POTD: Superficial Thrombophlebitis (feat. Dr. Doge Pologe)

Today's POTD is inspired by resident extraordinaire Dr. Doge Pologe. As usual, TL;DR is below the main text. 

Thrombophlebitis is essentially a composite of two diagnoses: phlebitis, which is a clinical diagnosis in the setting of an erythema and pain overlying a vein and an identified thrombus. In the lower extremities, this is most likely to occur in varicose veins. 

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In general, risk factors for thrombophlebitis are the same as for DVT (think Virchow's Triad of hypercoagulability, hemodynamic changes (stasis/turbulence), and endothelial injury/dysfunction). These include pregnancy, history of vein excision/ablation, history of prior thrombosis, malignancy, and prior IV catheter placement. 

Special cases:

  • "Mondor": thrombophlebitis of a breast vein, anterior chest vein, or of the dorsal penile vein. The two former should prompt a search for breast cancer and the later is usually due to repetitive trauma

  • "Trousseau's sign of malignancy": migratory thromboembolism, has a strong association with adenocarcinoma of the pancreas and lung


Diagnosis
:
Diagnosis of phlebitis is clinical. Ultrasound should be used to identify a thrombus to distinguish between phlebitis and thrombophlebitis. Patients should also have duplex ultrasound to identify a DVT especially if the area of concern is above the knee. This is important because the rate of concurrent DVT in all cases is 25% and the rate of concurrent PE is 5%. 

Thrombophlebitis on ultrasound will demonstrate heterogeneous internal echoes within a superficial vein. Unlike an abscess or a lymph node, this will not be discrete and you should be able to trace it out. in the words of the Doge:

"it looks like a weird continuous twisty spaghetti
abscess thing; 
but it's not to be feared, 
mostly superfluous, so get frisky and ultrasound that biddy, 
color doppler, diagnosis, ka-ching". 

There may be flow present (which can help distinguish an abscess from thrombophlebitis; abscess = no flow). Some examples (by the Doge Pologe and myself):

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Treatment:
As with treatment of below the knee VTE, the treatment of superficial thrombophlebitis is controversial. Patients can be considered low risk (for VTE) if they meet these criteria:

  • Affected vein segment < 5cm

  • Remote from the saphenofemoral/saphenopopliteal junction

  • Low risk for VTE

**Repeat duplex should be obtained in 7-10 days or for worsening symptoms to check for propagation!

NB: thrombophlebitis post-ablation are always low risk and do not require treatment

For these uncomplicated cases, treatment is aimed at alleviating symptoms and prevention of propagation. This includes the following:

  • NSAIDs

  • Warm/cool compresses

  • Elevation of the extremity

  • Compression stockings

Patients that do not qualify as low risk or if they have recurrent thromboembolism should be considered for anticoagulation. Although studies looking at anticoagulation for SVT are small and flawed, NSAIDsLMWH, and fondaparinux have all been shown to decrease incidence of DVT. Patients can also be discharged on Xarelto (this is the only NOAC to be studied for this indication). 

In addition, thromboembolism can become suppurative. Signs and symptoms include high fever (as opposed to the low-grade fever that accompany simple thrombophlebitis) and purulent drainage (duh). In these cases, consider antibiotics


TL;DR

  • Thrombophlebitis = phlebitis (redness/pain along vein) + thrombus

  • Find the thrombus on ultrasound! Look for internal echoes.

  • Low risk patients = below the knee, affected vein < 5cm, distance remove from saphenofemoral/saphenopopliteal junction can be managed with NSAIDs, compression stockings, warm/cool compresses, elevation

  • Low risk patients should get repeat study in 7-10 days to check for propagation

  • High risk patients: consider anticoagulation with LWMH, fondaparinux, or Xarelto

  • Antibiotics for suppurative thrombophlebitis

Special thanks to Dr. Jonas Pologe, Dr. Lawrence Haines, and Dr. Leily Naraghi Bagher Pour. 

Sources:
http://www.emdocs.net/core-em-superficial-venous-thrombosis-svt/
https://www.bmj.com/rapid-response/2011/10/31/superficial-thrombophlebitis-not-straightforward-we-may-think
https://emedicine.medscape.com/article/463256-overview
https://www.uptodate.com/contents/phlebitis-and-thrombosis-of-the-superficial-lower-extremity-veins
https://radiopaedia.org/cases/superficial-thrombophlebitis-1?lang=us

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Don't be Rash about Deadly Rashes

So, let's talk about why you went into Emergency Medicine - to talk about rashes, of course! Although you might not always (or rarely?!?) know the exact etiology of the rash, there are some Can't-Miss life threatening rashes that we must be able to recognize in the ED. And rashes account for 5% of all ED visits, so you should be diligent to identify these dangerous diagnoses. 

First things first: Describe the rash 

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Pertinent points on managing rashes: 

- STOP IT! Stop the offending agent. Known drugs that induce SJS-TEN include sulfa drugs, penicillin, barbituric acids, aspirins, pyrazolone drugs, and anticonvulsants.

- Rashes can be like a BURN, resulting in abnormal fluid balance, thermoregulation, infection control, and electrolytes. Treat appropriately!

- Treat their PAIN (Make Motov proud!) 

- Sepsis management (Make Dickman proud!). If underlying pathology is infectious, treat early and treat appropriately

- Utilize consultants, the sooner the better! Necrotizing infections - surgery. Toxic rashes - Dermatology. ICU and Burn Centers should be on board!

- Steroids??? WAIT  -  let Dermatology/Burn Center/ICU determine the disease pathology so that steroids will not be given that may cause more harm (SJS/Tens) than good. 

There's so much information, but this is just a rough guideline. Remember to rule out life threatening rashes before sending your patient home. 

You have to determine the TYPE of rash. The algorithm divides the rashes into 6 types: Maculopapular, Petechial/Purpura, Diffuse Erythematous, Non-erythematous, Vesiculo-bullous, Pustular. 

Then branch each type of the 6 rashes into the life threatening etiologies. 

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Keep in mind that this list is not comprehensive, but a guideline to help identify life threatening rash. If the patient looks ill, be concerned. 

Once you identify a life threatening rash, be aggressive and manage appropriately (too many points to address here.) Again, just a guide to look for the DANGEROUS RASHES!. Please see the original reference article attached!

REFERENCES: 

https://www.mdedge.com/emed-journal/article/71662/dermatology/emergent-diagnosis-unknown-rash-algorithmic-approach

https://jetem.org/em_derm_tbl/

http://www.emdocs.net/dont-rash-emergency-physicians-approach-undifferentiated-lesion/

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DRESS

DRESS – Drug Reaction with Eosinophilia and Systemic Symptoms

THE SHORT VERSION:Drug-induced hypersensitivity reaction        o Antiepileptics and allopurinol- Life threatening- Look for:        o Rash (morbiliform)        o Diffuse lymphadenopathy        o Diffuse facial edema (ask the pt as this may not be obvious on exam and something they forget to mention)        o Visceral involvement                - Liver (typically mild, can be severe liver failure)                - Kidneys (check Cr and BUN)                - Lungs (hypoxemia, pneumonitis, pleural effusion)- Typically resolves in weeks after offending agent is removed- Treat supportively (if renal/lung involvement consider corticosteroids)

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THE LONG VERSION THAT YOU LIKELY WONT REMEMBER AND WILL HAVE TO LOOK UP WHEN YOU SEE A PATIENT WITH DRESS:

- Drug-induced hypersensitivity reaction

- Life threatening

        o 80% drug related

        o Occurs 2-8 weeks after initiation of medication

        o Antiepileptic agents (eg, carbamazepine, lamotrigine, phenytoin, phenobarbital) and allopurinol are the most frequently reported causes

        o 10-20% a drug relationship cannot be established

- Look for:

       1. Rash - starts as a morbilliform rash and rapidly (hours – days) progresses to a diffuse, confluent, and infiltrated erythema with follicular accentuation covering ≥50% of the body

                 a. Associated with ≥2 of the following: facial edema, scaling, purpura

       2. Diffuse lymphadenopathy

       3. Inflammation and pain of mucous membranes without lesions/erosions

       4. Labs

                a. Leukocytosis with eosinophils with >700/microL

                b. Large activated lymphocytes, lymphoblasts, or mononucleosis-like cells

       5. Organ involvement

                a. Liver (60-80%) – typically mild transient asymptomatic hepatitis (^LFTs)

                        i. Severe hepatitis is responsible for the majority of deaths associated with DRESS.

                        ii. Most important predictors of death: markedly elevated aminotransferase, bilirubin levels and jaundice

                b. Kidneys (10-30%) - acute interstitial nephritis (seen with allopurinol)

                c. Lungs (5-25%) – hypoxemia secondary to interstitial pneumonitis and/or pleural effusion. On broncho-alveolar lavage: Drug-specific T-lymphocytes and eosinophils may be found

- Clinical course:

        o Rash and visceral involvement resolve in 6-9 weeks after withdrawal of offending agent

        o 20% of cases symptoms persist for months with remission and relapse

- Diagnosis:

        o Pt who received new medication in the last 2-6 weeks with the following:

                - Morbilliform rash

                - Fever

                - Lymphadenopathy

                - Facial edema

                - Eosinophilia

        o Labs: CBC (eosinophilia), BMP (creatinine/BUN), viral hepatitis panel, dermatology referral for skin biopsy

        o CT chest if pulmonary symptoms

- Management:

        o Drug withdrawal and supportive measures

        o If suspected medication is antiepileptic, substitute with valproate

        o For pts with hepatic involvement refer to hepatologist

        o For pts with severe interstitial nephritis or interstitial pneumonia, consider corticosteroids

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Drug Rashes

  • Unsurprisingly key in diagnosis is a good history.

  • Most commonly caused by antibiotics.

  • 90% are morbilliform: widespread erythematous macules or papules

  • Common timeframe is 1-2 weeks after starting drug (however some can take up to three weeks).

Rash Presenting Symptoms Onset After Drug Causes Treatment Erythema Multiforme Target like lesions symmetric on trunk and extremities (generally distributed acrally) Mucous membrane involvement in multiforme major.

 

3-14 days HSV primarily; also NSAIDS, sulfa drugs, antibiotics, anti-epileptics. Stop offending agent. Drug Rash with Eosinophilia and Systemic Symptoms Syndrome (DRESS)

 

Fever and rash. Must be organ involvement: hapatic (60-80%), renal, lung. 2-8 weeks Anticonvulsants and allopurinol, additionally sulfa medications, antibiotics, CCB, NSAIDs, and anti-retrovirals (LFTs and BMP should be trended). Topical corticosteroids for rash. Systemic corticosteroids (for interstitial lung disease or nephritis); supportive care/withdrawl of causative agent for organ involvement

 

Stevens-Johnsons

Sydrome

Blisters with mucous membrane involvement

SJS involves less than 10% of the skin surface.

+Nikolsy

4-28 days Allopurinol, sulfa drugs, anti-epileptics, nevirapine and oxicam NSAIDs Range from observation to ICU level care (consider burn unit for approaching >30% BSA)

IV-IG and systemic corticosteroids are controversial.

Stop drug. Supportive.

 

Toxic Epidermal Necrolysis Similar to above, however involves >30% of skin.

 

4-28 days Same as above, however >80% are due to drug. Same as above. Burn Unit/ ICU setting. Serum Sickness-Like Reaction* Rash: urticarial polycyclic wheals on trunk, limbs, face. Fever. Arthralgias in >2/3 patients. 1-2 weeks Penicillin, amoxicillin, cefaclor, bactrim Stop drug. Supportive

Note: True sereum sickness-- protein antigen from a nonhuman species (antitoxin for snake bites, rabies). 

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Fragile Skin Tears

Today we are going to try to focus on a practical skill which is increasingly important with our aging population: Fragile Skin Tears. Hemostasis/Pain Control:

  • Pressure

  • Use LET (Lidocaine-Epinephrine-Tetracaine)!

  • Topical TXA

  • Surgicel

Suture Techniques:

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  1. Apply a couple deep sutures to appose the wound edges. Then place steri strips across the wound and suture through them with 4.0 nylon sutures. This places tension on the tissue below rather than just on the skin.

  2. Place steri-strips parallel to the wound and suture through the steri strips with 4.0 nylon suture. Similar to approach above, however you are able to visualize the wound edges.

  3. Derma-Bond AND Steri Strips. Perform the above techniques, however derma-bond the edges of the wound, let dry, and place sutures through both the steri strips and derma bond. This will be the effective technique for preventing shearing of extremely fragile skin.

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Note there are many variations to this, you may also throw sutures behind the glue. Glue alone may work better for jagged edges than steri-strips. 

  1. Mattress sutures, tegaderm and wait etc.

Aftercare

When the steri strip techniques are used, try to keep wound dry (rather than using topical antibiotics such as bacitracin which will cause the steri strips to become ineffective.  Patients should be vigilant for signs of infection.

Sources:

EMDocs

Lacerationrepair.com

Aliem

Search Terms: Elderly Skin Parchment Laceration Fragile Skin Laceration Tear

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