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Describe about the Pathophysiology For the Sonographic Appearance.

Deep Venous Thrombosis

Deep venous thrombosis is caused by blood clots in the veins, specifically those found in the legs. When blood clots are dislodged from a vein, they move through blood and eventually find their way to the lungs, causing a condition known as a pulmonary embolism (Thompson 2015). Deep vein thromboses together with pulmonary embolisms make up a condition referred to as venous thrombo-embolism (VTE) (Stone et al. 2017).  The main function of clotting is to minimize blood clots through a process known as coagulation. When something goes wrong during the coagulation process, there is a potential for clot build up which leads to thrombosis (Blann 2015). Blood clots or thrombosis are caused by poor blood circulation, varicose veins, congestive heart failure, pregnancy, an injury to the vein, hormone therapy or susceptibility to blood clots (Thompson 2015).

The pathophysiology of deep vein thrombosis can trace its background to the work of a German doctor known as Rudolf Virchow. He identified three factors, known as Virchow’s triad, which caused blood clots to develop within the deep veins and these factors were venous stasis, injury/trauma and hypercoagulability (Rumbaut & Thiagarajan 2010). Venous stasis is seen to play the biggest role in the formation of blood clots within veins especially in post-surgical patients and those who have experienced vascular trauma (Behravesh et al. 2017).  While stasis can lead to the development of blood clots, research is still unclear on whether stasis alone can cause enough blood clot formation (Rumbaut & Thiagarajan 2010).

Endothelial injuries have been proposed by researchers to cause thrombosis if they are occur in the deep vein valve pockets. The endothelial injuries trigger an increase in P-selectin production which in turn increases production of platelet-endothelial and platelet-leukocyte-endothelial cells that create blood clots (Rumbaut & Thiagarajan 2010). Endothelial P-selectin contributes to inflammatory mechanisms that are localized and various inflammatory stimuli which lead to deep vein thrombosis. Hypercoagulability refers to conditions that exist in a procoagulant state because of hemostatic imbalances within the body that lead to thrombosis. Coagulation factors play an important role in venous thrombosis when they are activated because they concentrate in areas that have a reduce blood flow like the valve pockets found in the lower limbs (Rumbaut & Thiagarajan 2010).

Defects in the mechanisms that promote anticoagulation such as antithrombin deficiency or fibrin deposits play a significant role in causing deep vein thrombosis (Rumbaut & Thiagarajan 2010). In addition, the initiation of a coagulation cascade caused by the release of tissue factor due to tumors or tissue damage increases the risk of a person developing DVT (Behravesh et al. 2017).  Thrombosis mostly occurs in the deep vein valve pockets of the lower legs in areas that have decreased blood flow.

These valves usually help to promote blood flow but they also have a potential to be sites for venous stasis and hypoxia (Stone et al. 2017).  Blood clots are caused by tissue factor which leads to the conversion of prothrombin to thrombin and this process is later followed by fibrin deposition. Prothrombin, produced in the liver, is a protein essential in blood clotting while thrombin converts fibrinogen into fibrin during blood coagulation (Blann 2015).

Virchow's Triad

A venous duplex ultrasound of the lower limbs makes use of two components to detect deep vein thrombosis and these are a Doppler imaging of the leg using spectral waveform analysis and color-flow imaging or compression techniques using a transducer that makes use of B-mode or gray-scale images. The main criterion for diagnosing deep vein thrombosis is the inability to compress the vein. The secondary criteria for diagnosing the condition is the presence of a thrombus in the vein, distention within the veins, the lack of a Doppler spectral signal and no response to valsalva maneuvers (Karande et al. 2016). The Venous duplex ultrasound can also detect whether the thrombus is acute or chronic. For an acute diagnosis, there is venous distention with partial or no compression of the vein while for a chronic diagnosis, there is no compression and the vein has an irregular shape with blood clots present on the walls (Karande et al. 2016).

The American College of Radiology (ACR) has developed guidelines that can be used to diagnose deep vein thrombosis through the use of ultrasound. These guidelines are compression should be done in the lower extremity when using the ultrasound, the color and spectral Doppler should show there is adequate blood flow in the vein and also phasicity (Karande et al. 2016). The images below show acute DVT. Image A and B are gray-scale or B-mode ultrasound images of the left femoral vein with the arrow pointing to an enlarged vein that has no compression. Image C is a color image generated by a spectral Doppler showing a lack of flow within the vein (Karande et al. 2016). 

The right popliteal vein. Images A and B are a gray scale or B-mode ultrasound imaging of vein depicting compression of the lumen and an echogenic wall as shown by the arrow. The color image is generated from the spectral Doppler and it shows there is flow within the linear area of echogenic material (Karande et al. 2016).    


Behravesh, S, Hoang, P, Nanda, A, Wallace, A, Sheth, RA, Deipolyi, AR, Memic, A, Naidu, S & Oklu, R 2017, ‘Pathogenesis of thromboembolism and endovascular management,’ Thrombosis, pp. 1-13, viewed 2 December 2018, <> 

Blann, A 2015, Deep vein thrombosis and pulmonary embolism: a guide for practitioners. M&K Publishing, Glasgow, viewed 2 December 2018, <> 

Karande, GY, Hedgire, SS, Sanchez, Y, Baliyan, V, Mishra, V, Ganguli, S & Prabhakar, AM 2016, ‘Advanced imaging in acute and chronic deep vein thrombosis,’ Cardiovascular Diagnosis and Therapy, vol. 6, no.6, pp.493-507, viewed 11 December 2018, <> 

Rumbaut, RE & Thiagarajan, P 2010, Arterial, venous and microvascular hemostasis/thrombosis, Morgan and Claypool Life Sciences, San Rafael, CA, viewed 2 December 2018, <> 

Stone, J, Hangge, P, Albadawi, H, Wallace, A, Shamoun, F, Knuttien, MG, Naidu, S & Oklu, R 2017, ‘Deep vein thrombosis: pathogenesis, diagnosis and medical management,’ Cardiovascular Diagnosis and Therapy, vol. 7, viewed 2 December 2018, <> 

Thompson, AE 2015, ‘Deep vein thrombosis,’ JAMA, vol. 313, no. 20, viewed 2 December 2018, <>  

Factors Contributing to Thrombosis

Epididymitis is the swelling and inflammation of the epididymis as a result of a bacterial or fungal infection. If the infection is not treated, it can spread to the testicles, leading to a condition known as epididymo-orchitis. Currently there is not a lot of research to show the true prevalence of the disease. Data from the US shows that 600,000 people had epididymitis in 2002 with men between 18-35 years being the most infected (Taylor 2015). Epididymitis infections can be sexually transmitted or urinary tract infections even though UTIs are not common in men. UTIs are more likely to be the cause if the male has an indwelling urinary catheter, surgery in any of the male reproductive organs or an enlarged prostate gland (NHS 2018).

Epididymitis can be categorized as acute or chronic where acute is characterized by pain and swelling that lasts for less than six weeks. If no treatment is initiated, the infection can spread to the testis within a matter of days leading to epididymo-orchitis (Cek, Sturdza & Pilatz 2017). According to Campbell’s research in 1927, acute infections of the epididymis were caused by the ascension of microorganisms into the urethra. Another study found that patients with urinary catheters had bacterial pathogens that led to infections (Cek, Sturdza & Pilatz 2017). Chronic epididymitis occurs between six weeks to three months where the patient has pain and discomfort in the epididymis. The factors that lead to chronic infections include an obstruction in the urethra or an infection (Cek, Sturdza & Pilatz 2017).

Infections caused by STD begin when a bacterium is introduced to the genitourinary tract through sexual intercourse where it then migrates to the epididymis. UTI infections are caused when there is an obstruction in the flow of urine within the urinary tract, leading to an inflammation of the epididymis. This happens in patients who have indwelling catheters that have been in place for a long time (Rupp & Leslie 2018).

A hydrocele occurs when there is an accumulation of fluid in the membrane that covers the testicles. This fluid build-up is caused by severe diseases, trauma or imbalances in the secretion and absorption of fluids in the tunica vaginalis (Dagur et al. 2017). Hydroceles are usually painless but they can lead to complications if they are not treated. The most common cause of hydroceles is a disruption within the lymphatic system. Laparoscopic procedures like varicocelectomies have the potential to disrupt drainage within the testicles leading to hydrocele complications. Imbalances in the input and output of lymphatic tissue covering the scrotum are also another cause of hydroceles (Dagur et al. 2017).

Hydroceles can be congenital which are commonly found in pediatric patients and are caused when the tunica vaginalis closes, leading to spermatic cord hydroceles. Acquired hydroceles are commonly found in adult males and they are caused by increased secretion of fluids, reaction of the hydrocele to epididymitis, trauma and reduced lymphatic flow (Wright et al. 2012). They can also occur in patients who have undergone kidney transplants because of disruptions within the lymphatic system. The disruption causes hydroceles because the absorption of lymphatic fluid has been negatively affected despite the normal secretion of the fluid (Dagur et al. 2017).

Antithrombin Deficiency and Fibrin Deposits

If hydroceles are not treated, they can cause low sperm production due to the increased pressure within the testis. Both benign and malignant tumors can also be hidden by the hydrocele because the built-up fluid makes it difficult to detect underlying problems. They can also cause pressure to sensitive tissues within the body such as the testis (Dagur et al. 2017). The pressure from hydroceles can be very severe, surpassing that of blood vessels in the scrotum and this becomes a leading cause of ischemia in the testis. Hydroceles can be treated through invasive or non-invasive surgery. Hydrocelectomy is an invasive surgery for hydroceles that are particularly large and persistent while aspiration and sclerotherapy are non-invasive techniques that are used to treat hydroceles that are 750ml in size (Dagur et al. 2017).

Epididymitis is detected through the use of ultrasonography which is a noninvasive procedure for diagnosing abnormalities within the scrotum. A linear array transducer that uses a frequency of 12 to 17 MHz is used to provide grayscale and color Doppler images of the testicles, scrotum and epididymis (Kuhn et al. 2016). The scanning of the epididymis involves taking longitudinal imaging of the lateral, mid and medial parts of the head, body and tail of the epididymis. Transverse images include those of the upper, middle and lower parts of the epididymis (Kuhn et al. 2016).

The color Doppler imaging for the epididymis should be done bilaterally to assess the capsular, centripetal arteries and check for a reduction in velocity of venous flow. Arterial and venous flow on both sides should also be assessed using spectral waveforms (Kuhn et al. 2016). Ultrasonography results for diagnosing epididymitis show the presence of an enlarged and highly vascularized epididymis with a hypoechoic appearance. The color Doppler has a sensitivity of 100 percent and is an effective tool in detecting acute inflammations as well as diagnosing epididymitis. The formation of abscess is a complication found in acute epididymitis and it appears as a hypoechoic area that is avascular under sonography (Kuhn et al. 2016).

The images below are an ultrasonogram of a 48 year old male who complained of pain and swelling in the testicles. Image A is a gray-scale Doppler image of the epididymis which is enlarged (marked by the asterisk) and a right testicle that is also enlarged with edema. Image B is a color image which demonstrates increased vascularity consistent with epididymo-orchitis (Kuhn et al. 2016). 

The grayscale and color sonograms below depict an epididymis that is hypoechoic and has increased vascular flow. These findings are consistent with a diagnosis of epididymitis (Kuhn et al. 2016).   


Cek, M, Sturdza, L & Pilatz, A 2017, ‘Acute and chronic epididymitis,’ European Urology Supplements, vol. 16, no. 4, pp. 124-131, viewed 3 December 2018, <> 

Dagur, G, Gandhi, J, Suh, Y, Weissbart, S, Sheynkin, YR, Smith, NL, Joshi, G & Khan, SA 2017, ‘Classifying hydroceles of the pelvis and groin: an overview of etiology, secondary complications, evaluation and management,’ Current Urology, vol.10, no. 1, pp.1-14, viewed 3 December 2018, <> 

Sonographic Appearance

Kuhn, AL, Scortegagna, E, Nowitzki, KM & Kim, YH 2016, ‘Ultrasonography of the scrotum in adults,’ Ultrasonography, vol. 35, no. 3, pp. 180-197, viewed 11 December 2018, <> 

NHS 2018, Epididymitis, viewed 2 December 2018, <> 

Rupp, TJ & Leslie, SW 2018, Epididymitis. StatPearls Publishing, Treasure Island, FL, viewed 3 December 2018, <> 

Taylor, SN 2015, ‘Epididymitis,’ Clinical Infectious Diseases, vol. 61, viewed 3 December 2018, <> 

Wright, LA, Gerscovich, EO, Corwin, MT, Lynch, L & Lamba, R 2012, ‘Tension hydrocele: additional cause of ischemia of the testis,’ The Multidisciplinary Medical Ultrasound Journal, vol. 31, no. 12, pp. 2041-2043, viewed 3 December 2018, <>    

De Quervain’s tenosynovitis is condition that affects the tendons found within the wrists which irritate the muscles causing excruciating pain, swelling and increased difficulty grabbing onto objects (Patel, Tadisina & Gonzalez 2013). Painful inflammation occurs on the radial side of the wrists which is made worse when the wrist is used in a gripping or wringing motion. De Quervain’s has been found to affect women more than men and is likely to affect pre-menopausal, pregnant women and new born mothers (Satteson & Tannan 2018).

The cause of this disease is unknown even though it contributes to the degeneration of tissue deposits within the lining of the wrists. Tissue deposits within fibrous tissues cause thickening within the abductor pollicis longus (APL) and extensor pollicis brevis (EPB) tendon sheaths, entrapping these tendons (Satteson & Tannan 2018). The repetitive motion of the wrists together with the bending and extending of the thumb also contributes to this condition. The EPB and APL tendons move through a fibrous tunnel that is 2cm long under the fibers of the extensor retinaculum. The tendons can get trapped in these fibers especially if there is trauma or constant repetitive motion of the wrists (Satteson & Tannan 2018).

De Quervain progresses in three stages the first being the early onset or acute stage where there is inflammation, swelling and thickening of the tendon sheaths. The second stage known as the sub-acute phase is characterized by crepitus which is a grating or crackling sound under the skin (Yang & DeMola 2016). Pain is present in this stage limiting the patient’s ability to perform tasks such as grabbing or lifting. In the chronic stage, the superficial radial nerve becomes numb in the dorsolateral part of the hand, affecting the first three digits. The pain is very severe and moving the wrists becomes extremely difficult. Some medical conditions that are associated with De Quervain’s include carpal tunnel syndrome, rheumatoid arthritis and ruptured tendons (Yang & DeMola 2016).

An examination of the radial part of the hand will show tenderness and inflammation in the wrist. Finklestein’s test is also used to diagnose de Quervain’s by flexing the thumbs in a closed fist and moving the wrist either actively or passively to check for pain. The presence of pain is an indication that there is restricted gliding of the two tendons (Goel & Abzug 2015, p.1). The description of the Finklestein’s test states that when the thumb is grasped and the hand is abducted ulnarward, the pain is very excruciating. However some scientists have disputed this test because it can also diagnose cases of osteoarthritis, tendonitis in the wrists or joint tendonitis of the carpometaphalangeals (Yang & DeMola 2016).

Diagnosis of Deep Vein Thrombosis

Treatment for this disease includes surgical and non-invasive forms of treatment. Surgery is done when symptoms have been present for more than three months or when other treatments fail to work. Non-invasive treatments are recommended for patients who have mild to moderate pain (Ilyas 2007, p.759). Examples of these treatments include anti-inflammatory medication, splinting of the tendons and injecting steroids into the dorsal area of the wrist. Splinting is seen as an effective approach because it immobilizes the thumb and the wrist, reducing any movement or friction that leads to pain (2007, p. 759).

Corticosteroids are the most effective treatment regimen because many patients experience relief from symptoms with only one steroid injection. Various studies have shown that these injections have a higher percentage of effectiveness than the other forms of treatment when it comes to pain relief (Rowland et al. 2015). Research done by Richie et al. showed patients within the study had an 83 percent resolution of symptoms after a single steroid shot which further cemented the effectiveness of this treatment (Rowland et al. 2015).

Sonographic imaging of the affected hand is meant show changes in the structure of the APL and EPB tendons. The sonogram can also detect abnormalities, thickening and tissue perfusion within the tendons (Das & Prahbu 2017). Imaging is done over the radial styloid which shows swelling of the tendons and also thickening of the retinaculum compartment. Longitudinal imaging of the affected tendon shows the presence of distention and fluid surrounding the tendon sheath. Transverse images show thickening of the extensor reticulum at the radial styloid (Das & Prahbu 2017, p.4096).

The cutoff value for diagnosing de Quervain’s disease is a thickening of 0.45mm in the extensor reticulum. The tendons on imaging should be thickened when compared to tendons of the non-affected hand. Tendon sheath effusion distal to the extensor reticulum is also present when imaging is done (Das & Prahbu 2017, p.4096). The vertical septum in the sonogram appears as thin vertical bands that are hypoechoic between the tendons. The presence of a vertical septum poses a risk to the patient because it creates a barrier that makes it difficult to diffuse steroids injected in the tendons. Injections administered through the use of ultrasonography are the main treatment used in relieving symptoms of de Quervain’s tenosynovitis (Das & Prahbu 2017).

The sonograms below depict transverse and sagittal imaging of the radial styloid showing both the APL and EPB tendons. The stars in the image show the presence of thickening within the extensor retinaculum area (Das & Prahbu 2017, p.4094). 

The sonograms below are transverse images depicting hypoechoic thickening of the retinaculum over the extensor pollicis tendon. The second image shows the presence of a vertical septum between the two tendons (Das & Prahba 2017, p. 4095). 

This sonogram image is of the distal part of the first extensor retinaculum of the radial styloid. There is thickening of the two tendons surrounded by a small amount of fluid. There is also a hypoechoic septum dividing the abductor pollicis and extensor pollicis tendons (Das & Prahba 2017). 


Das, A & Prabhu, BJ 2017, ‘De Quervain’s disease; evaluation by high resolution ultrasonography,’ International Journal of Research in Medical Sciences, vol. 5, no.9, pp. 4093-4097, viewed 11 December 2018, <> 

Goel, R & Abzug, JM 2015, de Quervain’s tenosynovitis: a review of the rehabilitative options,’ Hand, vol. 10, pp. 1-5, viewed 4 December 2018, <> 

Ilyas, A, Ast, M, Schaffer, AA & Thoder, J 2007, ‘De Qervain tenosynovitis of the wrist,’ Journal of the American Academy of Orthopedic Surgeons, vol. 15, no. 12, pp. 757-764, viewed 4 December 2018,<> 

Patel, KR, Tadisina, KK & Gonzalez, MH 2013, ‘De Quervain’s disease,’ Eplasty, vol. 13, viewed 4 December 2018, <> 

Rowland, P, Phelan, N, Gardiner, S, Linton, KN & Galvin, R 2015, ‘The effectiveness of corticosteroid injection for De Quervain’s stenosing tenosynovitis (DQST): a systematic review and meta-analysis,’ The Open Orthopaedics Journal, vol. 9, pp. 437-444, viewed 4 December 2018, <> 

Satteson, E & Tannan, SC 2018, De Quervain Tenosynovitis. StatPearls Publishing, Treasure Island, FL, viewed 4 December 2018, <> 

Yang, J & DeMola, P 2016, De Quervain tenosynovitis. American Academy of Physical Medicine and Rehabilitation, Rosemont, IL, viewed 4 December 2018, <>

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