Why is my hospitalized patient with alcohol withdrawal syndrome so thrombocytopenic?

Although thrombocytopenia associated with chronic alcoholism may be related to complications of cirrhosis (eg, platelet sequestration in spleen due to portal hypertension, poor platelet production, and increased platelet destruction) (1), it may also occur in the absence of cirrhosis due to the direct toxic effect of alcohol on platelet production and survival (2).

 
In a prospective study of patients ingesting the equivalent of a fifth or more daily of 86 proof whiskey admitted for treatment of alcohol withdrawal—without evidence of severe liver disease, infection or sepsis— 81% had initial platelet counts below 150,000/µl, with about one-third having platelet counts below 100,000 µl (as low as 24,000/ul) (3).

 
In most patients, 2-3 days elapsed before the platelet count began to rise significantly, peaking 5-18 days after admission. Others have also reported that platelet counts rise within 5-7 days and normalize in a few weeks after alcohol withdrawal (1); bleeding complications have been uncommon in this setting.

 
Perhaps even more intriguing is the report of the association between thrombocytopenia in early alcohol withdrawal and the development of delirium tremens or seizures (sensitivity and specificity ~ 70%, positive predictive value less than 10% but with a negative predictive value of 99%) (4)! In fact, the authors suggested that, if their findings are corroborated, a normal platelet count could potentially be used to identify patients at low risk of alcohol withdrawal syndrome and therefore outpatient therapy. 

References
1. Mitchell O, Feldman D, Diakow M, et al. The pathophysiology of thrombocytopenia in chronic liver disease. Hepatic Medicine: Evidence and Research 2016;8 39-50. https://www.dovepress.com/the-pathophysiology-of-thrombocytopenia-in-chronic-liver-disease-peer-reviewed-article-HMER
2. Cowan DH. Effect of alcoholism on hemostasis. Semin Hematol 1980;17:137-47. https://www.ncbi.nlm.nih.gov/pubmed/6990498
3. Cowan DH, Hines JD. Thrombocytopenia of severe alcoholism. Ann Intern Med 1971;74:37-43. http://annals.org/aim/article-abstract/685069/thrombocytopenia-severe-alcoholism.

4. Berggren U, Falke C, Berglund KJ, et al. Thrombocytopenia in early alcohol withdrawal is associated with development of delirium tremens or seizures. Alcohol & Alcoholism 2009;44:382-86. https://www.ncbi.nlm.nih.gov/pubmed/19293148

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Why is my hospitalized patient with alcohol withdrawal syndrome so thrombocytopenic?

Can native valve infective endocarditis be associated with hemolytic anemia?

Yes, but it’s rare!  Hemolytic anemia (HA) in the setting of infective endocarditis (IE) has only been described in a few case reports (1-3).  Although diseased valves may cause shearing stress that fragments RBCs, similar to that associated with mechanical heart valves, an autoimmune hemolytic process has also been implicated. 

A 2018 case report describes a patient with hypertrophic obstructive cardiomyopathy (HOCM) with left ventricular outflow tract (LVOT) obstruction who had HA secondary to subacute IE due to Actinomyces israelii (1).   The anemia completely resolved after treating the IE (1). The cause was most likely mechanical shearing (schistocytes or fragmented RBCs present on peripheral smear) by the diseased valves; autoimmune hemolysis was considered unlikely in this case due to consistently negative Coombs tests and failure to respond to corticosteroids (1). 

An autoimmune mechanism was invoked by a 1999 report reviewing 6 cases of HA associated with IE (3).  All patients had fragmented erythrocytes, but several also demonstrated an immune-mediated mechanism for their HA, supported by the presence of spherocytes, splenomegaly, and + Coombs test (2,3).  The production of anti-erythrocyte antibodies, modification of antigenicity of erythrocyte antigens, or unmasking of antigens in IE may play a role (1,3). Additional evidence in support of an immune-mediated mechanism of HA in IE has been provided by an experimental study demonstrating significantly shorter RBC half-life in rabbits with intact spleen compared to that of splenectomized animals (4).

 

References

1. Toom S, Xu Y. Hemolytic anemia due to native valve subacute endocarditis with Actinomyces israellii infection. Clin Case Rep 2018;6: 376-79. https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccr3.1333 

2. Hsu CM, Lee PI, Chen JM, et al. Fatal Fusarium endocarditis complicated by hemolytic anemia and thrombocytopenia in an infant. Pediatr Infect Dis 1994;13:1146-48. https://www.ncbi.nlm.nih.gov/pubmed/7892087 

3. Huang HL, Lin FC, Hung KC, et al. Hemolytic anemia in native valve infective endocarditis. Jpn Circ J 1999;63:400-403. https://www.ncbi.nlm.nih.gov/pubmed/10943622 

4. Joyce RA, Sand MA. Mechanism of anaemia in experimental bacterial endocarditis. Scand J Haematol 1975;15:306-11. https://www.ncbi.nlm.nih.gov/pubmed/1198067 

 

Contributed by Scott Goodwin, Medical Student, Harvard Medical School, Boston, MA. 

 

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Can native valve infective endocarditis be associated with hemolytic anemia?

Should I order a blood transfusion based on the hemoglobin (Hgb) or the hematocrit (Hct)?

Despite the frequent interchangeability of Hgb (g/dL) and Hct (%) by a ratio of ~1:3, directly-measured blood Hgb levels may be preferred for assessing the need for blood transfusion for at least 3 reasons:

First, in contrast to the widely-used automated measurements of Hct, Hgb is not affected by conditions that affect the size of the RBCs or the mean corpuscular Hgb concentration (MCHC). This is because the Hct is not a direct measure of Hgb; rather it’s the proportion of blood occupied by RBCs which, in automated systems, is derived by multiplying the number of RBCs by the mean corpuscular volume (MCV).1-3

This may not be a significant issue when MCHC is normal, but when MCHC is abnormal, HCT may not accurately reflect the blood Hgb concentration. For example, in patients with hypochromic iron deficiency anemia with RBCs containing less hemoglobin (ie, low MCHC), the Hct may overestimate blood Hgb levels. Conversely in hereditary spherocytosis with its attendant low RBC volume and high MCHC, the Hct may underestimate Hgb levels.

Second, Hct results may also be more subject to technical factors in the lab. For example, blood at room temperature between 6-24 h may be associated with RBC swelling and increased Hct without any change in its Hgb concentration.4

Finally, national and international guidelines on blood transfusion generally target Hgb, not Hct results.5-7

For a related pearl, go to https://pearls4peers.com/2016/11/01/should-i-use-a-hemoglobin-level-of-7-or-8-gdl-as-a-threshold-for-blood-transfusion-in-my-hospitalized-patient.

 

References

  1. Tefferi A, Hanson CA, Inwards DJ. How to interpret and pursue an abnormal complete blood cell count in adults. Mayo Clin Proc 2005;80:923-36. https://www.ncbi.nlm.nih.gov/pubmed/16007898
  2. Macdougall IC, Ritz E. The Normal Haematocrit Trial in dialysis patients with cardiac disease: are we any the less confused about target hemoglobin? Nephrol Dial Transplant 1998;13:3030-33. https://academic.oup.com/ndt/article-pdf/13/12/3030/9907456/3030.pdf
  3. Kelleher BP, Wall C, O’Broin SD. Haemoglobin, not haematocrit, should be the preferred parameter. Nephrol Dial Transplant 2001;16:1085-87. https://www.ncbi.nlm.nih.gov/pubmed/11328933
  4. Hayuanta HH. Can hemoglobin-hematocrit relationship be used to assess hydration status? CDK-237/vol 43 no.2, th. 2016 http://www.kalbemed.com/Portals/6/20_237Opini-Can%20Hemoglobin-Hematocrit%20Relationship%20Be%20Used%20to%20Assess%20Hydration%20Status.pdf
  5. Blood transfusion. NICE guideline, November, 2015. https://www.nice.org.uk/guidance/ng24/chapter/Recommendations#fresh-frozen-plasma-2 uk
  6. National Blood Authority: Australia. Patient blood management, November 2016. https://www.blood.gov.au/system/files/documents/nba-patient-blood-management-resource-guide-nov_2016_v3_sm_web_file.pdf
  7. Carson JL, Guyatt G, Heddle NM, et al. Clinical practice guidelines from the AAABB: red blood cell transfusion thresholds and storage. JAMA 2016; 316:2025-2035. https://www.ncbi.nlm.nih.gov/pubmed/27732721

 

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Should I order a blood transfusion based on the hemoglobin (Hgb) or the hematocrit (Hct)?

Can my patient develop “anemia of chronic disease” acutely while hospitalized?

“Anemia of chronic disease” is better termed anemia of inflammation (AI) which may occur in acute as well as chronic inflammatory states. 1 As such, the view that anemia in the critically ill patients is simply caused by excess phlebotomy is inaccurate. 2 The CRIT study demonstrated that AI in critically ill patients develops even within 30 days, often despite blood transfusions. 3

In addition to the usual causes of AI (eg autoimmune disorders), AI can occur during bacterial, viral or yeast infections and sepsis 4,5.

Recent studies implicate both iron sequestration and impaired erythropoiesis as causes of AI. 1 Inflammation stimulates hepatic production of iron-regulatory peptide, hepcidin, which decreases delivery of iron from macrophages to developing erythrocytes.  Inflammation also causes production of pro-inflammatory cytokine, IL-6, which suppresses erythropoiesis.

Couple of cool studies using injection of heat-killed Brucella abortus in mice as a model of AI, showed dramatic hemoglobin drop by 7 days.6,7. In addition, not only were iron restriction from increase in hepcidin and transient erythropoiesis demonstrated, erythrocyte lifespan was also shortened in these experiments. AI is truly a multifactorial process.

 

References 

  1. Frankel PG. Anemia of inflammation: A review. Med Clin N Ame 2017;101:285-96. https://www.ncbi.nlm.nih.gov/pubmed/28189171
  2. Corwin HL, Krantz SB. Anemia of the critically ill: “Acute” anemia of chronic disease. Crit Care Med 2000;28:3098-99. https://www.ncbi.nlm.nih.gov/pubmed/10966311
  3. Corwin HL, Gettinger A, Pearl RG, et al. The CRIT study: anemia and blood transfusion in the critically ill-current clinical practice in the United states. Crit Care Med 2004;32:39-52. https://www.ncbi.nlm.nih.gov/pubmed/14707558
  4. Gabriel A, Kozek S, Chiari A, et al. High-dose recombinant human erythropoietin stimulates reticulocyte production in patients with multiple organ dysfunction syndrome. J Trauma:Injury, Infection, and Critical Care 1998;44:361-67. https://www.ncbi.nlm.nih.gov/pubmed/9498512
  5. Roy CN. Anemia of inflammation. Hematology Am Soc Hematol Educ Program. 2010;2010:276-80. doi: 10.1182/asheducation-2010.1.276. https://www.ncbi.nlm.nih.gov/pubmed/21239806
  6. Kim A, Fung E, Parikh SG, et al. A mouse model of anemia of inflammation: complex pathogenesis with partial dependence on hepcidin. Blood 2014;123:1129-36. https://www.ncbi.nlm.nih.gov/pubmed/24357728
  7. Gardenghi S, Renaud TM, Meloni A, et al. Distinct roles for hepcidin and interleukin-6 in the recovery from anemia in mice injected with heat-killed Brucella abortus. Blood 2014;123:1137-45. https://www.ncbi.nlm.nih.gov/pubmed/24357729
Can my patient develop “anemia of chronic disease” acutely while hospitalized?

My 35 year old patient with Crohn’s disease has peripheral neuropathy but no anemia or macrocytosis. Could he still have vitamin B-12 deficiency?

Absolutely! A significant number of patients with B-12 deficiency are neither anemic nor have macrocytosis but may still have related neurological symptoms.

A large study involving a nationally representative sample of older U.S. adults (aged >50 y) sponsored by the CDC reported a prevalence of B-12 deficiency without anemia or without macrocytosis of about 4% each . 1 Interestingly, in this study,  there was no evidence that mandatory folic acid fortification of certain foods was associated with lower prevalence of B-12 deficiency without anemia or macrocytosis.

In another study, the proportion of subjects with low serum B-12 but without macrocytosis was 70% or higher, irrespective of pre- or post-fortification period.2 Interestingly, in the age group <65 y, the post-fortification was associated with significantly higher proportion of patients without macrocytosis (85% vs. 45% in the prefortification period) in this study.

Younger age groups seem to also be overrepresented among patients with B-12 deficiency but no anemia, with a prevalence of 50% in <60 y age group with B-12 deficiency compared to 38% and 31% among older age groups (60-74 y and >74 y, respectively).3

So, keep B-12 deficiency in mind in the presence of compatible neurological symptoms even in the absence anemia or macrocytosis!

 

References

  1. Qi YP, Do AN, Hamner HC, et al. The prevalence of low serum vitamin B-12 status in the absence of anemia or macrocytosis did not increase among older U.S. adults after mandatory folic acid fortification. J Nutr 2014;144:170-76. http://jn.nutrition.org/content/144/2/170.abstract
  2. Wyckoff KF, Ganji V. Proportion of individuals with low serum vitamin B-12 concentrations without macrocytosis is higher in the post-folic acid fortification period than in the pre-folic acid fortification period. Am J Clin Nutr 2007;86:1187-92. https://www.ncbi.nlm.nih.gov/pubmed/17921401
  3. Mills JL, Von Kohorn I, Conley MR, et al. Low vitamin B-12 concentrations in patients without anemia: the effect of folic acid fortification of grain. Am J Clin Nutr 2003;77:1474-7. http://ajcn.nutrition.org/content/77/6/1474.full.pdf+html
My 35 year old patient with Crohn’s disease has peripheral neuropathy but no anemia or macrocytosis. Could he still have vitamin B-12 deficiency?

What is the connection between methemoglobinemia and hemolytic anemia?

Methemoglobinemia coupled with hemolytic anemia (HA) has been reported under different clinical scenarios and may have therapeutic implications for treatment of methemoglobinemia in the setting of G6PD deficiency.

Increased methemoglobin levels have been observed during the hemolytic crisis of patients with favism due to G6PD deficiency. This finding has been attributed to excessive oxidative stress generated by divicine, an oxidizing constituent of fava beans, and the inability to reduce its stress because of an insufficient G6PD-dependent hexose monophosphate shunt. 1Hemolytic anemia may also follow drug-induced methemoglobinemia, especially with exposure to dapsone, sulfasalazine, or phenacetin, and may be a feature of hemoglobin MSaskatoon and MHyde Park , abnormal hemoglobin variants associated with genetic methemoglobinemia. 2The concurrence of hemolysis due to G6PD deficiency and methemoglobinemia is not just an academic curiosity and may in fact pose a therapeutic quandary. This is because methylene blue, the treatment of choice for methemoglobinemia, is also an oxidant and works only after it is reduced to leukomethylene blue by (you guessed it!) nicotinamide adenine nucleotide phosphate (NADPH), a G6PD-dependent process. 2,3 With plenty of methylene blue on hand and little leukomethylene around in G6PD-deficiency, treatment may be ineffective or even cause worsening of methemoglobinemia. It’s never simple!

Final fun fact: Did you know that methylene blue is the first synthetic drug (>100 years ago) and has been used in the prevention of UTIs in the elderly, and treatment of pediatric malaria and Alzheimer’s disease? 4References

  1. Schuurman M, van Waardenburg D, Da Costa J, et al. Severe hemolysis and methemoglobinemia following fava beans ingestion in glucose-6-phosphate dehydrogenase: Case report and literature review. Eur J Ped 2009;168:779-782. https://link.springer.com/article/10.1007/s00431-009-0952-x
  2. Rehman HU. Methemoglobinemia. West J Med 2001;175:193-96. https://www.researchgate.net/publication/11817876_Methemoglobinemia
  3. Hassan KS, Al-Riyami AZ, Al-Huneini M, et al. Methemoglobinemia in an elderly patient with glucose-6-phosphate dehydrogenase deficiency: A case report. Oman Med J 2014;29:135-37. https://squ.pure.elsevier.com/en/publications/methemoglobinemia-in-an-elderly-patient-with-glucose-6-phosphate-
  4. Schirmer RH, Adler H, Pickhardt M, et al. “Lest we forget you—Methylene blue…” Neurobiology of Aging 2011; 32:2325. https://www.ncbi.nlm.nih.gov/pubmed/21316815
What is the connection between methemoglobinemia and hemolytic anemia?

What could be causing low serum haptoglobin in my patient with no evidence of hemolysis?

 

There are many causes of low serum haptoglobin besides hemolysis, including1-4:

  • Cirrhosis of the liver
  • Disseminated ovarian carcinomatosis
  • Pulmonary sarcoidosis
  • Elevated estrogen states
  • Repetitive physical exercise
  • Hemodilution
  • Blood transfusions
  • Drugs (eg, oral contraceptives, chlorpromazine, indomethacin, isoniazid, nitrofurantoin, quinidine, and streptomycin)
  • Iron deficiency anemia
  • Megaloblastic anemia (by destruction of megaloblastic RBC precursors in the bone marrow)
  • Congenital causes

Less well-known is that congenital haptoglobin deficiency (“anhaptoglobinemia”) may not be so rare in the general population at a prevalence of 1% among whites and 4% among African-Americans (>30% in blacks of West African origin)3. Measurement of serum hemopexin, another plasma protein that binds heme, may help distinguish between this condition and acquired hypohaptoglobinemia— in the absence of hemolysis, hemopexin levels should remain unchanged3,5.

Final Fun Fact: Did you know that serum haptoglobin is often low during the first 6 months of life?

References

  1. Shih AWY, McFarane A, Verhovsek M. Haptoglobin testing in hemolysis: measurement and interpretation. Am J Hematol 2014;89: 443-47. https://www.ncbi.nlm.nih.gov/pubmed/24809098
  2. Sritharan V, Bharadwaj VP, Venkatesan K, et al. Dapsone induced hypohaptoglobinemia in lepromatous leprosy patients. Internat J Leprosy 1981;307-310. https://www.ncbi.nlm.nih.gov/pubmed/7198620
  3. Delanghe J, Langlois M, De Buyzere M, et al. Congenital anhaptoglobinemia versus acquired hypohaptoglobinemia. Blood 1998;9: 3524. http://www.bloodjournal.org/content/bloodjournal/91/9/3524.full.pdf
  4. Haptoglobin blood test. https://medlineplus.gov/ency/article/003634.htm. Accessed August 6, 2017.
  5. Smith A, McCulloh RJ. Hemopexin and haptoglobin: allies against heme toxicity from hemoglobin not contenders. Front. Physiol 2015;6:187. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4485156/pdf/fphys-06-00187.pdf

 

In collaboration with Kris Olson, MD, MPH, Mass General Hospital, Boston, MA

What could be causing low serum haptoglobin in my patient with no evidence of hemolysis?

My middle age patient complains of night sweats for several months, but she has had no weight loss and does not appear ill. What could I be missing?

Night sweats (NS) is a common patient complaint, affecting about a third of hospitalized patients on medical wards1.  Despite its long list of potential causes, direct relationship between the often- cited conditions and NS is usually unclear2, its cause may remain elusive In about a third to half of cases in the primary care setting, and its prognosis, at least in those >65 y of age, does not appear to be unfavorable 2,3.

Selected commonly and less frequently cited conditions associated with NS are listed (Table)2-9.  Although tuberculosis is one of the first conditions we think of when faced with a patient with NS, it should be emphasized that NS is not common in this disease (unless advanced) and is rare among hospitalized patients as a cause of their NS1,9.

In one of the larger study of adult patients seen in primary care setting, 23% reported pure NS and an additional 18% reported night and day sweats5; the prevalence of NS in both men and women was highest in 41-55 y age group. In multivariate analyses, factors associated with pure NS in women were hot flashes and panic attacks; in men, sleep disorders. 

Table. Selected causes of night sweats

Commonly cited Less frequently cited
Neoplastic/hematologic (eg, lymphoma, leukemia, myelofibrosis)

Infections (eg, HIV, tuberculosis, endocarditis)

Endocrine (eg, ovarian failure, hyperthyroidism, orchiectomy, carcinoid tumor, diabetes mellitus [nocturnal hypoglycemia], pheochromocytoma)

Rheumatologic (eg, giant cell arteritis)

Gastroesophageal reflux disease

B-12 deficiency

Pulmonary embolism

Drugs (eg, anti-depressants, SSRIs, donepezil [Aricept], tacatuzumab)

Sleep disturbances (eg, obstructive sleep apnea)

Panic attacks/anxiety disorder

Obesity

Hemachromatosis

Diabetes insipidus

References

  1. Lea MJ, Aber RC, Descriptive epidemiology of night sweats upon admission to a university hospital. South Med J 1985;78:1065-67.
  2. Mold JW, Holtzclaw BJ, McCarthy L. Night sweats: A systematic review of the literature. J Am Board Fam Med 2012; 25-878-893.
  3. Mold JW, Lawler F. The prognostic implications of night sweats in two cohorts of older patients. J Am Board Fam Med 2010;23:97-103.
  4. Mold JW, Holtzclaw BJ. Selective serotonin reuptake inhibitors and night sweats in a primary care population. Drugs-Real World Outcomes 2015;2:29-33.
  5. Mold JW, Mathew MK, Belgore S, et al. Prevalence of night sweats in primary care patients: An OKPRN and TAFP-Net collaborative study. J Fam Pract 2002; 31:452-56.
  6. Feher A, Muhsin SA, Maw AM. Night sweats as a prominent symptom of a patient presenting with pulmonary embolism. Case reports in Pulmonology 2015. http://dx.doi.org/10.1155/2015/841272
  7. Rehman HU. Vitamin B12 deficiency causing night sweats. Scottish Med J 2014;59:e8-11.
  8. Murday HK, Rusli FD, Blandy C, et al. Night sweats: it may be hemochromatosis. Climacteric 2016;19:406-8.
  9. Fred HL. Night sweats. Hosp Pract 1993 (Aug 15):88.
My middle age patient complains of night sweats for several months, but she has had no weight loss and does not appear ill. What could I be missing?

What is the significance of smudge cells on peripheral blood smear?

Smudge cells (SCs)  also known as “basket cells”, are remnants of B lymphocytes ruptured during slide preparation (photo below). Although at low numbers (~0-5% of lymphocytes), SCs may be observed in healthy individuals, when found at higher numbers (>10%)they are associated with chronic lymphocytic leukemia (CLL) and other lymphoproliferative diseases1; the percentage of SCs may not discriminate between these malignancies, however2.

For nearly a century, SCs were thought to be just an artifact of slide preparation resulting from the fragility of CLL cells3. Although the mechanism accounting for the appearance of SCs is still unclear, their formation is inversely correlated with B cell content of vimentin, a cytoskeletal protein essential for rigidity and integrity of lymphocytes 3-5. High vimentin expression is associated with an aggressive variant of CLL and shorter survival times3-5. Therefore, higher number of SCs at the time of CLL diagnosis (>20% or >30%) may actually indicate a better prognosis4-6!

smudgecellsarrow

Photo courtesy of U.S. National Library of Medicine

References

  1. Petrakis NL, Lieberman E, Fullerton J. The dead leukocyte content of the blood in normal and leukemic patients. Blood. 1957 Apr;12:367-72.
  2. Matos DM, Perini G, Kruzich C, Rego EM, Falcao RP. Smudge cells in peripheral blood smears did not differentiate chronic lymphocytic leukemia from other B-cell chronic lymphoprolipherative diseases. Rev Bras Hematol Hemoter. 2009;31:333–6.
  3. Nowakowski GS1, Hoyer JD, Shanafelt TD, et al. Percentage of smudge cells on routine blood smear predicts survival in chronic lymphocytic leukemia. J Clin Oncol. 2009;27:1844-9.
  4. Nowakowski GS, Hoyer JD, Shanafelt TD, et al. Using smudge cells on routine blood smears to predict clinical outcome in chronic lymphocytic leukemia: a universally available prognostic test. Mayo Clin Proc. 2007;82:449-53.
  5. Johansson P, Eisele L, Klein-Hitpass L, et al. Percentage of smudge cells determined on routine blood smears is a novel prognostic factor in chronic lymphocytic leukemia. Leuk Res. 2010;34:892-8.
  6. Gogia A, Raina V, Gupta R, et al. Prognostic and predictive significance of smudge cell percentage on routine blood smear in chronic lymphocytic leukemia. Clin Lymphoma Myeloma Leuk. 2014;14(6):514-7.

 

 

Contributed by Khin-Kyemon Aung, medical student, Harvard Medical School, Boston.

 

 

 

 

 

 

 

 

 

What is the significance of smudge cells on peripheral blood smear?

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

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.

 

References

  • 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.
  • 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.
  • Hummel MC, Morse BC, Hayes LE. Reactive thrombocytosis associated with enoxaparin. Pharmacotherapy 2006;26:1667-1670.
Why has my hospitalized patient with head and neck cancer developed thrombocytosis few days following surgery?