Just another day.

History and Physical

NAME: Jack Black                       DOB: 03/28/1948                         SEX: Male

RACE: Caucasian                         Physician: Dr. L                       DATE:

2/17/2016

 

CHIEF COMPLAINT: Right leg pain and swelling with intermittent chest pain x 1 month.

 

HISTORY OF PRESENT ILLNESS: This is a 62 year old male presenting with right lower extremity swelling and calf pain with intermittent chest pain for approximately 1 month. He states that the swelling and pain has decreased, but is still present. The pain is only present upon compression or movement of the extremity, not constant as it was previously. He also states that he noted that his right foot was a blue color a few weeks ago. He also complains of “achy” substernal intermittent chest pains that began around the time his leg became swollen. He states that pain occurs at rest and is of gradual onset, usually 1-2 times per day, every other day. He states that the pain lasts 15-20 minutes and is resolved spontaneously. He rates the pain as a 5/10. He denies shortness of breath, wheezing, hemoptysis, cough, fever or chills, palpitations, dizziness/lightheadedness, headaches and any skin lesions or ulcers. He states he has been feeling more fatigued than usual lately. He also complains of increased sanguinous and fecal discharge from his abdominal fistulas in the past few days and periumbilical abdominal pain that has been constant for 4 years and has not changed in nature or intensity. He also states he has been experiencing unintentional weight loss over the past few weeks. He denies nausea, vomiting, and diarrhea. He states he has no change in his appetite, no change in bowel movements or blood in his stool.

PAST MEDICAL HISTORY: Abdominal fistulas s/p umbilical hernia repair in 2005 and anemia.

ALLERGIES: NKDA

MEDICATIONS: multivitamins, methadone and oxycodone.

SURGERIES/HOSPITALIZATIONS: umbilical hernia repair in 2005 and 2 past hospitalizations for anemia secondary to abdominal fistulas.

SOCIAL HISTORY: Denies tobacco use and drug use, drinks alcohol socially. Patient lives at home with his wife, Active, Works at ScrantonRoofingPros.com

FAMILY MEDICAL HISTORY: no related family history.

REVIEW OF SYSTEMS:

  • General: increased fatigue, unintentional weight loss, no fever, chills or sweats.
  • SKIN: no ulcers of lesions on extremities.
  • HEENT: denies any URI symptoms, eye pain or pressure, visual changes, hearing difficulty, dizziness or vertigo and headaches.
  • Cardiovascular: + chest pain + pedal cyanosis + edema of right lower extremity + increased fatigue. Denies dizziness, LOC, palpitations, orthopnea or PND.
  • Respiratory: Denies shortness of breath, wheezing, cough, hemoptysis. No history of tobacco use.
  • GI: + periumbilical abdominal pain and increased discharge from abdominal fistulas. Denies nausea, vomiting and diarrhea. No appetite change or change in bowel movements, no melena or hematochezia.
  • GU: denies dysuria, hematuria, urgency, frequency, or nocturia.
  • Neuro: denies memory problems, syncope, weakness, tremors, lightheadedness/dizziness, difficulty walking, changes in hearing, and headache. Denies paresthesias.

PHYSICAL EXAM:

  • Vital Signs: P 88 R 18 BP 107/61 T: 98.4 SpO2: 100% on room air.
  • General: alert and oriented x3. Well developed/well nourished male in no acute distress, speaking full sentences.
  • HEENT: Head-normocephalic, atraumatic; Eyes- PERRLA, EOM-intact, conjunctival pallor, no scleral icterus. Ears- intact, no discharge; Nose- patent, no discharge.
  • Skin: warm and dry, mild pallor and ecchymosis. No cyanosis, rashes, or ulcers.
  • NECK: supple, symmetric, trachea midline, no adenopathy, full ROM, no JVD.
  • CHEST: stable, equal rise and fall, no retractions, no instability or crepitus. Non-TTP. No accessory muscle usage.
  • LUNGS: Clear to auscultation bilaterally, equal breath sounds. No wheeze, rhonchi or rales. No pericardial friction rub, normal respiratory effort.
  • CVS: regular rate, regular rhythm, no murmurs, rubs, or gallops. 2+ radial pulses bilaterally, 2+ femoral, posterior tibial and dorsalis pedis pulses bilaterally. + non-pitting edema in right lower extremity.
  • Abdomen: soft, non-distended, tender to palpation periumbilically with involuntary guarding. 4 approximately 2-4 cm diameter abdominal fistulas, with peripheral erythema and sanguinous and fecal discharge. Bowel sounds present and normoactive in all 4 quadrants, no organomegally or masses. No abdominal jugular reflex.
  • Extremities: no obvious deformities. Delayed capillary refill. Full ROM. Sensation intact. + non-pitting edema in right lower extremity. + Homan’s sign, + calf tenderness. Non-tender in popliteal space.
  • Neuro: Cranial nerves II-XII grossly intact. Mental status: alert and oriented x 3. Sensation intact. 4/5 motor strength bilaterally. GCS of 15.

DIAGNOSTIC DATA:

  • Chemistry (CMP)
  • K: 3.7, Na: 139, Cl: 105, HCO3: 23, BUN: 14, Cr: 1.1, Glucose: 94.
  • Hematology
    • WBC: 5.4, Hgb: 5.5, Hct: 20.3, Plt: 599
  • CPK-30 Troponin- <0.30
  • PT- 1 INR-1.1
  • D-dimer: 804
  • Type and screen
  • Doppler U/S of right leg- + DVT
  • CXR- No cardiomegally. Normal pulmonary vasculature, no evidence of interstitial edema. No pleural effusion or infiltrates. No evidence of pulmonary embolus.
  • EKG- normal sinus rhythm with a rate of 80 beats per minute. Normal axis. No QT prolongation. No ST or T wave changes. No evidence of PE (S in I, Q in III, inverted T wave in III)

 ASSESSMENT/IMPRESSION:

Right lower extremity swelling/pain and chest pain

DDX:

  • DVT/Pulmonary Embolus
  • Myocardial Infarction
  • New onset CHF
  • Anemia

Other Diagnosis:

  • Chronic Abdominal Fistula

PLAN:

1.) Obtain IV access and Heparin Lock IV

2.) Type and Cross

3.) 2 units PRBCs- 1 unit over 2 hours

4.) Arixtra (fondaparinux) 7.5mg SC

5.) Surgery consult for abdominal fistulas

6.) Admit to internal medicine

 

In Conclusion

A number of studies suggest that successful thrombus elimination is correlated with better long-term venous function and improved clinical outcomes, with a lower incidence of PTS. Additionally, a published randomized trial found that the use of contemporary surgical venous thrombectomy with anticoagulation resulted in better venous patency and reduced PTS than anticoagulation alone. It has also been suggested by several studies that systemic DVT thrombolysis, which refers to venous thrombus dissolution using recombinant tissue plasminogen activator (rt-PA) achieves >50% clot lysis more often than heparin alone, with a trend toward reduced PTS. The use of intermittent rt-PA injections into nearby veins in the affected leg has also been studied in a randomized controlled study but was not found to be superior to systemic thrombolytic therapy in safety or efficacy. Catheter-directed intrathrombus thrombolysis (CDT) refers to the infusion of a fibrinolytic drug directly into the venous thrombus using imaging guidance. Once the thrombus has been broken up completely, the vein is evaluated using venography and any obstructive lesions are then treated with balloon angioplasty or stenting. In 2000, Comerota et al analyzed data from 68 CDT-treated acute iliofemoral DVT patients from a multicenter prospective CDT registry and found that they had fewer PTS symptoms, better physical function, less stigma of chronic venous insufficiency and less health distress at a mean follow-up of 16 months than 30 “matched” patients treated with anticoagulation alone. Another study by AbuRahma et al found that patients treated with CDT had more frequent venous patency at 6 months and absence of symptoms at 5 years. Click here for more info.

Thus, it seems that there is significant evidence to consider using endovascular thrombolysis to significantly reduce the incidence of post-thrombotic syndrome, which as it turns out is a common and significantly disabling condition.

Overview of Treatment…

A large spectrum of treatment options are available for DVT and PE and are chosen depending on the extent of the disease. The goal of treatment of DVT and PE is to minimize local extension of the disease in the acute phase and reduce the risk of recurrence in the months to years after the initial episode. The treatment of DVT has the added benefit of reducing the risk of post-thrombotic syndrome (swelling, stasis dermatitis, ulceration, and venous claudication). The standard treatment for DVT consists of an initial course of low molecular weight heparin given one-two times daily by subcutaneous injection at a dose of 100 units/kilogram or fondaparinux a factor Xa inhibitor followed by a vitamin K antagonist such as warfarin. Unfractionated heparin can be used in place of LMWH, but is becoming less common because if requires monitoring. These medications should be started as soon as diagnosis is confirmed or before if clinical suspicion is high. The dose of warfarin should be titrated to a target INR of 2-3. LMWH therapy should be continued for at least 5 days and can be discontinued if the INR is above 2 on two consecutive measurements at least 24 hours apart. For a first DVT, which was secondary to surgery, after immobilization, or associated with oral contraceptive use, warfarin therapy should be continued for 3 months. For patients with a first episode of idiopathic DVT, warfarin therapy should be continued for 6-12 months. Warfarin should be continued for 12 months in patients with documented antiphospholipid antibodies or two or more thrombophilic abnormalities. The risks and benefits of continuing anticoagulation therapy longer than 12 months must be weighed and the patients opinion taken into account. Warfarin therapy for a second DVT is always carried out for at least 12 months, usually longer. Thrombolytic therapy as well as surgical removal of the thrombus are controversial treatment approaches and are generally reserved for those with massive ileofemoral DVT who are at risk for limb gangrene. In order to prevent post-thrombotic syndrome, patients should be instructed to wear graduated elastic compression stockings to the knee with an ankle pressure of 30-40 mmHg for 2 years to reduce the risk. Most patients can now be treated at home for DVT or require only a short hospital stay.

The treatment of PE in hemodynamically stable individuals is exactly the same as the treatment for DVT. For those patients with PE who are not hemodynamically stable, a course of thrombolytic therapy should be considered. When no contraindications for thrombolysis exist (recent surgery or bleeding diathesis), this therapy reduces the short-term risk of recurrence or death from PE by 50%. The most widely used regimen is recombinant tissue plasminogen activator. For patients in which anticoagulation therapy is contraindicated or patients who have recurrent PE despite adequate treatment, a vena caval filter should be considered in order to prevent recurrent emboli.

Recently, with the significant evolution of endovascular techniques, considerations have been made as to weather it may be beneficial to institute endovascular thrombolysis as initial management of DVT to prevent the common complication of post-thrombotic syndrome. Despite the use of anticoagulant therapy, the postthrombotic syndrome (PTS) develops in 25% to 50% of patients who experience a proximal DVT episode. PTS most commonly causes chronic, daily limb pain/aching, fatigue, heaviness, or swelling. In severely affected patients activity limiting venous claudication, stasis dermatitis, subcutaneous fibrosis, or skin ulceration may develop. PTS clearly impairs quality of life and the recent Venous Thrombosis Outcomes cohort study found the presence and severity of PTS to be the leading predictors of patients’ health-related quality of life 2 years after a DVT episode. PTS also leads to venous leg ulcers that are difficult to treat and that often recur. The direct medical costs of treating PTS and the indirect costs of the related work disability have been shown to result in substantial economic burden to the healthcare systems of several North American and European countries. The mechanism behind the occurrence of PTS in the initial weeks after DVT is thought to occur by at least 2 pathways. First, even with anticoagulant therapy, incomplete clearance of thrombus is common, so residual thrombus physically blocks venous blood flow causing obstruction. Second, the inflammatory response that occurs secondary to acute thrombosis directly damages the venous valves and alters the adjacent vein wall, leading to valvular reflux. Uninvolved distal deep veins and superficial collaterals may dilate and become incompetent as well. When reflux and/or obstruction is present, venous hypertension develops and results in edema, tissue hypoxia and injury, progressive calf pump dysfunction, subcutaneous fibrosis, and skin ulceration.

 

The Risks…

Risk Factors for DVT/PE

            There are several risk factors and causes for DVT, all of them related to either immobilization or hypercoagulability. Risk factors associated with limb immobilization include orthopedic surgery, neurosurgery, major abdominal surgery, major trauma, travel, plaster cast and prolonged bed rest. Other acquired causes include central venous catheters, malignancy, antiphospholipid syndrome, pregnancy, obesity, oral contraceptives, hormonal replacement therapy, myeloproliferative disorders, polycythemia vera, or you could be like my recent patient – working as a concrete contractor in Ashburn Va. Inherited disorders that increase the risk of venous thrombosis include antithrombin deficiency, protein C and S deficiency, factor V Leiden, prothrombin 20210A, non-O blood group, dysfibrinogenemia and factor XIII 34val. Other conditions that also increase the risk of thrombosis include high levels of factor VIII, factor IX, factor XI, or fibrinogen and hyperhomocysteinemia. Often several of these risk factors are present in one individual.

The symptoms of DVT are very nonspecific, making clinical diagnosis difficult and imaging essential in the diagnosis of DVT. Some of the common symptoms of DVT are swelling, pain, redness, superficial venous dilation, and Homan’s sign (pain behind the knee or in the calf upon dorsiflexion of the ankle). These symptoms can occur in a number of conditions as mentioned previously and thus are nonspecific and not very helpful in diagnosing DVT. The signs and symptoms of PE are also very nonspecific and include dyspnea, pleuritic chest pain, cough and hemoptysis.

The classic “gold standard” for diagnosis of DVT is contrast venography; however, this study is being largely replaced by ultrasonography. The single criterion for diagnosis of DVT on ultrasonogrpahy is noncompressability of the vein. This investigation is unfortunately limited to the femoral vein and the popliteal vein, but still has a high sensitivity and specificity in symptomatic patients for proximal DVT. It is less accurate for isolated DVT in the calf veins and therefore, the study must be repeated in about 1 week in those patients with an initial normal test. When combined with clinical probability and measurement of the D-dimer level, ultrasonography is very useful and accurate in diagnosing DVT. It has been found that withholding further diagnostic testing and anticoagulant therapy in patients with a low probability of DVT based on ultrasound, clinical probability and negative D-dimer (which constitutes 30-50% of patients) is acceptable. As an alternative to this diagnostic plan, it is also acceptable to perform whole leg imaging. An advantage to this approach is that repeat testing and correlation with clinical probability and D-dimer level is not necessary; however, this approach may result in increased and unnecessary treatment which unnecessarily increases a patients bleeding risk. The classic “gold standard” for diagnosis of PE is pulmonary angiography, which, similar to the diagnosis of DVT is being replaced by other less invasive and complicated tests. Two strategies are accepted for the diagnosis of PE, the first is assessment of clinical probability correlated with the D-dimer level, and the second is spiral CT of the chest. Patients who have an elevated D-dimer level need to undergo a spiral CT. It is safe to rule out PE in patients with a low clinical probability and negative D-dimer level. The multi-slice CT is the best method for diagnosing PE because it detects pulmonary embolus well and if negative has been shown to safely rule out the presence of PE. Another advantage is the probability of detecting alternative diagnoses in the thorax if PE is excluded. Alternative methods for diagnosing PE when spiral CT is unavailable or contraindicated include ventilation-perfusion scintigraphy, ultrasound of the legs and pulmonary angiography.

 

Lets Discuss…

CASE DISCUSSION:

            The lower extremities can swell for a number of reasons, such as increased venous or lymphatic pressures, decreased intravascular oncotic pressures, increased capillary leak, and local injury or infection. Chronic venous insufficiency is by far the most common cause of lower extremity edema and is a common complication of previous DVT, which is the most life threatening cause of lower extremity edema. Normal lower extremity venous pressures in the erect position are 80 mmHg in the deep veins and 20-30 mmHg in the superficial veins. In order to maintain this pressure muscle contraction must be adequate, valves must be competent, and respiration must be normal. If any one of those components fail, venous hypertension occurs. Clues suggesting DVT as a cause of lower extremity edema include a history of cancer, recent limb immobilization, or confinement to bed for at least 3 days following major surgery. Bilateral involvement and improvement upon wakening suggest more systemic causes such as CHF, venous insufficiency or cirrhosis. Other causes of a painful, swollen calf include ruptured popliteal cyst, calf strain or trauma, cellulitis, nephrotic syndrome, or renal failure.

            Venous Thrombosis is the result of occlusive clot formation in the veins. It occurs most commonly in the deep veins of the legs (DVT), but can occur in other sites as well. These sites include the arm (often associated with central venous catheters), the brain, the digestive system (mesenteric vein thrombosis), the liver (portal vein thrombosis), and hepatic vein thrombosis, also known as Budd- Chiari syndrome. Local abnormalities in these vessels often play a role, but a procoagulant state due to cancer or hereditary abnormalities increases the incidence of thrombosis in these more rare locations. DVT’s are common and often occur spontaneously, but can be a complication of certain medical and surgical conditions. The incidence is 1-3 per 1,000 persons per year, 2/3 of these being DVT and 1/3 presenting as PE. Half of patients with PE have no symptoms of DVT beforehand and 1-3% of venous thromboses prove fatal. The incidence of venous thrombosis increases with age and has a high recurrence rate.