Hemoglobinuria After Fraternity Hazing

Hemoglobinuria After Fraternity Hazing Barbara A. Baker, M.D., Kenneth A. Schwartz, M.D., Douglas J. Segan, M.D., and Gilbert H. Mayor, M.D. We describe a 19-year-old male who presented with traumatic hemoglobinuria . We hypothesize that this patient has a genetic haptoglobin variant with a low hemoglobin binding capacity which resulted in hemoglobinuria after physical fraternit y hazing. A

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EMOGLOBINURIA in soldiers after marching was initially described by Fleischer in 1881. 1 The acute red cell destruction leading to hemoglobinuria appears related to repeated trauma, thus the designation traumatic hemoglobinuria has supplanted the initial term , march hemoglobinuria. Hemoglobinuria has also been associated with other trauma to the feet after either running2 or playing basketba1l 3 in thin soled shoes, or with trauma to the hands after conga drum playing3-7 or karate exercise. 8 Similarly hemoglobinuria has been associated with child abuse , 9 closed cardiac massage,10 and in a psychotic patient with selfinflicted trauma to his forehead and thigh. 11 We describe hemoglobinuria in a college student subjected to severe paddling and other trauma while participating in fraternity " hazing" and suggest that the hemoglobinuria is related both to the trauma and a genetic haptoglobin variant with decreased hemoglobin binding capacity leading to hemoglobinuria after destruction of a relatively small number of red cells. CASE REPORT A 19-year-old muscular black male was admitted with complaints of dark colored urine and abdominal pain of 12 hr duration . While pledging a fraternity , he sustained trauma to his chest and back as well as multiple swats to his buttocks with the fraternity paddle . Personal or family history of hematologic or renal disease was denied . The patient was afebrile with diffu se muscle swelling and tenderness most prominent over the right latissimus dorsi , anterior chest, both gluteus maximi , the abdominal muscles and the muscles of the anterior and lateral thighs . Slight ecchymosis was observed in the coccyalgeal area.

From the Nephrology Division, Department of Medicine, Michigan State Universiry , East L anSing. Mich. Reprint requests should be addressed t o Gilbert H. Mayor, M .D ., B-220 Life Sciences Building, Department of Medicin e, Michigan Stare Universiry. East L ansing, Mich . © 1982 by The National Kidney Foundation, Inc. 0272-6386/82/020268-03$01 .00/0

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review of the literature regarding traumatic hemoglobinuria supports the association between decreased baseline plasma haptoglobin levels and hemoglobinuria after trauma .

Laboratory investigation revealed a muddy brown urine with a large amount of hemoglobin and 2- 3 red cells per high-power field. Urine electrophoresis confirmed a large amount of hemoglobin but no myoglobin . The hematocrit wa s 38.4% , the urea nitrogen 14 mg/ IOO ml, creatinine 1.6 mg/ IOO ml, and the potassium 4.0 mmol/liter. Plasma hemoglobin was greater than 38 mg/ IOO ml plasma haptoglobin was less than 25 mg/IOO ml. Initial serum enzyme studies showed an elevated creatine phosphokin ase of 2230 IU/ liter, lactic dehydrogenase of 1125 IUlliter and aldolase 13 lLu/milliler (normal up to 6). Total bilirubin was 4.8 mg/ IOO ml with an indirect fraction of 4.5 mg/ IOO ml. Serum for myoglobin and urine for porphyrin and porphobilinogen were negative. No schistocytes or fragmented red cells were seen on peripheral blood smear. The prothrombin time , partial thromboplastin time, platelet count, sickle cell screen, Hams acid hemolysis, and total serum proteins were all normal. The patient's urine became progressively less discolored and creatine phosphokinase, lactic dehydrogenase and bilirubin values returned toward normal. He was discharged and instructed to avoid further physical hazing. Five months later the patient reported no further episodes of hemoglobinuria, however, the plasma haptoglobin remained less than 25 mg/ IOO ml.

DISCUSSION

We hypothesize that our patient has a genetic haptoglobin variant with a low hemoglobin binding capacity which resulted in hemoglobinuria after physical fraternity hazing. Hemoglobinemia may be common after trauma such as running but hemoglobinuria is not. Gilligan et al. found hemoglobinemia in 18 of 22 marathon runners , but hemoglobinuria in just four. 12 Genetic haptoglobin variants with decreased hemoglobin binding capacity occur with increased frequency in black people . 14 In this patient the serum haptoglobin of less than 25 mg/ 100 ml observed 5 mo after the traumatic episode, suggests a haptoglobin variant with decreased binding capacity. A literature survey reveals 17 of 19 traumatic hemoglobinuria patients had decreased baseline plasma haptoglobin levels after they had recovered from their traumatic episodes (Table 1) . Thus patients with either congenital

American Journal of Kidney Diseases, Vol. II, No. 2, September 1982

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HAZING HEMOGLOBINURIA Table 1. Low Baseline Haptoglobin Levels in 17/19 Patients with Traumatic Hemoglobinuria

Precipitating Event Conga Drum and Basketball Running Conga Drum Conga Drum Conga Drum Conga Drum Karate Cardiac massage Child Abuse Running Running Running Running Conga Drum Running Walking Running Running Fraternity Hazing

AgelSex

201M 27/F 201M 311M 321M 29!? 261M 781M 21f2IM 181M 211M 181M 18(M 311M 201M 54/M 161M 191M

Acute Episode Haptoglobin mgliOO ml

H 38 20 33 91 103 <20 260 100 20-30 70-80 0 19 23 25 5 0 Normal <25

Steady State Haptoglobin mgliOO mi'

75 46 59 42 181 79 120 N.D. N.D. 20-30 70-80 20 28 31 60 80 81 37 <25

Reference

Schwartz' Spicer' Furie5 Caro7 Caro7 Caro 7 Streeton'

Narasimhan 10 Rimer9 Davidson 16 Davidson 16 Payne 13 Banga18 Mehbod 19 Buckle'· Flatmark21 Chaplin22 Pollard" Baker

'N.D. = not done.

variants of haptoglobin and low hemoglobin binding activity or with repeated bouts of hemolysis and low haptoglobin levels have increased susceptibility to hemoglobinuria with trauma. Red cell survival measurements, using (51) Cr, have revealed accelerated destruction of red cells during the traumatic episode. 15 The hemolysis is attributed to mechanical forces transmitted to the red cells as they traverse the capillaries of the "traumatized" tissue. 1 Atraumatic exercise like swimming or bicycling is not associated with

hemoglobinuria. Decreasing trauma by altering running style, running on grass instead of pavement, or using padded running shoes to lessen the impact of the foot striking the ground can decrease or alleviate hemoglobinuria in runners. 16 Intrinsic red cell abnormalities resulting in an increased propensity to lyse after trauma have also been proposed. It has been suggested by Blum et al. that paroxysoral nocturnal hemoglobinuria (PNH) may masquerade as traumatic hemoglobinuria. 17 These authors report intravascular hemolysis in two patients with PNH after forearm exercise and a resultant acidosis. The negative Hams test in this patient militates against a diagnosis of PNH. A report by Banga et al. described abnormalities in the low molecular weight protein bands of red blood cell ghosts of three patients with traumatic hemoglobinuria. 18 The pattern described was different from that seen with hereditary spherocytosis or elliptocytosis. The pathophysiologic relationship of a protein membrane abnormality is not clear. Davidson demonstrated that red blood cells from runners with traumatic hemoglobinuria are no more prone to lysis than normal red cells when subjected to similar traumatic stresses. 16 Although it is remotely possible that an intrinsic red cell abnormality was present in this patient we think it is more likely that his congenitally low haptoglobin binding capacity resulted in hemoglobinuria after traumatic lysis induced by the fraternity paddle of a relatively small number of red cells trans versing the capillaries of his glutii.

REFERENCES 1. Fleischer R: Ueber eine neue form von haemoglobinurie biem menchen. Berl Klin Wschr 18:691-694, 1881 2. Spicer AJ: Studies on march haemoglobinuria. Br Med J 1:155-156, 1970 3. Schwartz KA, Flessa HC: March hemoglobinuria: report of a case after basketball and congo drum playing. Ohio State Med J 69:448-449. 1973 4. Kaden WS: Traumatic haemoglobinuria in conga drum players. Lancet 1:341-342. 1970 5. Furie B, Penn AS: Pigmenturia from conga drumming: hemoglobinuria and myoglobinuria. Ann Intern Med 80:727729, 1974 6. Fenichel RR: Conga drumming and pigmenturia (letter). Ann Intern Med 81:570, 1974 7. Caro XJ, Sutherland PW, Mitchell DB, et al: Traumatic hemoglobinuria associated with conga drumming. West J Med 123:141-144, 1975 8. Streeton JA, Melb MB: Traumatic haemoglobinuria caused by karate exercises. Lancet 2:191-192, 1967

9. Rimer RL, Shane R: Child abuse and hemoglobinuria. JAMA 238:2034-2035, 1977 10. Narasimhan P, Sabetghadam R: Hemoglobinuria following closed cardiac massage. JAMA 228:1520, 1974 11. Ensor CW, Barrat JOW: Paroxysmal haemoglobinuria of traumatic origin. Med-Chir Trans 86:165-195, 1903 12. Gilligan DR, Altschule MD, Katersky EM: Physiological intravascular hemolysis of exercise: hemoglobinemia and hemoglobinuria following cross-country runs. J Clin Invest 22:859-869, 1943 13. Payne RB: Low plasma haptoglobin in march haemoglobinuria. J Clin Pathol 19: 170~ 172, 1966 14. Giblett ER: Haptoglobin types in American negroes. Nature 183:192-193, 1959 15. Joshua H, De Vries A: Effect of exercise on red blood cell in march haemoglobinuria. Am J Clin PathoI46:341-344, 1966 16. Davidson RJL: Exertional haemoglobinuria: a report on

270 three cases with studies on the haemolytic mechanism. J Clin Pathol 17:536-540, 1%4 17. Blum SF, Sullivan 1M, Gardner FH: The exacerbation of hemolysis in paroxysmal nocturnal hemoglobinuria by strenuous exercise. Blood 30:513-517, 1969 18. Banga JP, Pinder lC, Gratzer WB , et al: An erythrocyte membrane-protein anomaly in march haemoglobinuria. Lancet 2:1048-1049, 1979 19. Mehbod H: Bongo drum hematuria. Ohio State Med 1 70:169-171 , 1974

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20. Buckle RM: Exertional (March) haemoglobinuria. Lancet 1:1136-1138,1%5 21. Flatmark T: Studies on the hemolytic mechanism in March hemoglobinuria. Acta Med Scand 173:307-313, 1%3 22. Chaplin H, Perkoff GT, Frisbie JH, et al: March hemoglobinuria associated with asymptomatic congenital heart disease. JAMA 208: 1700-1702, 1969 23. Pollard TD, Weiss IW: Acute tubular necrosis in a patient with march hemoglobinuria. N Engl J Med 283: 803-804, 1970