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History and Physical. Pulmonary Embolism

History and Physical. Pulmonary Embolism

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History and Physical #1. Pulmonary Embolism

  • Date: 1/26/2012
  • Name: N.N
  • Date of Birth: 11/11/1976
  • Age: 35
  • Health Insurance Plan: QualCare
  • Gender: Female
  • Marital Status: Single
  • Language: English
  • Referral: None.
  • Source and Reliability: Self-historian

CHIEF COMPLIANT:

Palpitations and shortness of breath

HISTORY OF PRESENT ILLNESS:

Patient is a 35 years old Caucasian female who presents to the Emergency Department witha 2-week history of episodic palpitations, 3-4 times a day, with each episode started abruptlyand lastedapproximately 1 to 2 hours before abating gradually.The palpitations were not associated with any specific activity or time and did not significantly affect patient’s daily routine. Patient went to an urgent care center 5 days prior to ED visit due to a concern of palpitations. The work-up included blood work, ECG and chest X-ray that appeared to be negative. Despite negative work-up, patient continued to have persistent symptoms. Today, the symptoms were precipitated by walking up stairs to the second floor at which time she became acutely short of breath and called 911. Patient denies syncope/ near-syncope, lightheadedness, chest pain, fever, chills, weight loss, hemoptysis, cough, diaphoresis, calves tenderness or swelling. Patient denies recent sick contact; immobilization,prolong air or ground travelling, recent trauma and history of previous similar episodes.


PAST MEDICAL/SURGICAL/OBSTETRIC HISTORY

  • Patient denies medical history of cardiac disease, HTN, hyperlipidemia, arrhythmias, anemia, thyroid disorders, coagulopathies, deep vein thrombosis, autoimmune or rheumatic disorders, malignancies, SLE, TB, asthma, HIV/AIDS, kidney and hepatic disease, rheumatic fever
  • Patient denies childhood medical history
  • Patient is G0P0A0, LMP 1/15/12
  • Patient denies psychiatric history
  • Patient denies surgical history and previous hospitalizations.

Health Maintenance

  • Patient’s immunization status: annual influenza (10 /2011), DTaP (04/2010)
  • Last complete physical: 10/2011
  • Last pap smear test: 06/2011, negative
  • Blood pressure screening -2011, negative
  • Lipid disorder screening -2011, negative

Family History

  • Patient is unaware of health history of grandparents.
  • Mother alive, aged 66, history of HTN and osteoporosis
  • Last pap smear test: 06/2011, negative
  • Father alive, aged 67, history BPH and HTN.
  • Patient’s brother, aged 33, alive and well
  • Patient denies family history of arrhythmias or premature cardiovascular conditions, kidney or liver disease, anemias, bleeding/clotting disorders, vein thromboembolism; thyroid disease, diabetes, cancer, epilepsy, autoimmune, rheumatic and mental illness.

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MEDICATIONS

  • Oral contraceptive Yasmin 28 (drospirenone 3mg/ ethinyl estradiol 0.2 mg). Patient has been taking Yasmin 28 since age 21.
  • Patient denies taking OTC medications, herbal supplements or vitamins Allergies
  • No known food/drug or environmental allergies

PERSONAL/SOCIAL HISTORY

  • Patient is single
  • Patient lives with her boyfriend in a two-bedroom townhouse which she owns
  • Patient is a high school graduate, works as an assistant director in a local game store. Her working hours are 9-7 pm

Monday through Friday.

- Patient has no religious preferences.


Current Health Habits

  • Patient smokes 1 pack/day since age 18
  • Patient drinks alcohol socially, every Saturday night, 2 drinks of beer
  • Patient denies illegal drug use
  • Patient denies illegal drug use
  • Patient drinks caffeinated coffee regularly, 1-2cups daily
  • Patient eats regularly, mostly restaurant food
  • Patient doesn’t exercises regularly
  • Patient denies exposure to firearm at home, have a smoke detector at home, wears a seatbelt while driving

REVIEW OF SYSTEMS

  • General:denies fever, chills, night sweats, fatigue, or weight changes (loss or gain).
  • Head and Neck:Skin, Hair, Nails:denies rash/lesions/moles/birthmarks, itching, skin texture changes, and unusual hair or nail growth.
  • Head: Denies recent head injury, headaches, dizziness, light headedness, forgetfulness, and loss of consciousness.
  • Neck: denies difficulty swallowing, neck stiffness,
  • Eyes:Does not wear glasses, denies visual disturbances, double vision, pain discharge or any recent changes in vision, difficulty seeing at night.
  • Ears:Denies changes in hearing, pain, discharge, vertigo, ringing in ear, or increased pressure/obstruction of the ear.
  • Nose and Sinuses: Denies problems or changes with sense of smell, obstructions, nosebleeds, postnasal drips, sinus pain or frequent colds.
  • Mouth and Throat:Denies hoarseness, changes in voice, sore throats, bleeding gums, oral ulcers, dental appliances, difficulty chewing food or changes in taste.
  • Cardiovascular:See HPI.
  • Peripheral vascular:denies claudication, extremities pain, swelling, discoloration,changes in temperature or sensation.
  • Chest and Lungs:denies cough, pleurisy, hemoptysis, orthopnea, chest tightness or wheezing.
  • Endocrine:Denies polyuria, polydipsia, polyphagia, skin or hair changes, heat/ cold intolerance, weight changes, menstrual irregularities
  • Hematologic: Denies unexplained bleeding or bruising
  • Lymphatic:Denies lymph node enlargement, tenderness or suppuration.
  • Gastrointestinal:Denies changes in appetite, constipation, diarrhea, abdominal pain, nausea, vomiting, heartburn, hemorrhoids, bleeding or tarry stools.
  • Genitourinary:Denies dysuria, increased/decreased frequency or urgency of urination, nocturia, polyuria, or incontinence.
  • Gynecological:Denies dysmenorrhea, heavy menstrual periods, menstrual irregularities, vaginal bleeding, discharge or pelvic pain.
  • Musculoskeletal:Denies joint pain, stiffness or swelling,restriction of movement, myalgia.
  • Neurologic:Denies syncope, seizures, weakness, and changes in sensation, coordination, or tremors.
  • Mental Status and Psychiatric:Denies difficulty concentrating, anxiety, tension, irritability, sleep disturbances or any suicidal ideation.

PHYSICAL EXAMINATION

  • General: Patient is a 35 year old Caucasian female appears anxious and in mild distress.She is well-groomed, dressed appropriately, maintains good eye contact and expresses appropriate concerns. Patient speaks in full sentences but pauses frequently to take a deep breath.
  • Vital Signs: Temp: 97.8 F , HR: 112/ min,BP: 130/85 mmHg,RR 30/min SaO2: 89% RA, HT: 4’6’’, WT: 145 lbs., BMI 24.6 kg/m2
  • Mental Status: alert and oriented to person, place, and time; short term memory and attention span intact.
  • Skin, hair, and nails: skin pink, warm, and dry to touch. Nail beds are pink and smooth. No lesions, rashes, scars or moles.Capillary refill is 2 seconds.
  • Head:head normocephalic, erect, midline;scalp moveable, no lesions. Symmetrical facial features, no orbito-facial edema, erythema or discoloration. Temporal arteries soft, non-tender, no bruits
  • Eyes:Eyelids pink without ptosis, edema, lesions; conjunctiva pink and dry without discharge; sclera white without increased vascularity or lesions. PERRLA; EOMs intact; no nystagmus; visual field equals, corneal light reflex equal bilaterally. Red reflex present, disc cream colored with well-defined border bilaterally; no crossing changes noted; cornea, lens and vitreous clear; retina pink, no hemorrhages or exudates; macula yellow; Snellen 20/20 each and both eyes
  • Ears: Auricles in proper alignment, without lesions, masses, or tenderness; canals with small amount of dry cerumen; tympanic membranes gray, translucent, light reflex and bony landmarks present; no perforations; repeats whispered words at 2 ft. bilaterally.
  • Nose and Sinuses: No flaring, septum midline, patent bilaterally, mucosa pink and moist, no polyps or discharge; no frontal or maxillary sinus tenderness with palpation
  • Throat and mouth. Buccal mucosa pink and moist, no lesions, discolorations; salivary glands nontender; gingivae pink, no swelling, lesions, bleeding; tongue in midline without fasciculation, no lesions; uvula midline with elevation of soft palate; pharynx without erythema; tonsils without erythema, exudate, enlargement, ulcers; no hoarseness.
  • Neck:Trachea midline, thyroid and cartilages move with swallowing, thyroid lateral borders palpable, no enlargement or nodules noted, lymph nodes nonpalpable, full range of motion and appropriate strength.
  • Chest and Lungs:AP/lateral diameter 1:2 ratio;tachypnea (RR 30); use of accessory muscles on inspiration; tactile fremitus symmetric; no egophony; resonant percussion throughout, vesicular breath sounds throughout all lung fields, no adventitious sounds.
  • Heart: Apical impulse non-palpable;tachycardia (112), regular rhythm; S1 and S2 without splitting; no murmurs, gallops, rubs;no audible S3, S4
  • Blood vessels:+2 symmetric palpable pedal (DP, PT), radial, and brachial pulses bilaterally. No jugular vein venous distention, no bruit/thrill present over carotid, temporal arteries, or abdominal aorta. No edema, swelling, tenderness or varicosity of lower extremities.No cord-like sensation over deep vein distribution; negative Homan’s sign bilaterally
  • Abdomen:soft, rounded, non-distended; active bowel sounds in all quadrants; tympanic percussion tones over epigastrium, remainder dull to percussion; liver span 6 cm at Rt. midclavicular line by percussion; spleen percussed at Lt. midaxillary line; liver, spleen, and kidney not palpable; no tenderness on palpation; no CVA tenderness
  • Lymphatic:no palpable lymph nodes in neck, supraclavicular, axillary or inguinal areas.
  • Musculoskeletal:muscles symmetric, muscle strength 5/5 all extremities, equal bilaterally. Spine and extremities in good alignment, no loss of muscle bulk, normal tone. No joints swelling, tenderness, deformities, full ROM of all extremities
  • Neurologic: smooth and coordinated gait, good balance, no sensory focal deficits, no motor focal deficits. Motor strength 5/5 all extremities; Cranial nerves I-XII intact. DTRs (biceps, triceps, patella, ankle) +2 ,symmetric.
  • GYN: deferred Diagnostics (1/21/2012):
  • CBC: WBC 6.5, RBC 4.3, HGB12.1g/dl HCT 39% , MCV 90 fL, MCH 29.5 pg, MCHC 34.1 pg, PLT225. Automated differential: neutrophils 43.6%, lymph 40.5%, monos 10.9%, eos 2.7%, baso 0.3%
  • BMP: Sodium 138 mEq/l , Potassium4.0mEq/l, Chloride105mEq/l, total CO225mEq/l, Glucose 97g/dl , BUN 12 mg/dl, Creatinine 0.7 mg/dl
  • TSH: 1.4 mIU/L
  • ECG: ST (106/min), P-R Interval: 142 ms, QRS duration: 80 ms, Q-T interval: 352 ms, QTC calculation: 465 ms, no pathological Q waves, isoelectric ST segments, normal T waves, good R wave progression, axis 30 degrees
  • CXR: no cardiopulmonary pathology
  • Urine pregnancy test –negative

ASSESSMENT:

1. Pulmonary embolism


PLAN:

  • Admit to telemetry floor
  • Obtain D-dimer , troponin (q 8 h x 3), BNP
  • Obtain Contrast-enhanced CT arteriography (CTA)
  • Obtain transthoracic echocardiography (TTE)
  • Obtain Venous Doppler US
  • Repeat ECG
  • Initiate Enoxaparin 1 mg/kg (70 mg) subcutaneously every 12 hoursand Warfarin 5 mg/d PO. Discontinue Enoxaparin as soon as INR has been in the therapeutic range (between 2.0 and 3.0) on 2 consecutive days. Monitor INR daily to adjust warfarin dose accordingly. Monitor for possible complications of anticoagulants : bleeding , HIT (obtain PLT every 2 days) and hypersensitivity reaction (urticaria, angioedema)
  • Continue warfarin treatment for 3 months. Monitor INR daily while in the hospital, then weekly until the therapeutic level has been achieved and then every 4 weeks for the duration of warfarin therapy.
  • Discontinue drospirenone 3mg/ ethinyl estradiol 0.2 mg.
  • Supplement oxygen and titrate to SPO2 above 90%
  • Encourage oral hydration. Place on regular diet and encourage oral intake. If patient cannot tolerate oral intake, initiate gentle parenteral hydration with D5%NaCl 0.9% at rate 100 ml/hr
  • Place on bed rest initially, increase physical activity gradually as tolerated
  • Monitor vital signs, SPO2 q 4 hours or more frequently, maintain continuous telemetry monitoring, measure I and O and daily weight.
  • Consider discharge from the hospital when patient is clinically stable
  • Before discharge instruct patient regarding duration, laboratory monitoring and side effects of warfarin. Teach patient regarding drug-drug and drug-food interactions, signs of bleeding and safe practices while on anticoagulation therapy
  • Before discharge teach patient regarding risk factors for VTE and measures to prevent recurrent VTEs. Strongly recommend smoking cessation. Assess patient’s readiness to quit smoking
  • Counselregarding alternative contraceptive methods. Prescribe Norethindrone 0.35 mg OC pills for the duration of warfarin therapy and reconsider their use at follow-up.
  • Counsel about preventive measures during prolong travelling and pre-/postnatal period
  • Obtain d-dimer level one month after discontinuation of anticoagulation to assess a risk for recurrent PE. Repeat TTE after resolution of acute PE to monitor for chronic pulmonary hypertension
  • Consider thrombophilia screening if patient develops recurrent idiopathic VTE or VTE while on anticoagulation therapy
  • Consult a specialist with expertise in coagulation disorders if patient develops recurrent VTE or complications necessitating alternatives to anticoagulation, in cases of suspected or proven hypercoagulability and for management of VTE during pregnancy.

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RATIONAL:

N.N is a 35 years old Caucasian woman with no medical conditions who presents to the Emergency Department with a two week history of episodic palpitations and an acute onset of shortness of breath today. Her physical examination reveals tachypnea, accessory muscle use, hypoxemia and tachycardia. Her history is positive for tobacco and oral contraceptives (OC) use.Her diagnostic tests are benign. Most common conditions to consider as an explanation of patients symptoms are: thyrotoxicosis, anemia, electrolyte imbalance, pheochromocytoma, cardiac arrhythmias, anxiety and pulmonary embolism (Thavendiranathan, Bajai, Khoo, & Dorian, 2009). Thyrotoxicosis will often manifest with tachycardia. However, in the absence of elevated TSH, characteristicskin findings (diaphoretic and warm) and ocular signs(stare and lid lag), overt hyperthyroidism is less likely.In the setting of a significant anemia, palpitations can beperceived secondary to compensatory increases in HR andstroke volume in order to maintain adequate tissue oxygenation.In the absence of risk factors for bleeding and normal HGB values, this wouldbe uncommon. Normal chemistry values exclude electrolyte imbalance as an etiological cause of palpitations.

Pheochromocytomas are rare catecholamine-secreting tumors that are classically associated with the triad of episodic headaches, diaphoresis, and tachycardia. Hypertension, not present in this patient, is the most common finding. Hypoxemia is not associated with this condition.Although anxiety-related disorders are in the differential diagnosisfor the patient’s symptoms, it would be prematureto accept this as the sole etiology, especially without the usual accompanying symptoms and before further diagnostics.Although substances such as nicotine that increaseadrenergic tone or diminish vagal activity could be a causeof palpitations, such palpitations would not usually presentacutely and intermittently if the substances had been usedlong-term, as they were in this patient.Arrhythmias are a common cause of palpitations. Theetiology can vary from benign premature atrial ectopic activityto more worrisome ventricular arrhythmias. Sinus tachycardia of 106 beats/min was evident onthe previously done (5 days ago) ECG. The absence of signs of left ventricular hypertrophy, atrial enlargement, AV blocks, prolonged QT, old myocardial infarction, and delta waves (as seen in WPW syndrome), ST-segment elevation in leads V1 to V3 (Brugada syndrome) indicates non-pathologicalECG.Yet, even normal ECG cannot completely exclude cardiac pathology. Given the abrupt onset and persistency of the symptoms, additional tests will be warranted. ECG will be repeated because patient’s conditions have changed and sudden onset of shortness of breath has been developed since last ECG. Also, transthoracic echocardiography (TTE) will be ordered to rule out valvular abnormalities as a potentialcause of tachycardia. Troponin (q 8 hours x3) will be monitored to exclude myocardial injury.However, there is a high level of suspicion that patient developed acute pulmonary thromboembolism. Pulmonary embolism is suspected since the patient presents with unexplained resting tachycardia, tachypnea and hypoxemia and risk factors for thromboembolism such as tobacco and oral estrogen use that predispose to blood hypercoagulability.

Pulmonary embolism (PE) is a difficult diagnosis to establish because of the non-specificity of presenting signs and symptomsand the probabilistic nature of the most common noninvasive diagnostic tests (Chalikias, Tziakas, Stakos, & Konstantinides, 2010). The choice of diagnostic tests for PE is established on pretest probability based on validated prediction scores, clinical presentation and risk factors. Patient’s risk factors include exposure to tobacco and oral estrogen that predispose to hypercoagulability, which is one of the tree components of Virchow triad (endothelial injury, stasis or turbulence of blood flow and hypercoagulability). Wells prediction score can be served for the purpose of predicting individual risk of actually having PE (Chalikias et al., 2010). Based on the Wells prediction score, patient is at moderate (21%) risk to develop PE. Moderate calculated risk for PE in combination of high level of clinical suspicion dictate to pursue additional tests.

When clinical prediction rule results indicate that the patient has a low or moderate pretest probability of pulmonary embolism, D-dimer testing is the usual next step.A negative an ELISA-based D-Dimer test,which measures a degradation product produced by plasmin-mediated proteases of cross-linked fibrin is very sensitive in patients with a low to moderate pretest probability of pulmonary embolism and can reliably exclude this condition.D-dimer testing is most reliable in younger patients who have no associated comorbidity or history of venous thromboembolism and whose symptoms are of short duration. The use of the d-dimer assay is of limited value in patients with high clinical probability of pulmonary embolism.Although a positive test indicates that venous thrombosis and pulmonaryembolism are possible diagnoses, this test is nonspecific. In patients with a high pretest probability,however, imaging should be performed instead ofd-dimer testing(Angnelli & Becattini, 2010). Since the patient has a moderate pretest probability score, d-dimer test will be obtained first. A negative result will exclude pulmonary embolism and spare the patient from unnecessary additional tests and exposure to high CT scan radiation. On the contrary, a positive result, because of its low specificity to diagnose PE, will require further investigation. Contrast-enhanced CT arteriography(CTA)has advantagesover ventilation–perfusion scanning,including speed, characterization of nonvascularstructures, and detection of venous thrombosis.CTarteriography has the greatest sensitivity andspecificity for detecting emboli in the main, lobar,or segmental pulmonary arteries(Angnelli & Becattini, 2010). Because of the concern for PE, D-dimer was obtained and indicated positive results (515 mcg/l). Subsequently, CTA was performed (BUN and Creatinine WNL) and showed small, acute-appearing, sub-segmentalPEs in the posterior basal segments of the lower lobes bilaterallywith associated peripheral infarction and hemorrhage.

The initial goal of PE management is identification of severity of the pathologic process and early death risk. The literature reports the death rate is nearly 58% among hemodynamically unstable patients and about 15% among hemodynamically stable PE patients(Angnelli & Becattini, 2010). The early mortality is associated with right ventricular overload thatleads to hemodynamic instability, dilatation, ischemia and dysfunction of the right ventricle. Death results from right ventricular failure(Chalikias et al., 2010). Riskstratification has potential clinical implications. Patients who are atimmediate risks (hemodynamic instability and right-sided heart failure) require thrombus removal from the pulmonary circulation (thrombolysis or surgical embolectomy);on the other hand, low-risk patients can be safely discharged earlier and even treated at home with anticoagulants (Chalikias et al., 2010). No clear evidence-based guidelines are available for inpatient versus outpatient treatment of acute PE. Cardiac biomarkers together with TEE have been used to stratify patients’ risk of death anddetermine disease severity. Elevated cardiac troponin and BNP levels together with evidence of right ventricular dysfunction on TTE are very sensitive indicators of poor prognosis even in stable patients with acute PE. However, it remains unclear whether normotensive patients with right ventricular dysfunction, detected by TTE plus evidence of myocardial injury indicatedby a positive troponin test, may benefit from earlythrombolytic treatment(Chalikias et al., 2010). Moreover, it has been proposed that selected patients with low-risk PE (i.e. normotensive patients with neither RV dysfunction nor myocardial injury) can be treated as outpatients. However, excessive optimism is not warranted at present, since a randomized study of home treatment versus hospitalization of low-risk patients with PE was recently discontinued because of high mortality in the early discharge group. Indeed, current evidence suggests that only a very small proportion (less than 10%) of patients with PE may be eligible for home treatment, and this management option cannot be recommended at present until further data become available regarding its safety and practicability (Chalikias et al., 2010). The patient’s resting hypoxemia (Spo2 ≤90%), tachycardia (HR ≥110 beats/min), and tachypnea (RR, ≥30 breaths/min) are suggestive of substantial hemodynamic strain. Therefore, outpatient management of this patient would be less than ideal. Patient will be admitted to telemetry floor for close observation, frequent vital signs and continuous cardiac monitoring.

In addition to troponin, BNP and TTE, venous Doppler of both low extremities will be ordered. About 79% of patients who present with PE have evidence of deep venous thrombosis in their legs(Angnelli & Becattini, 2010). The patient has no physical signs of DVT (unilateral calf erythema, edema and tenderness, positive Homan’s sign or cord-like sensation over distribution of major veins). However, lack of clinical signs and symptoms doesn’t rule out diagnosis of DVT. Although Doppler’s findings will not affect the treatment and prognosis of PE, it will be obtained in order to detect the origin of the embolus.

The treatment of acute PE should be initiated upon clinical suspicion without awaitingdefinitive confirmationbecause of a high potential of early mortality(Chalikias et al., 2010).The initial treatment for this patient with objectively confirmedPE is a parenteral antithrombotic agent alongsidewith a vitamin K antagonist. The choice of antithromboticagent should be individualized. For sub-massive PE,treatment with low-weigh molecular heparin (LMWH) has been shown to be as safe andeffective as intravenous unfractionated heparin (UFH). Given its superior convenienceand lower risk of heparin-induced thrombocytopenia (HIT),LMWH would be favored over UFH for this patient.Intravenous UFH is preferred in morbidly obese patients,in whom inadequate subcutaneous absorption is a concern,and in patients with renal failure, in whom decreasedclearance of LMWH can increase the risk of hemorrhage.UFH is also preferred in patients at highrisk of hemorrhage or if invasive procedures are likely becauseintravenous UFH can be stopped more quickly andreversed more reliably with protamine than LMWH(Kearon et al., 2008).

Warfarin decreases carboxylation of factors II, VII, IX, and X as well as proteins C and S by competitivelyinhibiting vitamin K epoxide reductase. This leads to decreasedinitiation of the coagulation pathways and aidsin preventing further thrombotic events. In patients withacute PE, warfarin should be initiated on the first dayof antithrombotic treatment and overlap (bridge) withLMWH for at least 5 days or until 24 hours afterthe international normalized ratio (INR) has reached thetherapeutic range (INR, 2.0-3.0)(Kearon et al., 2008). The utility of bridgingis 3-fold. First, warfarin inhibits only the new synthesis ofvitamin K–dependent factors, and therefore preexistingclotting factors require 36 to 72 hours to clear from thecirculation. Second, during the first 2 to 3 days of therapywith warfarin, the elevated prothrombin time reflectsdepletion of factor VII, which has a short half-life (5 to 7hours); however, it does not reflect adequate anticoagulationbecause of incomplete suppression of the intrinsiccoagulation pathway. Finally, rapid reduction of proteinC, an endogenous anticoagulant with a short half-life (6to 8 hours), can yield a transient hypercoagulable state,potentially leading to increased clot burden and, rarely,warfarin-induced skin necrosis(Goodacre, 2008). Therefore, patient’s medications will include Enoxaparin 1 mg/kg (70 mg) subcutaneously every 12 hours and Warfarin 5 mg/d PO. Enoxaparin will be discontinued when INR will reach therapeutic range (between 2.0 and 3.0) on 2 consecutive days. INR will be checked daily.Measurement of antifactorXa levels, is not necessary in patients receivingLMWH(Kearon et al., 2008).Patient will be monitored for bleeding complications and heparin-induced thrombocytopenia (incidence below 1% in patient receiving LWMH). Platelet count will be obtained every 2-4 days. Upon clinical suspicion of heparin-induced thrombocytopenia, all sources of heparin should be discontinued and therapy with direct parenteral thrombin inhibitors, particularly argatroban or lepirudin, initiated (Kearon et al., 2008).Drospirenone 3mg/ ethinyl estradiol 0.2 mg will be discontinued. Patient will be monitored for changes in clinical status (VS and pulse oxymetry every 4 hours). Non-pharmacologic measures will include oxygen (titrate to SPO2 > 90%) to correct hypoxemia secondary to ventilation/perfusion mismatch.Patient will be encouraged to maintain oral hydration to compensate for insensible fluids loss related to tachypnea. If patient is unable to tolerate PO, gentle parenteral hydration will be initiated at slow rate of 100 ml/hr D5%NaCL0.9 % since a significant increase in intravascular volume can cause right ventricular strain and exacerbate right-sided heart failure. I and O and patient’s weight will be closely monitored.

The discharge will be considered when patient is clinically stable(HR< 100 / min, RR< 24 / min, SBP> 90 mm Hg, and SPO2> 90% on room air). Before discharge patient will be instructed regarding Warfarin treatment that needs to be continued for three months. The recommendedduration of oral anticoagulation after an episodeof acute PE weighs the risk versus the benefits of vitaminK antagonists. As a rule, treatment with vitaminK antagonists should be continued for 3 monthsafter a first episode of PE triggered by a transient riskfactor (trauma, surgery, immobilization, pregnancy,contraceptive use or hormonal replacement therapy),and for at least 3 months for patients with unprovokedPE(Kearon et al., 2008).INR should be monitored weekly initially and then every 4 weeks for the durationof warfarin therapy once thelevel of anticoagulation is stable(Goodacre, 2008). Patient should be taught about warfarin and other drug-drug and drug-food interactions. Patient should be warned not to change diet abruptly, stick to routine and not to take medications OTC without consulting with a practitioner. Foods with large amounts of vitamins A, E, K, and C can decreasethe INR level in patients on warfarin.Green leafy vegetables containthe most vitamin K. Other examplesinclude green and herbal teas, whichcan also alter the prothrombin time.Proteolytic enzymes, such as papainin fried or boiled onions, increasefibrinolytic activity(Goodacre, 2008). Patient will be encouraged to take warfarin as prescribed, not to skip dosages and be aware to signs of bleeding (bleeding gums, heavy menstrual flow, tarry stool). Patient needs to seek immediate help if she develops dizziness, weakness, severe headache or abdominal pain. Rarely, warfarin can cause hair loss or skin rashes. Patient needs to be instructed to be careful and protect from injuries:use electric razors, soft toothbrushes, always wear shoes, wear gardening gloves while doing yard work, and avoid contact sports. Upon discharge from the hospital, patient will be taught about risk factors of venous thromboembolism and how to avoid its recurrence. The patient’s PE was thought to be provoked by exogenous estrogen in the setting of tobacco use.It will be strongly recommended to quit smoking. The U.S. Public Health Service recommends that clinicians use the five A’s (Ask about tobacco use , Advise to quit smoking , Assess patient’s willingness to quit , Assist with patient’s attempt to quit , and Arrange follow-up) model when treating patients with nicotine addiction. Patient’s willingness to quit smoking will be assessed using the “stages of change” model (pre-contemplation, contemplation, preparation, action and maintenance). Interventions based on the “stages of change” model have been shown to enhance motivation and predict cessation. Patients who are willing to attempt cessation should receive specific advice about how to proceed. Even brief (five minutes or less) advice on smoking cessation increases cessation rate(Okuyemi, Nollen, & Anluwalia, 2006).

Patient will be counseled about alternativecontraceptive methods that will not increase risk of VTE, for example, barrier methods. If patient intend to continue OC,norethindrone 0.35 mg (Micronor) will be a preferred option. Also, it seems to be appropriate, due to high teratogenicity of warfarin,to continue the OC pills for the duration of anticoagulationtherapy and reconsider their use at follow-up. Norethindrone is a progestogen-only contraceptive pill.Although this remains controversial, progestogen-onlycontraceptive pills have not convincingly been shown tobe an independent risk factor for VTE (Bonnema, McNamara, & Spencer, 2010). Therefore, norethindronewithout ethinyl estradiol would be the preferredOC pill for this patient. Patient will be educated that before prolong travellingbelow-kneecompression stockings should be used starting 2 to3 hours before flights longer than6 to 8 hours. Also,a single dose of subcutaneousLMWH can be given to individuals with previous history of VTE 2 to 4 hours before long-haultravel in addition to compressionstockings. If patient wishes to become pregnant in the future, she needs to know that pregnancy increases risk of VTE in women with previousVTE related to a temporary riskfactor.Therefore, prenatal and postnatal prophylaxis with LMWH will be considered in her case(Goodacre, 2008).

At a follow-up visit after discontinuation of warfarin, D-dimer level will be obtained. Recent evidence suggests that a normal D-dimer level 1 month after discontinuation of anticoagulation is associated with a lower risk of recurrence (3.7% vs 11.5%)(Angnelli & Becattini, 2010).After an acute pulmonary embolism, patients should be monitored for chronic thromboembolicpulmonary hypertension. The incidence ofchronic thromboembolic pulmonary hypertension2 years after the acute event ranges from0.8 to 3.8%(Angnelli & Becattini, 2010). TTE will be repeated after resolutions of acute PE. There is an ongoing debate regarding screening patients for inherited thrombophilia. In general, thrombophilia screening should only be considered in the given indications if the test results will affect the patient’s management and usually not indicated if venous thrombosis has developed in the presence of clear provoking factors(Goodacre, 2008). Since the patient’s PE was thought to be provoked by exogenous estrogen in the setting of tobacco use,additional thrombophilia screening is not warranted at this time. Thrombophilia screening will be recommended if patient develops recurrentidiopathic VTE or VTE during therapeutic anticoagulation therapy.

Consulting a specialist with expertise incoagulationdisorders will be considered if patient will develop recurrentVTEor complications necessitating alternatives to anticoagulation, in case of suspected or proven hypercoagulability and for management of VTEduring pregnancy(Goodacre, 2008).

References

Angnelli, C., & Becattini, C. (2010).Acute pulmonary embolism.N Eng J Med, 363, 266-74. doi: 10.1056/NEJMra0907731

Bonnema, R. A., McNamara, M. C., & Spencer, A. L. (2010).Contraception choices in women with underlying medical conditions.Am Fam Physician, 86(2), 621-628. Retrieved from http://www.mdconsult.com.libproxy2.umdnj.edu/das/article/body/315112783-3/jorg=journal&source=MI&sp=23646579&sid=1260399197/N/765809/s0002838x10603656.pdf?SEQNO=1&issn=0002-838X

Chalikias, G. K., Tziakas, D. N., Stakos, D. A., & Konstantinides, S. K. (2010). Management of acute pulmonary embolism: a contemporary, risk-tailored approach. Hellenic J Cardiol, 51, 437-450. Retrieved from www.hellenicjcardiol.org/archive/full_text/2010/5/2010_5_437.pdf

Goodacre, S. (2008, September 2). In the clinic.Deep vein thrombosis.Ann Intern Med, 149(5), ITC3-1. Retrieved from http://www.annals.org.libproxy2.umdnj.edu/content/149/5/ITC3-1.long

Kearon, C., Kahn, S. R., Agnelli, C., Goldhaber, S., Raskob, G. E., & Comerota, A. J. (2008, June).Antithrombotic therapy for venous thromboembolic disease.American College of Physicians Evidence-Based Clinical Practice Guidelines (8th Edition).Chest, 133(6), 454S-545S.doi: 10.1378/chest.08-0658

Okuyemi, K. S., Nollen, N. L., & Anluwalia, J. A. (2006, July 15). Interventions to facilitate smoking cessation.Am Fam Physician, 74(2), 262-271. Retrieved from http:// http://www.aafp.org.libproxy2.umdnj.edu/afp/2006/0715/p262.html

Thavendiranathan, P., Bajai, A., Khoo, C., & Dorian, P. (2009). Does this patient with palpitations have a cardiac arrhythmia? JAMA, 302(19), 2135-2143. doi: 10.1001/jama.2009.1673 Grade 100% Excellent H&P!!


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