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Subjective: HPI
Pt is 54 y/o male with PMH of protein S deficiency with h/o unprovoked DVT x 2
(1997, 2005) and heavy EtOH use x 30 years presents from Bear Valley Hospital
with palpitations and associated SOB. Palpitations were intermittent for 2 weeks
then became constant for the past week. SOB exacerbated by exertion and lying flat
x 5 days. Pt admits to typical CP. Pt denies HA, fever, chills, nausea, vomiting,
LOC.
Subjective: History
PMH: BPH, DVT x 2, Venous Stasis with RLE ulcer
PSH: Splenectomy 2/2 MVA (1997), exploratory laparotomy 2/2 stab wound
Medications: Terazosin
Allergies: NKA
Family: Brother- DVTs, unknown protein deficiency. Sister- unknown protein
deficiency
Social: Tobacco/smoking quit 20 years ago, THC daily, 6 beers per day
ER Course
VS: BP: 125/96, P: 121, RR: 19, T: 98.1, O2: 98% RA
Cardizem 20 mg IV x 2
Cardizem 30 mg PO
Labs:
145
3.7
109
22
15
0.9
8.8 73
112
13.3
13.37
46.1
284
6.5 106
3.9 61
0.4
Objective
VS: BP: 105/72, P: 98, RR: 18, O2: 99% on 2L
Gen: WDWN. NAD. Lying comfortably
HEENT: EOMI, PERRLA, oral mucosa moist
Neck: Supple, No LAD + ND??
Resp: decreased bibasilar breath sounds, b/l apical crackles
CV: irregular irregular. No m/g/r. Peripheral pulses erratic
GI: Soft. NTND. Normoactive Bowel Sounds x 4.
Ext: 1+ pitting edema LLE, 2+ pitting edema RLE w venous stasis ulcer
Neuro: No focal defecits. CN II-XII grossly intact b/l. Gross sensation intact. Muscle Strength 5/5 b/l.
Etiology
Abnormalities or damage to the hearts structure -- most common cause
Other possible causes
HTN
MI
CAD
Structural valve disease
Congenital heart disease
Hyperthyroidism
CHA2DS2-VASc
- Estimation of Ischemic Stroke Rate http://www.mdcalc.com/cha2ds2-vasc-score-for-atrial-fibrillation-stroke-risk/
CHA2DS2VASc acronym
Unadjusted ischemic
stroke rate (% per
year)*
0.2%
0.6%
2.2%
3.2%
4.8%
7.2%
9.7%
11.2%
10.8%
12.2%
Algorithm
Protein S deficiency
Background
Protein S is mainly synthesized in hepatocytes, but also in megakaryocytes,
osteoblasts, and endothelial, Leydig and vascular smooth muscle cells.
The major function of protein S is as a cofactor to facilitate the action of activated
protein C (APC) on its substrates, activated factor V (FVa) and activated factor
VIII (FVIIIa). Protein S deficiencies are associated with thrombosis.
A deficiency can be inherited or acquired due to vitamin K-antagonist therapy, oral
contraceptives, pregnancy and various disorders, such as liver disease, nephritic
syndrome, disseminated intravascular coagulation and chronic infections (e.g. HIV).
Protein S has both APC-dependent and independent anticoagulant properties and
is an important regulator of thrombin generation and fibrinolysis.
Management
Management of protein S deficiency generally takes place in the event of acute venous
thromboembolism (VTE).
Following an acute thrombosis, administer heparin therapy and then transition to warfarin oral
anticoagulation.
Initial heparin treatment x 5 day minimum may be administered as intravenous unfractionated heparin or as
subcutaneous low molecular weight heparin (LMWH)
Warfarin administration can start on day 1 or 2 of heparin therapy.
After two consecutive International Normalized Ratio (INR) clotting tests and a minimum of 5 days of
heparin therapy, continue on warfarin alone. 6-9 months of initial treatment with warfarin is recommended.
Recommended life long therapy if the first thrombotic event was life threatening or occurred in
multiple or unusual sites (eg, cerebral veins, mesenteric veins)
If precipitated by a strong event (eg, trauma, surgery) and the thrombosis did not meet the
criteria of life threatening or multiple or unusual sites, can perform a trial without warfarin
after 9 months on the basis of low rate of recurrence.
Management
Prophylaxis for Asymptomatic carriers of protein S deficiency
In such patients, avoid drugs that predispose to thrombosis, including oral contraceptives. In these
patients, if surgery or orthopedic injury occurs, prophylaxis with heparin is mandatory.
In pregnancy, experts recommend prophylaxis with heparin; however, the timing is controversial.
Treatment from the second trimester through 4-6 weeks postpartum is generally recommended.
Patient bleeding risks must be assessed on an individual basis for any of these prophylactic
recommendations.