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Deep Venous Thrombosis and Pulmonary Embolism


For 2 months, a 31-year-old woman had had dyspnea anddull, continuous retrosternal pain. She was admitted to thehospital, and a helical CT scan of the thorax identified asaddle pulmonary embolism. An ultrasonogram revealeddeep venous thrombosis (DVT) in the left leg. Intravenousheparin was given; the patient was discharged,and warfarin was prescribed.

For 2 months, a 31-year-old woman had had dyspnea anddull, continuous retrosternal pain. She was admitted to thehospital, and a helical CT scan of the thorax identified asaddle pulmonary embolism. An ultrasonogram revealeddeep venous thrombosis (DVT) in the left leg. Intravenousheparin was given; the patient was discharged,and warfarin was prescribed.Within a few days, the symptoms returned and becameincreasingly severe. A second helical CT scan ofthe chest again showed a saddle pulmonary embolism(A, arrow). The patient was immediately hospitalized.Her history included asthma, type 2 diabetes mellitus,hypertension, and an ovarian cyst (which had beenresected). A hip fracture 19 years earlier had required pinplacement. Medications included warfarin, hydrochlorothiazide,glyburide, and an oral contraceptive.She had no known drug allergies and denied tobacco,alcohol, and illicit drug use. The family history wassignificant for stroke and myocardial infarction (MI); hermother had had DVT at age 44 years.Temperature was 36.1oC (97oF); blood pressure,104/70 mm Hg; and heart rate, 134 beats per minute.Pulse oximetry showed an arterial oxygen saturation of91% on room air. S1 and S2 were audible; P2 was louderthan A2, and no S3 or S4 were heard. Sinus tachycardiawas noted on the ECG. No sternal heave, apical beat,jugular venous distention, or murmurs were detected. Thelungs were clear with decreased breath sounds in thebase of the left lung field.The slightly obese abdomen was soft, nontender,and not distended. Bowel sounds were audible; no hepatomegaly,splenomegaly, or pulsatile abdominal masseswere found.There was no lower extremity edema or erythema.The patient complained of left calf and thigh tenderness; apositive Homans sign was elicited in the left leg. Cranialnerves were intact; no sensory or motor deficits weredetected.Warfarin was discontinued, and the international normalizedratio decreased from 2.47 to 1.92. Tissue-typeplasminogen activator (tPA) was then given, which amelioratedthe patient's shortness of breath and retrosternalpain. A third helical CT scan of the chest revealed significantdissolution of the clot, especially around the left pulmonaryartery (B, arrow). A Greenfield filter was placed.After 1 week, the patient was discharged. Warfarin(5 mg and 7.5 mg on alternate days) was prescribed; herregular medications for diabetes and hypertension werecontinued. She was advised to discontinue the oral contraceptive.There have been no further complications.About 650,000 cases of pulmonary embolism occurin the United States each year; over 200,000 of affectedpatients are hospitalized, and about 50,000 die.1 Of these deaths, 8% to 10% occur within the first hour after onset ofsymptoms.2 More than 90% of pulmonary emboli originatein the deep venous system of the lower extremities.3Risk factors for pulmonary embolism include prolongedimmobilization, postoperative state, lower extremitytrauma, estrogen-containing oral contraceptives, historyof DVT or pulmonary embolism, congestive heart failure(CHF), pregnancy, cancer, advanced age, obesity, chronicobstructive pulmonary disease (COPD), deficiencies inantithrombin III or protein C and S, and factor V Leidenmutation. This patient had a decreased protein S level.Dyspnea, shock, tachycardia, tachypnea, cyanosis,hemoptysis, gallop rhythm, increased jugular venous distention,pleural rub, right ventricular heave, loud P2, andcough may be associated with pulmonary embolism.Most of these signs and symptoms are seen with a massiveor saddle pulmonary embolus; however, multiplesmall emboli can cause similar but less severe symptoms.Because MI, pneumonia, pneumothorax, CHF, pleuritis,and pericardial tamponade can have a similar presentation,include these conditions in the differential diagnosis.If you suspect pulmonary embolism, order an ultrasonogramof the lower extremities initially to find thesource of the emboli and to rule out DVT. In addition toan ECG and chest films, obtain blood gas levels to evaluatefor hypoxia, and calculate the A-a gradient, which iselevated in patients with pulmonary embolism. A D-dimerstudy is highly sensitive for detecting clots but is notspecific for their location.Results of ventilation-perfusion (V/Q) scans can bemisleading. If the scan is read as "low probability" andthe clinical suspicion of pulmonary embolism is high,initiate anticoagulation and perform more specific tests.Conversely, high probability V/Q results can be found inpatients with chronic lung conditions, such as COPDand interstitial fibrosis. A helical CT scan of the chest ismore useful in diagnosing pulmonary embolism in thesepatients. If these studies are inconclusive, a pulmonaryangiogram--the "gold standard" for diagnosis--can beperformed.When pulmonary embolism is suspected, administeroxygen, obtain intravenous access, and admit the patientfor close monitoring. Thrombolytic therapy with tPA orstreptokinase is the treatment of choice for hemodynamicallyunstable patients with a massive pulmonary emboluswho have no contraindications to anticoagulation.An alternative is intravenous heparin followed bylong-term warfarin therapy after discharge. A Greenfieldfilter is necessary for patients in whom pulmonary embolicontinue to develop despite anticoagulation.




Ferri FF.

Ferri’s Clinical Advisor: Instant Diagnosis and Treatment

. St Louis:Mosby; 2001.


Hope RA.

Oxford Handbook of Clinical Medicine

. Oxford, England: OxfordUniversity Press; 1998.


Kirby RR, Taylor RW, Civetta JM, eds.

Handbook of Critical Care

. 2nd ed.Philadelphia: Lippincott-Raven; 1997:596.(Case and photographs courtesy of Drs Brian L. Patterson and Kamran Zakaria.)

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