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Dr Timur Krivitsky
Executive Producer
Hickams Dictum
Krivitskys Conundrum
It doesnt really matter, because at 3am on a
night shift, as the medical registrar, despite your
best efforts to obtain a thorough history and
examination from the cognitively impaired, NESB,
hypoxic patient and after altering the provisional
ED diagnosis of ceftriaxone, prednisolone and
frusemide deficiency, your diagnosis of infective
exacerbation of COPD, NSTEMI and UTI will be rediagnosed in the morning consultant ward round
as non-infective exacerbation of CCF, type 2 ACS
and asymptomatic bacteriuria.
Mrs I D, 83F
Past
medical history
Hypercholesterolaemia
DM2
- Insulin dependant
HTN
GORD
GOUT
Medications
Social History
Lives with son (primary carer)
Walks with 4ww
Home help q2/52
HOPC
Worsening epigastric pain over 4 months
10kg weight loss over 4 months
1
0
21/12/2016:
Gastroscopy
Likely malignant gastric biopsy in the incisura and anterior wall of gastrum
Biopsy
Ulcerated poorly differentiated adenocarcinoma
of intestinal type.
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1
02/01/16:
Histopathology:
Adenocarcinoma
Local invasion to serosal surface (pT4)
No perforation
1/8 lesser curve LN
5/8 greater curve LN
http://www.gastrotraining.com/category/gi-surgery/gastric-operations
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2
12/02/2016 29/03/2016: Admission UGIG
# epigastric pain (presenting complaint)
# fistula and gastrectomy wound dehiscence, managed with dressings,
slowly resolved.
# Iron deficiency anaemia infused with iron.
1
3
Since discharge from UGIG admission.
Recurrent exertional angina, relieved with rest
Serial troponin negative
Serial ECG negative
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Since discharge from UGIG admission.
Recurrent exertional angina, relieved with rest
Serial troponin negative
Serial ECG negative
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5
Distal gastrectomy
02/01/16
10.3
85
9.4
84
2PRBC
1
1
6.9 8
87 9
Fe
7.
6
92
1
6
2PRBC
9.5
96
7.0
105
9.5
97
2PRBC
7.2
99
Fe
B12
Current admission
5/5/16 - .
1PRBC
7.0
96
8.0
95
B12
Fe
Folat
e
WHF ED 20/4/16
Aberrant Hb 9.5 in setting of
?reaction to PRBC?
Lymphocytosis, APO and
transaminitis resolving.
1
7
Causes of anaemia?
1. GI bleed? Recurrence of malignancy?
- Pt denied malena/haematochezia, multiple PR negative
2. Anaemia secondary to Iron or B12 deficiency post RYG
- Timing?
3. Intra-abdominal bleed
- Complicated surgery
4. Haemolysis?
5. Allo antibodies?
1
8
Haemolysis screen:
Haptoglobin: 0.73 (0.36-1.95)
LDH: 251 (240-480)
Br: 3
Direct coombs text: negative
Reticulocyte count: 6% (0.3-2.0)
Absolute reticulocyte count: elevated
Urinary haemosiderin: not done
Blood film:
Known malignancy.
1. Red cell dimorphism and marked polychromasia,
suggestive of blood loss
+/- recent red cell transfusion.
2. Transient lymphocytosis, in keeping with
reactive process
1
9
CT abdo/pelvis 5/5/2016:
Resolution of the previously demonstrated anterior intra-abdominal collection with
communication with abdominal wall. No other appearance is essentially stable when
compared with imaging from 04/03/2016.
Gastroscopy 9/5/16:
Mild gastritis
Normal anastomosis
Mild perianastamotic inflammation
Suggest colonoscopy if continued Hb drop
2
0
TTE 08/07/2015:
Well seated TAVI/AVR. Normal iEOA of 14mm^2/m^2, DPI = 0.82.
PG 12mmHG, MG 5mmHg. No regurgitation.
TTE 07/01/0216:
Well seated bioprosthetic valve. Trivial regurgitation, likely
para-valvular at the native non coronary annulus.
2
1
Medication Safety
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4
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* Sadler JE, Mannucci PM, and Berntorp E et al, Impact, diagnosis and treatment of von Willebrand disease. Thromb Haemost.
2000;84(2):160.
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TYPE
1. Partial deficiency
2. Functional impairment
2A
2B
2M
2N
3. Severe deficiency
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7
Laboratory
Normal platelets
Normal PT
Normal or increased APTT (depending on degree of factor VIII
involvement)
Screening tests
1. Plasma vWF antigen (quantitative)
2. Plasma vWF activity (qualitative)
i. ristocetin cofactor activity
ii. vWF collagen binding
3. Factor VIII activity
TYPE 2 A,B,M,N (functional) = low vWF activity to antigen
ratio
vWFCB:vWFAg ratio < 0.7= suggests Type2 disease
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2
9
Experimental
1. Platelet function analyser assay (PFA 100)
- assesses the VWF-platelet interaction
- measures platelet plug formation in citrated whole blood,
- sample is aspirated through a capillary tube to a collagen + epinephrine
or a collagen + adenosine diphosphate-coated membrane that contains a
central aperture. The time to closure of the aperture by the forming
platelet plug is measured.
- closure time is dependent upon both VWF and intrinsic platelet function.
3
0
HADES
3
1
Heyde syndrome
Described in 1958 by Edward C Heyde, a Canadian internist.
Severe aortic stenosis (AS) + gastrointestinal bleeding due to
angiodysplasia
Acquired type 2A vWD
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2
https://en.wikipedia.org/wiki/Heyde%27s_syndrome
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n Batur, MD; William J. Stewart, MD; J. Harry Isaacson, MD. Increased Prevalence of Aortic Stenosis in
ents With Arteriovenous Malformations of the Gastrointestinal Tract in Heyde Syndrome. Arch Intern Med. 2003;163(15):1821-1824
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Gordon E. Pate, Mann Chandavimol, Sheldon C. Naiman et al. Heyde's Syndrome: A review. The Journal of
heart valve disease (Impact Factor: 0.75). 10/2004; 13(5):701-12.
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1. Review Heyde's syndrome: a review.Pate GE, Chandavimol M, Naiman SC, Webb JG. J Heart Valve Dis.
2004 Sep; 13(5):701-12.
2. Bleeding from the right colon associated with aortic stenosis.Boss EG Jr, Rosenbaum JM. Am J Dig Dis.
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4
0
(r = 0.56, P<0.001).
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2
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Retrospective study assessing Major Late Bleeding complications (>30days post TAVI)
from PARTNER-1 trial (multicenter, randomized clinical trial TAVR vs surgical AVR in
high risk patients)
2,401 pts
Gastrointestinal complications (n = 58 [40.8%]), neurological complications (n = 22
[15.5%]), and traumatic falls (n = 11 [7.8%])
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Conclusion
Post-TAVR paravalvular aortic regurgitation may represent the
perfect storm for acquired thrombophilia, ultimately leading to
major bleeding events.This biological phenomenon may
beamplified byusing aggressive antiplatelet therapy and/or
anticoagulation therapy
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Summary
The correlation between angiodysplasia and severe AS is compelling, but potentially
corrupted by age as a confounder.
The aeitiology of the relationship between angiodysplasia and AS is unclear.
The current evidence, despite a lack of prospective studies seems to point toward a
preponderance towards inherited thrombophillia in high grade AS, which is temporarily
but not sustainably reversed by aortic valve replacement (both surgical and TAVR)
Thank you