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
- 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
- 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
- Engoren M. Lack of association between atelectasis and fever. CHEST 1995;107:81-84. https://www.ncbi.nlm.nih.gov/pubmed/7813318
- Lansing AM, Jamieson WG. Mechanisms of fever in pulmonary atelectasis. Arch Surg 1963;87:168-174. https://jamanetwork.com/journals/jamasurgery/fullarticle/561080
- Jamieson WG, Lansing AM. Bacteriological studies in pulmonary atelectasis. Arch Surg 1963;87:1062-66. https://www.ncbi.nlm.nih.gov/pubmed/14063816
- 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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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
- Young-Fadok TM. Diverticulitis. N Eng J Med 2018;397:1635-42 https://www.nejm.org/doi/full/10.1056/NEJMcp1800468
- 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
- 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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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
- 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
- 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/
- 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
- 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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An acute rise in platelet count is not uncommon among hospitalized patients and may be related to several factors, including “tissue damage” from a surgical procedure, infection, and acute blood loss1. 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 circulation1. 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 inflammation2.
Less well known is that enoxaparin (Lovenox), an anticoagulant commonly used for prevention of thromboembolic events in hospitalized patients, may also cause reactive thrombocytosis, usually within the first 2 weeks of therapy and resolving 2 weeks following its discontinuation3.
Although malignancy is also associated with secondary thrombocytosis, given its acute nature in our patient, it is less likely to be playing a role.
- . 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
- 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
- Hummel MC, Morse BC, Hayes LE. Reactive thrombocytosis associated with enoxaparin. Pharmacotherapy 2006;26:1667-1670. https://www.ncbi.nlm.nih.gov/pubmed/17064215
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