2. History of
Present
Illness
45 y/o WF is seen at bedside at AM rounds. Pt
complains that she feels lousy and had a
difficult time sleeping last night. Pt is 2 days
s/p triple arthrodesis of the right foot for
severe acquired flatfoot. Pt denies F/V/CP/SOB
and states that she feels cold and lousy.
3. Subjective
• Allergies: PCN; codeine
• Meds:
• Clinda 600 mg q6h
• Atenolol 50 mg qd
• Glucotrol XL 5 mg qd
• ASA 325 mg every other day
• Premarin .625 mg qd
• Depomedrol injection every three months
• PMH: HTN, DM2 x 10 years
• SHX: Smokes 2ppd x 25 yrs. EtOH occasionally
• FHX: Mother deceased at 82 gunshot to the head; Father
deceased at 74 from massive MI ROS: HEENT: occasional
headaches; CV: dx with a heart murmur in 1998
4. Physical
Exam
Vitals: Ht 62 inches; Wt 168 lbs; T 101.1; P: 92; R 24;
BP 185/90
Integ: upon removal of the cast, medial and lateral
incisions appear intact with some tension noted;
suture intact; some periwound erythema and edema;
right calf appears swollen compared to the left.
Vasc: Non-palpable, right due to edema. Palpable
pedal pulses, left.
Neuro: decreased to SWM b/l
M/S: pain to palpation of the right posterior calf
5. What do you
have to rule
out at this
point? And
how do you
rule it out?
• Atelectasis – chest x-ray
• UTI – UA with cultures
• DVT – venous duplex doppler
• Wound infection – clinical correlation
• Drug fever
6. What are the
five causes of
post – op fever
and what is the
time period in
which they
occur?
• Wind: 12 hours
• Water: 24 hours
• Walking: 12 – 48 hours
• Wound: 2 – 4 days
• Wonder Drug: anytime
7. Results
• Chest x-ray is negative; pt has been using the incentive
spirometer once every hour for five minutes; pt does not
complain of shortness of breath or chest pain
• UA results are the following
• pH: 6.5
• Specific gravity: WNL
• Bacteria: 0
• Leukocyte esterase: negative
• Color: straw
• WBC 2/field
• Nitrities: negative
• Duplex Doppler was positive for acute DVT in the
posterior tibial vein of the right leg
• No work up needed because no wound infection
suspected. Normal post op changes to the peri-wound
areas.
8. Treatment
example
- Pt started on 15,000 u bolus of heparin IV
- Pt given 1400 u heparin IV/hr
- PTT was checked four hours after initiation of therapy and found to be
46 sec (normal = 25 – 35s)
- Pt was given a bolus of 3000i IVP and 1452u/hr
- PTT was checked again four hours after adjustment of therapy: 75 sec
(you want the PTT to be 70 – 95here)
- Pt was started on 10 mg of coumadin 24 h after initial diagnosis of
DVT; pt was give 10 mg of coumadin the next day
- PT was taken and INR was found to be 2.5 (you want it between 2 and
3)
- Heparin was continued for five days after coumadin was started
- Coumadin was continued for 3 months
9. 1. What is
virchow’s
triad?
1. States of hypercoaguability
2. Venous stasis
3. Damage to the endothelial lining in the
blood vessel
10. 2. Pneumonic
for risk
factors of
developing
DVT.
I AM CLOTTED
• Inactivity
• A Fib/Age
• MI
• Coaguable state
• Longevity of surgery
• Obesity
• Tobacco/tourniquet
• Tumor/trauma
• Estrogen (oral contraceptives)
• DVT hx
11. 3. What are
the common
locations for
DVT?
• 20 % of calf emboli will become thigh emboli
• 1/5th of PE come from the calf
12. 4. How do
you diagnose
a DVT?
• Clinically: red, hot, swollen, painful calf
- edema is the most reliable sign of DVT
(compare suspected calf to the contralateral
side)
• Homan’s test: DF foot elicits pain in the calf
• Pratt’s sign: compression of calf elicits pain
13. Diagnostic
Tests:
Non-invasive
• Duplex Doppler: lack of venous compression indicates DVT
• Can have color flow imaging to enhance sensitivity
• Allows to determine direction of blood flow and the
amount of reduction in
• lumen diameter
• Good for symptomatic DVT
• Grady-Bensmetal JBJS, 1994: duplex ultrasound has the
positive predictive
• value of 7/9
• Ciccone et al JBJS 1998: duplex ultrasound with color flow
imaging is
• unreliable in detecting asymptomatic DVT post THR/TKR
• Impedence plethysmography
14. Diagnostic
Tests:
Invasive
a. Contrast venography
i. Gold standard for detecting DVT
ii. Not as reliable in detecting recurrent DVT
iii. Has been known to cause PE during testing iv.
New contrast media has decreased this risk
15. 5. How do
you diagnose
a PE
Clinically?
• Sudden onset of chest pain, dyspnea,
hemoptysis, tachycardia
• Pt may be febrile, hypotensive and cyanotic
16. 5. How do
you diagnose
a PE?
1. Blood gasses
1. PaO2 < 80 mmHg
2. Chest x-ray:
1. 50% are normal; a normal or near normal
chest x-ray in a dyspneic patient suggests PTE.
Well – established abnormalities include
• Focal Oligemia (Westermark’s sign),
• A peripheral wedged shaped density above the
diaphragm (Hampton’s hump) or
• An enlarged right descending pulmonary artery.
17. 5. How do
you diagnose
a PE?
3. Ventilation – Perfusion Scan (V/Q Scan)
• A mismatch demonstrating an area of ventilation
but no perfusion suggests
• PE
• Ventilation: inhalation of xenon 133
• Perfusion: T99 labeled albumin
• V/Q mismatch: acute PE, previous PE, centrally
located cancer, radiation
• therapy
4. Pulmonary angiography
• Definitive test
• Indicated if V/Q scan is inconclusive
• Diagnostic signs: intraluminal filling defect,
abrupt vessel cutoff, loss of
• side branches
18. PE
Prophylaxis?
A. Non-pharmacologic
- Compression stockings
- Intermittent compression pumps
- Increases levels of prostacyclin and fibrinolytic
byproducts
- Prevents stasis due to increased venous return
B. Heparin
- 5000u SQ q2h pre-op
- 5000u SQ q8-12h
19. Treatment
for PE?
a. Heparin IV
- Loading dose: 10,000 – 15,000u or 80u/kg
- Maintenance dose: start with 1,000 u/hr
(18u/kg/hr)
- Adjust according to PTT (goal 57 – 90 seconds)
- Protamine sulfate reversed heparin
- 1 mg protamine pre 100 u heparin
- Use with care in pts on NPH insulin
- Complications: Hemorrhage,
thrombocytopenia, osteoporosis with long
term use
20. Treatment
for PE?
b. Coumadin
- Start after heparin is therapeutic
- Commonly 2.5 mg qd
- Adjust according to PT (1 – 1.15 x
normal/INR 2 – 3)
- PT normal = 11 – 13
- INR normal 0.8 – 1.2
- Vitamin K reversal
21. Treatment
for PE?
c. LMWH
- Safer than regular heparin
- No need to monitor PTT, easier dosing
- i. Lovenox
- Theraputic: 30 mg SQ BID Prophylatic: 1
mg/kg
- ii. Fragmin
- 2500 u SQ qd
- iii. Normiflo
- 5000 u – 10000 u SQ BID
Compartment syndrome has been implicated with
their use (McLaughlin et al JBJS 1998)
22. Treatment
for PE?
d. Thrombolytic therapy
- Urokinase, streptokinase to dissolve clot
- Must be initiated within 24 – 48 hours
e. Surgical therapy
1. Venous interruption operation
- Greenfield filter: placed in IVC below renal veins
2. Pulmonary embolectomy
23. 8. Post-
phlebetic
syndrome
(post
thrombotic
syndrome)
• Result of venous HTN due to recanalization
of major thrombi which lead to patent but
scarred/incompetent valves occurs in 50 –
60% of patients with proximal DVT; 30% of
patients with symptomatic calf DVT.
• Blood can now flow from the deep to
superficial veins which leads to persistent LE
edema, stasis dermatitis may occur and
breakdown of skin and ulceration develops.
24. 9. Pt has a DVT in his
lower extremity. Clots
are thrown and pt is
found dead at home.
Upon autopsy pt is
found not to have died
from a pulmonary
embolism but from a
massive CVA. How is this
possible?
• Pt had an undiagnosed patent foramen
ovale. This is called a paradoxical embolism.
25. Pt had an
undiagnosed
patent foramen
ovale. This is
called a
paradoxical
embolism.
• Right sided heart failure.
Right ventricular dysfunction. Progressive right heart
failure is the usual immediate cause of death from PTE. As
pulmonary vascular resistance increases, right ventricular
wall tension rises and perpetuates further right ventricular
dilation and dysfunction. Consequently, the inter-
ventricular septum bulges into and compresses an
intrinsically normal left ventricle. Increased right
ventricular wall tension also compresses the right coronary
artery and may precipitate myocardial ischemia and right
ventricular infarction. Underfilling of the left ventricle may
lead to a fall in left ventricular output and systemic arterial
pressure, thereby provoking myocardial ischemia due to
compromised coronary artery perfusion. Eventually,
circulatory collapse and death may ensue.
