Surgery;

My patient recently underwent total knee arthroplasty (TKA) and is now found to have a Baker’s cyst. Is Baker’s cyst a postoperative complication of TKA?

FA Manian MD, MPH, , , , , , , , , , , , Leave a comment

Not likely! There is no evidence that TKA causes Baker’s cyst (also known as popliteal cyst). Instead, the finding of Baker’s cyst following TKA may be best explained by its well-known association with osteoarthritis, one of the main indications for TKA.1,6,7

In a study of 2025 patients who underwent primary TKA, 0.6% were diagnosed with Baker’s cysts within 6 weeks to 2 years postoperatively (75% symptomatic), but whether the cysts were present prior to TKA was unclear. There was no reported association between surgical technique or perioperative course and Baker’s cyst diagnosis.9

Actually, there might be a correlation between TKA and Baker’s cyst resolution.2,3 Among patients with known cysts preoperatively, 15% and 67% of patients may experience resolution of the cyst at 1 year and 4-6 years following surgery, respectively. 2,3

A Baker’s cyst is a fluid-filled pocket in the posterior aspect of the knee, typically seen in adults with degenerative changes in the patellofemoral joint, as may occur with meniscal tears and arthritis. When symptomatic, it can be treated non-operatively with ultrasound-guided aspiration and corticosteroid injection or operatively with surgical excision or attempted repair of the underlying defect. 4,8

 

Bonus Pearl: Did you know that the ‘crescent sign’ (bruising below the medial malleolus associated with fluid from ruptured cyst moving inferiorly toward the ankle) was first described in 1976 and may help distinguish calf pain due to Baker’s cyst from that of deep venous thrombophlebitis? 5

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 Contributed by Anamika Veeramani, Medical Student, Harvard Medical School

 

References

  1. Guermazi A., Hayashi D., Roemer F, et al. Cyst-like lesions of the knee joint and their relation to incident knee pain and development of radiographic osteoarthritis: The MOST study. Osteoarthritis and Cartilage 2010; 18:1386-1392. doi:10.1016/j.joca.2010.08.015. https://pubmed.ncbi.nlm.nih.gov/20816978/
  2. Hommel H., Becker R., Fennema P., et al. (2020). The fate of Baker’s cysts at mid-term follow-up after total knee arthroplasty. The Bone & Joint Journal, 2020;102-B(1):132-136. doi:10.1302/0301-620x.102b1.bjj-2019-0273.r2. https://pubmed.ncbi.nlm.nih.gov/31888367/
  3. Hommel, H., Perka, C., Kopf, S. The fate of Baker’s cyst after total knee arthroplasty. The Bone & Joint Journal 2016;98-B(9):1185-1188. doi:10.1302/0301-620x.98b9.37748. https://pubmed.ncbi.nlm.nih.gov/27587518/
  4. Leib AD, Roshan A, Foris LA, et al. Baker’s Cyst. [Updated 2020 Mar 16]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430774/
  5. Mizumoto, J. The crescent sign of ruptured baker’s cyst. Journal of General Family Medicine, 2019;20(5): 215-216. doi: 10.1002/jgf2.261. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6732489/
  6. Rupp, S., Seil, R., Jochum, P., & Kohn, D. Popliteal Cysts in Adults. The American Journal of Sports Medicine 2002; 30(1): 112-115. doi:10.1177/03635465020300010401. https://pubmed.ncbi.nlm.nih.gov/11799006/
  7. Sansone, V., Ponti, A. D., Paluello, G. M., & Maschio, A. D. Popliteal cysts and associated disorders of the knee. International Orthopaedics 1995;19(5): 275-279. doi:10.1007/bf00181107. https://pubmed.ncbi.nlm.nih.gov/8567131/
  8. Smith, M., Lesniak, B., Baraga, M., Kaplan, L., Jose, J. Treatment of Popliteal (Baker) Cysts with Ultrasound-Guided Aspiration, Fenestration and Injection: Long-term Follow-up. Sports Health 2015; 7(5): 409-414. doi: 10.1177/1941738115585520. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4547114/
  9. Tofte, J. N., Holte, A. J., & Noiseaux, N. Popliteal (Baker’s) Cysts in the Setting of Primary Knee Arthroplasty. The Iowa Orthopedic Journal 2017;37:177-180. https://pubmed.ncbi.nlm.nih.gov/28852354/

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

My patient recently underwent total knee arthroplasty (TKA) and is now found to have a Baker’s cyst. Is Baker’s cyst a postoperative complication of TKA?

Why is my diabetic patient complaining of arm pain and localized edema for couple of weeks without an obvious cause?

FA Manian MD, MPH, , , , , , , , , , , , , , Leave a comment

Aside from the usual suspects associated with a painful extremity (eg, trauma, deep venous thrombosis and soft tissue infections), think of spontaneous diabetic myonecrosis (DMN), also known as diabetic muscle infarction (1-3).

DMN is characterized by abrupt onset of painful swelling of the affected muscle, most often of the lower extremities, but also occasionally upper extremities. DMN occurs in patients with longstanding DM whose blood glucose control has deteriorated over time, often with nephropathy, retinopathy and/or neuropathy (1-3).

Couple of things to remember when considering DMN in your differential of a painful extremity. First, except for localized edema and tenderness over the involved muscle, the exam may be unremarkable. Specifically, there is no erythema or signs of compartment syndrome and fever is absent in the great majority of patients (~90%) (2). Even white blood cell count and creatine kinase (CK) are usually normal. The reason for normal CK at presentation is not clear but CK might have already peaked by the time of patient presentation (3). In contrast, C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) are usually elevated (>80%) (1).

MRI (without contrast in patients with renal insufficiency) is the imaging of choice with muscle enlargement and edema with hyperintense signal on T2-weighted images and other changes, including perifascial, perimuscular and or subcutaneous edema (1-3). Muscle biopsy is not currently recommended because of its adverse impact on time to symptomatic improvement. Non-surgical therapy, with rest, analgesia and glycemic control is usually recommended (1-3).

 
Though its exact cause is still unclear, atherosclerosis, diabetic microangiopathy, vasculitis with thrombosis and ischemia-reperfusion injury have been posited as potential precipitants for DMN. The role of anti-phospholipid syndrome, particularly in patients with type I DM, is unclear (1,2).

 
Bonus pearl: Did you know that symptoms of DMN may last for weeks with at least one-third of patients having a recurrence in the same muscle or elsewhere (1)?

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Reference
1. Horton WB, Taylor JS, Ragland TJ, et al. Diabetic muscle infarction: a systematic review. BMJ Open Diabetes Research and Care 2015;3:e000082.
2. Trujillo-Santos AJ. Diabetic muscle infarction. An underdiagnosed complication of long-standing diabetes. Diabetes Care 2003;26:211-15.
3. Diabetes muscle infarction in end-stage renal disease:A scoping review on epidemiology, diagnosis and treatment. World J Nephrol 2018;7:58-64.

Why is my diabetic patient complaining of arm pain and localized edema for couple of weeks without an obvious cause?

Does my patient on chronic prednisone need stress doses of corticosteroids perioperatively?

FA Manian MD, MPH, , , , , , , , , , Leave a comment

There are wide-ranging opinions on stress doses of corticosteroids (CS) in patients on chronic prednisone undergoing surgery, largely due to lack of adequately-sized randomized controlled studies.  Most experts seem to agree, however, that the age-old practice of routinely administering very high doses of hydrocortisone (eg, 100 mg IV every 8 hours) with prolonged taper postoperatively is excessive. 1-7

Couple of questions to consider before you decide on stress doses of CS for your patient with CS-induced (not primary) adrenal suppression. First, is your patient likely to have a suppressed adrenal function? And if so, what type of surgery is he or she about to undergo?

As for the first question, keep in mind that exogenous CS suppress the production of corticotropin (ACTH) and can induce adrenal atrophy that may persist for up to 12 months, an effect that’s dependent not only on their dose but also on their duration and may vary greatly from person to person. 2,4

Generally, a daily prednisone dose of 5 mg or less —irrespective of the duration— is considered unlikely to cause adrenal suppression (unless it’s given at bed time) and therefore should not require stress doses of CS.1 Conversely, clinical features of Cushing’s syndrome and prednisone doses of 20 mg or more daily for more than 3 weeks are likely to be associated with hyphothalamic-pituitary-adrenal (HPA) axis suppression.  Due to possible delay in the recovery of the HPA axis after discontinuation of exogenous CS, you should review not only your patient’s current dose and duration of CS but his or her regimen during the previous year. 2

When in doubt, particularly in patients receiving intermediate doses (eg, between 5 to 20 mg of prednisone daily) or duration of CS, testing the HPA axis (eg, by cosyntropin stimulation) has been suggested by some with the caveats that it’s a grade 2C (weak recommendation, low quality evidence) recommendation,7 and the results may not necessarily predict clinical adrenal insufficiency or be available before surgery. 4  

Once you have decided that your patient may be at risk of adrenal insufficiency during the perioperative period, the stress dose and duration of CS will likely depend on the type of surgery: “minor” (eg, inguinal herniorrhaphy); “moderate” (eg, total joint replacement, peripheral vascular surgery) and “major” (eg, pancreatoduodenectomy, cardiac surgery with cardiopulmonary bypass). 

A popular online resource suggests the following:4

  • Minor surgery or local anesthesia: Give only the morning maintenance dose of CS without any stress doses
  • Moderate surgery: Give the usual morning dose plus hydrocortisone IV 50 mg (or equivalent) just before the procedure followed by 25 mg IV every 8 hours for 24 hours, followed by the maintenance regimen
  • Major surgery: Give the usual morning dose plus hydrocortisone 100 mg IV before anesthesia induction, followed by 50 mg IV every 8 hours for 24 hours, tapering the dose by half each day to maintenance.

Alternatively, for minor and moderate procedures, other authors suggest usual daily dose plus hydrocortisone 50 mg IV before incision, followed by hydrocortisone 25 mg IV every 8 h for 24 h, then the usual daily dose.1  Yet others have recommended giving IV hydrocortisone 25 mg/day for 1 day for minor surgeries, 50-75 mg/day x 1-2 days for moderate surgeries, and 100-150 mg/day for 2-3 days for major surgeries.2-4 Whichever regimen you chose, make sure to give the morning maintenance dose.  

Why is less aggressive stress dosing being favored in these patients? Several reasons come to mind, including:

  •  In normal subjects, endogenous cortisol production rarely rises above 150-200 mg /day even in response to major surgery 2-4   
  • High doses of CS, particularly with long taper, may unnecessarily subject patients to adverse effects, such as hyperglycemia and poor wound healing 3,4
  • Published reports of CS-treated patients having complications such as hypotension or even death in the postoperative period have generally only implicated, not proven, adrenal insufficiency as a cause. 1-4

 

Bonus pearl: Did you know that the hypotension of secondary adrenal insufficiency in patients treated with CS is not caused by mineralocorticoid deficiency? Instead, it may in part be related to the action of CS in enhancing vascular responsiveness to vasopressors (eg, catecholamines).2 

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References

  1. Liu MM, Reidy AB, Saatee S, et al. Perioperative steroid management: Approaches based on current evidence. Anesthesiology 2017;127:166-72. https://anesthesiology.pubs.asahq.org/article.aspx?articleid=2626031
  2. Axelrod L. Perioperative management of patients treated with glucocorticoids. Endocrinol Metab Clin N Am 2003;32:367-83. http://pggweb.com/doc/glucocorticoids.pdf
  3. Salem M, Tainsh RE Jr, Bromberg J, et al. Perioperative glucocorticoid coverage. A reassessment 42 years after emergence of a problem. Ann Surg 1997;219:416-25. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1243159/
  4. Shaw M. When is perioperative ‘steroid coverage’ necessary? Clev Clin J Med 2002;69:9-11. https://www.ncbi.nlm.nih.gov/pubmed/11811727
  5. Urmson K. Stress dose steroids: the dogma persists. Can J Anesthe 2019;September 23. https://www.ncbi.nlm.nih.gov/pubmed/31549340
  6. Wax DB. One size fits all for stress-dose steroids. Anesthesiology 208;128:674-87. https://anesthesiology.pubs.asahq.org/article.aspx?articleid=2672525
  7. Hamrahian AH, Roman S, Milan S. The management of the surgical patient taking glucocorticoids. Uptodate 2019, accessed October 21, 2019. https://www.uptodate.com/contents/the-management-of-the-surgical-patient-taking-glucocorticoids
Does my patient on chronic prednisone need stress doses of corticosteroids perioperatively?

My postop patient now has fever with atelectasis on her chest X-ray one day after surgery. Does atelectasis cause fever?

FA Manian MD, MPH, , , , , , Leave a comment

Although fever and atelectasis often coexist during the early postop period, there is no evidence that atelectasis causes fever.

A 2011 systematic analysis of 8 published studies found that all but 1 study failed to find a significant association between postop fever and atelectasis.1  A 1988 study reported a significant association between postop fever during the first 48 h and atelectasis on day 4 postop, but not each postop day.2  Even in this study, however, fever as a predictor of atelectasis performed poorly with a sensitivity of 26%, specificity of 75% and accuracy of 43%.

In another study involving postop cardiac surgery patients, despite a fall in the incidence of fever from day 0 to day 2, the incidence of atelectasis based on serial chest X-rays actually  increased. 3

Experimental studies in dogs and cats in the 1960s also support the lack of a causative relationship between atelectasis and fever. 4,5 Although fever was observed within 12 hrs of placement of cotton plugs in the left main bronchus of these animals, almost all animals also developed pneumonia distal to the plug.  Antibiotic treatment was associated with resolution of fever but not atelectasis.

So if it’s not atelectasis, what’s the explanation for early postop fever? The great majority of postop fevers during the first 4 days postop are unlikely to be related to infections. Instead, a more plausible explanation is the inflammatory response to the tissue injury as a result of the surgery itself causing release of cytokines (eg, interleukin-1 and -6 and tumor necrosis factor) associated with fever. 6

References

  1. Mavros MN, Velmahos GC, Falagas ME. Atelectasis as a cause of postoperative fever. Where is the clinical evidence? CHEST 2011;140:418-24. https://www.ncbi.nlm.nih.gov/pubmed/21527508
  2. Roberts J, Barnes W, Pennock M, et al. Diagnostic accuracy of fever as a measure of postoperative pulmonary complications. Heart Lung 1988;17:166-70. https://www.ncbi.nlm.nih.gov/pubmed/3350683
  3. Engoren M. Lack of association between atelectasis and fever. CHEST 1995;107:81-84. https://www.ncbi.nlm.nih.gov/pubmed/7813318
  4. Lansing AM, Jamieson WG. Mechanisms of fever in pulmonary atelectasis. Arch Surg 1963;87:168-174. https://jamanetwork.com/journals/jamasurgery/fullarticle/561080
  5. Jamieson WG, Lansing AM. Bacteriological studies in pulmonary atelectasis. Arch Surg 1963;87:1062-66. https://www.ncbi.nlm.nih.gov/pubmed/14063816
  6. Narayan M, Medinilla SP. Fever in the postoperative patient. Emerg Med Clin Nam 2013;31:1045-58. https://www.ncbi.nlm.nih.gov/pubmed/24176478 

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My postop patient now has fever with atelectasis on her chest X-ray one day after surgery. Does atelectasis cause fever?

When should surgery be considered in my hospitalized patient with divertculitis?

FA Manian MD, MPH, , , , Leave a comment

Severe diffuse abdominal pain, fever, tachycardia, leukocytosis or other signs of sepsis and diffuse peritonitis indicative of free perforation requires emergent surgery. Urgent surgery should be considered when your patient fails to improve (eg, abdominal pain or the inability to tolerate enteral nutrition, bowel obstruction, or infection-related ileus) despite medical therapy or percutaneous drainage. 1,2

Lower threshold for surgical intervention is also needed in transplant patients, patients on chronic corticosteroid therapy, other immunosuppressed patients and those with chronic renal failure or collagen-vascular disease because these patients have a significantly greater risk of recurrent, complicated diverticulitis requiring emergency surgery. Overall, up to 20% of patients with acute diverticulitis undergo surgery during the same hospitalization.2

For patients with recurrent uncomplicated diverticulitis, decision regarding future elective surgery should be individualized. Although older guidelines recommended surgery after 2 attacks of uncomplicated diverticulitis, more recent guidelines place less emphasis on the number of episodes and stress the importance of considering the severity of the attacks, chronic or lingering symptoms, inability to exclude carcinoma, overall medical condition of the patient, risks of surgery, and the impact of diverticulitis on the patient’s lifestyle.1,2

Of interest, a decision analysis model suggests that elective resection after a fourth episode may be as safe as earlier resection.3

 

References

  1. Young-Fadok TM. Diverticulitis. N Eng J Med 2018;397:1635-42 https://www.nejm.org/doi/full/10.1056/NEJMcp1800468
  2. Feingold D, Steele SM, Lee S, et al. Practice parameters for the treatment of sigmoid diverticulitis. Dis Colon Rectum 2014;57:284-94. https://www.fascrs.org/sites/default/files/downloads/publication/practice_parameters_for_the_treatment_of_sigmoid.2.pdf
  3. Salem L, Veenstra DL, Sullivan SD, et al. The timing of elective colectomy in diverticulitis: A decision analysis. J Am Coll Surg 2004;199:904-12. https://www.journalacs.org/article/S1072-7515(04)01000-2/fulltext

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When should surgery be considered in my hospitalized patient with divertculitis?

Should I be concerned about the umbilical hernia in my patient with cirrhosis and ascites?

FA Manian MD, MPH, , , , , , , , , , , Leave a comment

Although umbilical hernia in patients with cirrhosis and ascites is common and often “expected” (a rate of 20% during the course of their disease), it can be associated with significant risk of complications such as incarceration, ascites drainage, peritonitis, and spontaneous rupture or evisceration from necrosis of overlying skin.1,2

A 2007 retrospective study involving patients with cirrhosis and umbilical hernia reported a complication rate of 77% and related mortality of 15% among those managed conservatively (mean period of observation ~ 5 years); MELD score could not predict failure of conservative management (median 22 in complicated vs 24 in uncomplicated).3

Because the risk of death with hernia repair in urgent settings is 7x higher than for elective hernia repair in cirrhotic patients, there has been increasing interest in elective repair in patients with well-compensated cirrhosis.3 Interestingly, the reported surgical complication rates among patients with well-compensated cirrhosis appear similar to those in noncirrhotic patients.3 If the patient is expected to undergo liver transplantation in the near future, elective hernia repair can be postponed and managed concomitantly.

Bonus pearl: Did you know that spontaneous umbilical hernia rupture is also known as “Flood syndrome” (should be easy to remember!), first described by Frank B Flood, a surgical resident back in 1961? 4

References

  1. Marsman HA, Heisterkamp J, Halm JA, et al. Management in patients with liver cirrhosis and an umbilical hernia. Surgery 2007;142:372-5. https://www.ncbi.nlm.nih.gov/pubmed/17723889
  2. Coelho, JCU, Claus CMP, Campos ACL, et al. Umbilical hernia in patients with liver cirrhosis: a surgical challenge. World J Gastrointest Surg 2016;8:476-82. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4942747/
  3. Martens P, Laleman W. Umbilical hernia in a patient with cirrhosis. Cleveland Clin J Med 2015;82: 404-5. https://www.mdedge.com/ccjm/article/100682/hepatology/umbilical-hernia-patient-cirrhosis
  4. Nguyen ET, Tudtud-Hans LA. Flood syndrome: spontaneous umbilical hernia rupture leaking ascitic fluid-a case report. Perm J 2017;21:16-152. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5499604/ 

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Should I be concerned about the umbilical hernia in my patient with cirrhosis and ascites?

Why has my hospitalized patient with head and neck cancer developed thrombocytosis few days following surgery?

FA Manian MD, MPH, , , , , , , , , , , Leave a comment

Thrombocytosis or elevated platelet count is not uncommon among hospitalized patients and may be related to several factors, including “tissue damage” from a surgical procedure, infection, acute blood loss, iron deficiency, and less well known, enoxaparin.1-4 

Postoperative thrombocytosis is thought to be related to increased platelet production as well as redistribution of platelets from the splenic platelet pool to the general circulation.1  Increased levels of megakaryocytic growth factors such as thrombopoietin, and pro-or anti-inflammatory cytokines such as interleukin (IL)-1, 3, 6, or 11 may also stimulate megakaryopoeisis in the setting of inflammation.2 The mechanism of iron deficiency causing thrombocytosis is unknown.4

Enoxaparin-related thrombocytosis usually develops within the first 2 weeks of therapy and resolves 2 weeks following its discontinuation.3

In our patient, although malignancy is also associated with secondary thrombocytosis, given its acute nature in our patient, it is less likely to be playing a role.

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References

  1. Griesshammer M, Bangerter M, Sauer T, et al. Aetiology and clinical significance of thrombocytosis: analysis of 732 patients with an elevated platelet count. J Intern Med 1999;245:295-300. https://www.ncbi.nlm.nih.gov/pubmed/10205592
  2. Kulnigg-Dabsch S, Schmid W, Howaldt S, et al. Iron deficiency generates secondary thrombocytosis and platelet activation in IBD: the randomized, controlled thromboVIT trial. Inflamm Bowel Dis 2013;published online, DOI10.1097/MIB.0b013e318281f4db. https://www.ncbi.nlm.nih.gov/pubmed/23644823
  3. Hummel MC, Morse BC, Hayes LE. Reactive thrombocytosis associated with enoxaparin. Pharmacotherapy 2006;26:1667-1670. https://www.ncbi.nlm.nih.gov/pubmed/17064215
  4. Dan K. Thrombocytosis in iron deficiency anemia. Intern Med 2005;44: 1025-6. https://www.jstage.jst.go.jp/article/internalmedicine/44/10/44_10_1025/_pdf

 

Why has my hospitalized patient with head and neck cancer developed thrombocytosis few days following surgery?