Assignment Two

Intro – 200~300 words

VTE/ prophylaxis is a major challenge for patients in theatre because _____

Ive chosen a patient who had a fractured ankle however patient has high risk of VTE such as
______

And I would like to take this opportunity to explore her management in relation to both national
and international guidelines

I have decided to discuss John’s recovery as I believe he experienced some common post
anaesthetic complications requiring me to plan and perform nursing interventions to ensure
he remained safe. I will reflect upon my actions, discuss their purpose and compare them to
literature. By doing this I hope to demonstrate my level of practice but also gain insight
towards improving my future practice.

Venous thromboembolism is associated with significant morbidity and mortality in hospitalized patients [1]. Factors

associated with a high risk of VTE in this population include obesity, cancer, older age, surgery and immobility [2–4].

Surgery poses a significant risk for VTE, and as many as 40% of patients undergoing surgery can experience VTE without

appropriate thromboprophylaxis

One of the most common adverse events after orthopaedic

surgery, with a potential for subsequent serious morbidity and
mortality is venous thromboembolism (VTE).1 The incidence of
deep venous thrombosis (DVT) has been reported to be as high as
60% in major orthopaedic surgery, with mortality of 6% associated
with DVT and 12% with pulmonary embolism (PE).2 The economic
cost to the health system has been estimated to be more than twice
as high for patients with VTE than without, for various orthopaedic
surgery procedures,3e5 with costs increasing over time.6
There are many different prophylactic anticoagulation regimens
available for treatment of VTE.2,7 Similarly, various professional
societies and countries have different guidelines for prevention of
DVT in orthopaedics.8 The American College of Chest Physicians
(ACCP) published guidelines in 2012 for antithrombotic therapy for
patients undergoing various orthopaedic procedures.9 A recent
comparison of guidelines highlights the ACCP recommendations to
still be the most thorough and appropriate.2
Treatment and prevention of VTE in orthopaedic surgery is one
of the most heavily studied topics in orthopaedic surgery, and is
ever evolving.

Select a client from my area of clinical practice as a case study

Heavy rain, on the way to the bus station, slipped on sidewalk and hit the kerb with left ankle, fell
on ground denies head collision, concussion or loss of consciousness, alert, left ankle pain ++
swollen ++, unable to weight bare, transferred to ED, minor abrasions on elbow during the fall
washed with saline and applied dressing, CT head scan okay, radiography shows left ankle
trimalleolar fracture, cast situ in ED, ortho team to review, leg too swollen for OT, consider 48hrs,
NBM 0200 for OT next morning.

Patient: Health condition and its impact on the patient ( 500 words)

- Relevant health history (smoker 2packs a week, obese 130kg, high BMI 42, Type 2
diabetes, Hypertension, family history of DVT/VTE / previous DVT/VTE episodes?)

- Sociocultural/genetic consideration (Social worker, otherwise lives a sedentary lifestyle,

DVT/VTE prone gene)

- Drug therapy (what medication regime were they on for diabetes and high blood
pressure etc)

Synthesis of underlying physiological and pathophysiological processes occurring for this

client

800 words

Pathophysiology of VTE/DVT/PE

And its relation in regard to ortho

Thrombus formation and propagation depend on the presence of abnormalities of blood flow,
blood vessel wall, and blood clotting components, known collectively as Virchow's triad.
Abnormalities of blood flow or venous stasis normally occur after prolonged immobility or
confinement to bed. Venous obstruction can arise from external compression by enlarged
lymph nodes, bulky tumours, or intravascular compression by previous thromboses.

 (Diane K. Dressler Advanced Critical Care Nursing, )

Following an injury, hemostasis is accomplished by the harmonious interaction of

three components: the injured blood vessel wall, platelets, and the plasma
coagulation factors. The multiple events involved in blood clotting begin with spasm
of the injured vessel wall and progress through a series of steps that result in clot
formation. Vascular spasm is initiated by nerves in the vessel wall, and slows the loss
of blood. The spasm is enhanced by the release of thromboxane A 2 from circulating
platelets, and by the release of other potent vasoconstrictors, including
endothelin. 19 The degree of spasm is proportional to the amount of trauma, with
more spasm occurring with greater injury.

The subsequent hemostatic process entails two major steps. During the first step,
platelet adhesion and aggregation occurs, resulting in formation of a platelet plug at
the site of blood vessel injury. The second step involves the formation of a fibrin clot
( Fig. 27.1 ). 1928

Activation of the clotting cascade, as well as aggregation of platelets and blood

cells, occurs simultaneously to form a thrombus. The thrombus can cause
complete or partial occlusion of the vein leading to venous stasis,

Finally, through a series of events involving factor XIII (the fibrin stabilizing factor), fibrin monomers
become fibrin polymers, which become stable fibrin, forming the actual blood clot. The mesh-like clot
consists of fibrin strands, red blood cells, and platelets. Clot formation usually occurs within minutes,
and rapid clot formation is necessary to prevent the platelet plug and clot from washing away from the
shear forces of blood flow

Virchows triad

When dvt detach, they follow the natural course of venous blood flow by traversing the vena cava
to the right heart chambers and ultimately a pulmonary artery where they lodge to become a PE
(PE patho)

Clinical manifestations of DVT are often absent. If a symptom is present, it is typically pain. Other
signs of DVT include unilateral leg swelling, dilation of superficial veins, calf tenderness, and skin that
is mottled or cyanotic. Because DVT is usually asymptomatic and difficult to detect clinically,
prevention of DVT is a high priority. (AUT patho)

National best practice guideline relevant to the clients management regime & International
best practice guideline relevant to the clients management regime ( 500 words)

Critically analyse the treatment regime for this client in the context of the national and
international guidelines (500 words)

Current treatment regime for DVT/VTE/PE

Mechanical – TEDS/ SCDS etc

Chemical – Clexane (LWMH), aspirin, rivaroxaban.

RATIONALE FOR PROPHYLAXIS

The risk of VTE is significantly increased in patients who are hospitalised after trauma, surgery or
immobilising medical illness, and also in pregnant and puerperal women, and DVT is common
in such individuals. In many patients, DVT remains asymptomatic but in others it can cause
morbidity and mortality.3,7,11,26 The rationale for prophylaxis is based on its efficacy, the clinically
silent nature of VTE, its high prevalence in hospitalised, pregnant or puerperal patients, and its
potentially disabling or fatal consequences.3,23,26-29
There is evidence that routine prophylaxis reduces morbidity, mortality and health service
costs in hospitalised patients at risk of DVT and PE, as highlighted in national and international
guidelines.3 (Scottish guideline)
Critically discuss the clinical implication of the treatment regime and the appropriateness of
this regime for the client (500 words)

nursing profession is pivotal in the prevention of this fatal complication.

Patient’s current health? Diabetes, obesity, high BMI, family history of VTE/DVT etc

(physio input, family involvement, support etc)

Conclusion 200-300 words

A group of 600 international experts have issued a new set of guidelines that
address virtually all aspects of venous thromboembolism (VTE) related to
orthopedic surgery. The 328-page report, with scores of recommendations, is
divided into 10 topics (general, hip/knee, foot/ankle, hand/wrist, shoulder/elbow,
spine, oncology, pediatrics, sports, and trauma).

Key Points and Recommendations

Here we present selected points, drawn from the “general” and “hip/knee”
sections, that might be of interest to nonorthopedists who comanage elective
surgical patients with orthopedists.

 A history of VTE is a well-known risk factor for postoperative VTE.

However, presence of varicose veins and a history of unprovoked
superficial venous thrombosis also are risk factors for VTE in lower-limb
orthopedic surgery.
 Because scoring systems for VTE risk stratification generally have not
been validated in large orthopedic surgery populations, they are not
reliable for such patients.
 Although VTE prophylaxis lowers the incidence of postoperative VTE
generally, no strong evidence shows that it lowers the incidence of fatal
pulmonary embolism.
 The recommended duration of posthospital VTE prophylaxis after hip or
knee arthroplasty is 14 to 35 days. Aspirin is the optimal choice,
accounting for efficacy, safety, ease of administration, and cost-
effectiveness.
 Intermittent compression devices lower the incidence of VTE after hip or
knee arthroplasty, but the authors don't specify precisely when such
devices should be used in addition to (or as a substitute for)
chemoprophylaxis, and they acknowledge that adherence is low after
patients leave the hospital.
  For patients with postoperative isolated distal deep venous thrombosis, it is
acceptable either to monitor the thrombus (with a follow-up ultrasound in 1
week) or to institute full anticoagulation.
 Taking a nonsteroidal anti-inflammatory drug (NSAID) at the same time as
aspirin can negate aspirin's antiplatelet effect. If a patient is receiving
postoperative VTE prophylaxis with aspirin plus an NSAID for pain, aspirin
should be taken 2 hours before the NSAID (and not with, or immediately
after, the NSAID)

The risk of thrombosis from orthopaedic surgeries stems from the use of a tourniquet, which
causes stasis of blood flow and hypoxia [1]. Mechanistically, the hypoxia causes damage
secondary to inflammation and activation of the coagulation cascade, leading to elevated levels of
thrombin–antithrombin complex, plasmin–antiplasmin complex and D-dimer.

The risk factors for VTE following surgery are well-defined and include immobility, older age,
malignancy, COCPs and thrombophilias [3]. In our patient, use of COCPs was the only
identifiable risk factor. The estrogen found in COCPs creates a hypercoagulable state by
simultaneously increasing levels of procoagulant factors such as fibrinogen, prothrombin and
factors VII, VIII and X, and decreasing anti-thrombin III and tissue factor pathway inhibitor.
These effects, albeit dose-dependent, lead to an increased risk of VTE, especially during the
initial months of COCP use [4]. COCPs are associated with an increased risk for symptomatic
DVT and PE (1.70 and 0.27%, respectively) following arthroscopy of the knee [5].

CONCLUSION
The majority of episodes of post operative VTE occur after discharge from hospital, even when
prophylaxis has been employed during the admission.1 (Scottish guideline)

Understanding these factors involved in thrombus formation and subsequent thromboembolic events enables the
clinician to stratify risk, direct clinical decision-making regarding treatment, and establish preventative
measures. 

Given the serious nature of thrombosis, an interprofessional healthcare team, including clinicians, nurses, mid-
level providers, and specialists, should be familiar with Virchow's triad and recognize the presentation when
examining or interacting with patients. Prompt recognition can lead to further testing and specialized
intervention, resulting in better patient outcomes.

coagulation activation from tissue and bone injury; venous in juries; heat due to cement polymerization;
reduced, venous emptying intra-or post-surgery; immobilization
Vignon P, Dequin PF, Renault A, et al. Intermittent pneumatic compression
to prevent venous thromboembolism in patients with high risk of bleeding
hospitalized in intensive care units: the CIREA1 randomized trial. Intensive
Care Med 2013; 39:872–880.