbar Puncture:

○ Glucose 151, Protein 1277, 85, MEP negative, Herpes Negative, Lyme Negative, VDRL negative ○ Cytology: No malignant Cells ○ Fat stain and Lipid panel: Unable to be performed ○ Antibiotics/Antiviral discontinued

  • Concern for Right to Left Shunting

○ TCD w/ Bubble study: Did not show right to left shunting ○ TTE: “ Doppler shows no evidence of shunt. There is no evidence of right to left shunting with injection of agitated saline contrast” ■ EF 54%, RWMA noted consistent with Takotsubo Cardiomyopathy

  • Trach/PEG, discharged to SNF
slide-29
SLIDE 29

Update on Patient

  • Esophageal Stent removal and TEE performed 07/09:

○ CFD and doppler positive. There is evidence of shunting with injection of agitated saline contrast

  • Returned secondary to “concern for seizures”, started on Keppra at SNF
  • Intermittent episodes of lucency, eyes to fix and follow, with occasional command following (closing eyes), nonverbal
  • Palliative Care/Hospice

○ Patient with minimal improvement

  • Patient expired on 09/06/2019
slide-30
SLIDE 30

Sedation Medications History

  • Laparoscopic LAR 04/16/2017: Propofol 200mg, via 20 gauge in PIV
  • Colonoscopy 06/20/2017: Propofol 560mg, via 20 gauge in Right AC
  • EGD 05/17/2019: Propofol 350mg, via 20 gauge in Right AC
  • EGD w/ Dilation 05/21/2019: Propofol 200mg, via 20 gauge in Right AC
  • EGD w/ Stent Placement 06/07/2019: Propofol 200mg, via PIV
  • Propofol 300mg PIV (re-sedated)
slide-31
SLIDE 31

Chemical Meningitis

  • Caused by certain substance or chemical

○ Drugs ○ Rupture of benign tumors

  • Sterile
  • Treatment: supportive care, steroids, surgical
slide-32
SLIDE 32

Opisthotonos

Uptodate: truncal rigidity and back arching Thought to be secondary to enduring refractoriness in inhibitory pathways of the cerebellum, brainstem, and spinal cord

slide-33
SLIDE 33

Treatment

  • Recommended to avoid antiepileptic drug
  • Agents that accentuate glycinergic and GABAergic inhibition

○ Benzodiazepines: Accentuate GABA 1 receptors ○ Physostigmine: restpore spinal inhibition by stimulating Renshaw cell inhibition ○ Baclofen: GABA B agonist properties ○ Hydrocortisone: Potentiate glycine actions

  • Avoid propofol, morphine, fentanyl - can all antagonize glycine
  • Anaesthetic induced opisthotonos/”Seizure-like” movements - Benzos
slide-34
SLIDE 34

Layman's Odds

  • What is the likelihood of propofol able to transverse the venous system to the Right Atrium, cross through a ASD through a low

to high pressure gradient (Right-to-left shunt) in an otherwise structurally normal heart, and then shoot up to the brain, all while withstanding rapid redistribution to the tissues and on-going metabolism?

  • Alternative theories

○ Accumulation on surfactant with microemulsions absorbed by capillaries

slide-35
SLIDE 35

Acknowledgements

  • Dr. Susanna Bowling
  • Dr. Eric Espinal
  • Dr. Shelly Barker
slide-36
SLIDE 36

References

  • Uptodate
  • Opisthotonos following propofol: a nonepileptic perspective and treatment strategy - CAN J ANESTH 1994
  • Seizures and Opisthotonos After Propofol Anesthesia - Anesth Analg 1992
slide-37
SLIDE 37

Questions?