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Morning Report, Bettina Manduca, 2014

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Bettina Manduca

on 5 May 2016

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Transcript of Morning Report, Bettina Manduca, 2014

MICU Evolution
Organizing Pneumonia
Increase pulmonary vascular congestion can not exclude mild interstitial pulmonary edema
Labs and Ancillary

DM type II uncontrolled
HTN Class 1
Chronic Anemia
Obesity
S/P amputation of right fourth and fifth toe secondary to gangrene/acute osteomyelitis
Former tobacco smoker and cocaine abuser
From Odyssey House

PMH
Pertinent positive findings include:
Chills
Fever
Malaise
Anorexia
Odynophagia
Cough with yellowish phlegm in the last week

ROS
ER
Laboratory
CBC:

17
(neut%
79
) >
9.1
/
28
< 377 MCV
76
RDW 14.5
BM
P:
132
/4
.0/98/25 Glucose
314
BUN/Cr
33
/
1.5

Lactate: 1.0
LFT: 23/23/
161
/0.54/0.17/7.1/
2.1
ESR:
111

CRP:
205
A1C:
10
UA: negative nitrate and Leuk Esterase

ER (continued)
Admitted to Medicine Wards for:
SIRS secondary to gangrene on right foot r/o acute osteomyelitis
Podiatry evaluation stat
Vascular duplex of extremities
Blood cultures sent
IV empiric antibiotics to cover MRSA and based on prior cultures and sensitivity
IV fluids
AKI work up

Initial Orders
Hospital Course
Patient presented s/p amputation second right toe with:
Tachypnea
Tachycardia
Hypoxemia
Pleuritic chest pain
Bi-basal crackles

MICU consulted
Hospital Course
What do you think is happening?
Pulmonary Embolism
Pneumothorax
Acute Heart Failure
Pneumonia
Acute Coronary Syndrome
CC: bluish-black discoloration of the second right toe

36 year old male who presented to the ED complaining of discoloration of second right toe for the last three days associated to malaise and fever for the last 24 hours, moderate pain on ambulation and swelling of the right leg
HPI
Morning Report

Vital Signs
BP:
153
/73
P: 85
RR: 16
O. Sat: 100% RA
T:
100.4
F
Physical Exam
Extremities: right second toe with black eschar, edema and rubor
Distal pulses non palpable bilateral
Images
Right foot XR: soft tissue emphysema consistent with gangrene
AKI improving
UA: no active sediment, glycosuria and proteinuria
FENa: <1%
Renal and Bladder US:
- no hydroneprhosis
- high post void residual
Medical clearance for I&D.
Vascular duplex: 7/14/14 left GSV thrombosis below the knee


Differential Diagnosis
EKG
CXR


ABG at FIO2 30%:
PH 7:44
PCO2: 35
PO2:
53

HCO3: 24
Management
First Impression
Type 1 respiratory failure with high suspicion of PE
R/O other causes of acute onset of dyspnea
Superficial Venous Thrombosis (Left GSV)
Right foot gangrene s/p second toe amputation
DM type 2 uncontrolled
AKI improving
Hypertension
Obesity, class II
Moderate protein caloric malnutrition
Patient started on Heparin drip/prior coagulation panel ordered
Echo:
- EF >55%
- normal RSVP
- no wall abnormalities
Pro BNP:
2057
ACS: unremarkable
Chest CT with PE protocol done

No evidence of acute central PE

Bilateral lower lobe airspace disease consistent with pneumonia

Small to moderate bilateral pleural effusion more in the right side

Patient started on Azithromycin to cover atypical microorganisms

D/C heparin drip

Hypercoagulability panel negative

No indication for long term anti-coagulation on SVT

ID agreed on antibiotic therapy (vanco/zosyn and zithromax)

High flow oxygen, incentive spirometry, bronchodilators and OOB to chair
Despite appropriate treatment patient condition continued to deteriorate:
- severe respiratory hypoxic failure
- worsening bilateral lower infiltrates
Reviewed of prior CXR showed chronic underlying lung parenchymal disease
- history of former smoker and crack use
High suspicion of AIP
Titrate FIO2 to keep O2 Sat >90%
Serial ABGs to check P/F ratio
BiPap settings IPAP:15, EPAP: 7, FiO2: 50%
Blood cultures negative
Sputum culture negative for organism, few white blood cells
Legionella Ag negative
Mycoplasma Ab Ig M negative
HIV 1 - HIV 2 negative
Cryptococcal Ab negative
Histoplasma Ab negative
ID Work Up
ANA negative
RF negative
DNA DS negative
Centromere Ab <1
SCL- 70 Ab <1
Jo-1 Ab <1
C-ANCA negative
P-ANCA negative
Anti- GBM negative
Low C3 and C4




Connective and Vasculitis Work Up
Patient hemodynamics stable but acute respiratory failure with worsening infiltrates on CXR and P/F ratio <
200
Patient
was unable to tolerate bronchoscopy

Repeat Echo EF preserved and moderate pulmonary HTN / RSVP 50-60 mm Hg
Pro BNP:
4493

ARDS secondary most likely secondary to AIP
Started on
Methylprednisolone 500 mg

IVPB q 6hr
and continued on broad spectrum ATB
07/15/2014
07/27/2014
Mini- thoracotomy with wedge resection of RML and RLL 7/28/14

Patient remained intubated post procedure

Pleural fungal and anaerobic culture partial negative

Preliminary virus culture of pleural fluid after 7 days of incubation negative

Pleural AFB smear: negative

Pleural cytology: negative for malignancy
Organizing Pneumonia (OP) pattern

Type 2 pneumocyte hyperplasia and alveolar histiocytes, edema and hemorrage

Focal interstitial inflammation

Vascular congestion and microemboli
Pathology Report
Pathology Report
No hyaline membranes

No granulomas or viral inclusions

GMS stain negative for fungi

Kinyoun ’s stain negative for AFB
Many Thanks!
Inflammatory lung disease with distinctive clinical radiological and pathological features
Definition
Types
COP (
Cryptogenic Pneumonia) formerly
BOOP

SOP (
Secondary Organizing Pneumonia)
COP incidence 6-7 cases over 100.000 hospital admission
Epidemiology
OP is more likely the result of a type of alveolar epithelial injury and repair rather than a disease with one defined etiology
Pathogenesis
COP equally affect men and women usually at aged between 50-60 years old

Sub acute onset of symptoms
Malaise
Anorexia
Weight loss
Fever
Persistent dry cough
Dyspnea

PE: inspiratory sparse crackles
Clinical Features
CXR
CT chest high resolution
Laboratory test
infection, malignancy, connective tissue disorder
PFT
mild restrictive pattern
BAL
mixed pattern with lymphocytes predominance
Lung biopsy
trans-bronchial versus thoracoscopy
Diagnosis

Community Acquired Pneumonia

persistent of symptoms and lack of response to ATB. As OP can be a consequence of certain infections, positive culture results do not necessary exclude the diagnosis

Idiopathic Interstitial Pneumonias
COP is one type of idiopathic interstitial pneumonia (IIP), and the other types of IIP are in the differential of COP
Differential Diagnosis
Differential Diagnosis

Chronic Eosinophilic Pneumonia
Hypersensitivity Pneumonitis
Pulmonary Lymphoma
Pulmonary Lymphomatoid Granulomatosis
Diffuse Alveolar Damage
Unilateral of bilateral consolidation (90%)
Subpleural or peribronchial distribution (50%)
Lower lobes predominate
Migratory
Pleural effusion uncommon or rare
Treatment
Mild to moderate disease

Prolonged course of
three to six months of macrolide
(Clarithromycin 250 to 500 mg BID) and tapering to once daily dose


Prednisone 60 mg daily for 4 to 8 weeks
then taper to
0.5- O.75 mg/kg per day
(using ideal body weight) for 4 to 6 weeks and if patient remains stable continue gradually tapering to zero

Fulminant disease:

Methylprednisolone 125 to 250 mg IV every 6 hr.
or a pulse of 750 to 1000 mg daily for three to five days and transition to
Prednisone 0.75 to 1 mg/Kg/ day
to a maximum of 100 mg/day

Cyclophosphamide
if unresponsive to steroids and/or respiratory failure on mechanical ventilation support
Initial dose 50 mg daily
and increase over two or four weeks up to a maximum of 150 mg /day
Prognosis
Relapses are common upon stopping or tapering dose of steroids

Follow-up with
CXR and PFTs
every 2-3 months during therapy
and up to one year after discontinuing steroids
Bettina Manduca
PGY-2
Cryptogenic organising pneumonia is a particular form of inflammatory and fibroproliferative lung disease. The disease onset is subacute with cough, dyspnoea, fever, weight loss, and elevation of biological inflammatory markers.

Chest imaging usually shows multifocal alveolar opacities predominating in the subpleural regions. Lung biopsy reveals budding connective tissue filling the distal airspaces.
The diagnosis is established by combining clinical, radiological and histological criteria. Similarities with other disease processes can lead to a delayed or erroneous diagnosis. Most patients respond well to corticosteroid therapy (prednisone or methyl-prednisolone). Relapses are frequent but can generally be controlled.

There are literature data about the immunomodulatory properties of some macrolides in cryptogenic organizing pneumonia (COP) as an alternative to corticosteroids in mild disease or as adjuvant to standard therapy.
CONCLUSION
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