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Perirenal Hematoma Primary with Polycythemia1
PERIRENAL HEMATOMA PRIMARY WITH POLYCYTHEMIA 1 DAVID W. MAcKENZIE From the Department of Urology, Royal Victoria Hospital, Montreal
The case which we wish to bring to your attention ls one of spontaneous perirenal hemorrhage, occurring in a male suffering from polycythemia. So far we have been unable to find a similar case reported in the literature. Spontaneous or non-traumatic perirenal hematoma itself has been described by Rayer as far back as 1839, and also by Willis in 1841. Since then many writers, among them Doll, Richer, Laewen, Baggard, Koch, Greco, Schloss, Eigler, Chauvent, J\Iyeres and Singer have reported similar cases. Caenan has given us a classification of these hematomata, dividing them mainly into t,, o grours. 1. Primary non-traumatic or essential type. 2. Secondary type or those due to known causes, such as tuberculosis, tumor, aneurysm or perinephritic abscess.
It is in the first group into which our case falls, and with which we are mainly interested. Richer ha.s suggested that the lesion occurs by means of diapedesis due to a pathological lesion of the vasomotor system. Baggard believes that alterations in compression as found in hydronephrosis may be the cause, while others think that a degenerative inflammation of the veins is the etiological factor. While some 66 cases such as these have been reported, not one has occurred jn a patient suffering from polycythemia. Four have occurred in patients who were hemophilics as reported by Caenan, Laewen, Bollag and Saint Cene. The question naturally arises was the polycythemia the cause or the result of the perirenal hemorrhage. 1 Read at the annual meeting of the American Association of Genito-urinary Surgeons, Manchester, Vermont, June 13, 1929. 535
536
DAVID W. MACKENZIE
The resume of the case report is as follows : J. D., male, thirty-five years of age, admitted to the Urological Service of the Royal Victoria Hospital at 1 p.m., December 18, 1928. Complaints on admission were: (1) Severe sharp pain in the left loin and left upper quadrant; (2) mass in the left loin. (3) nausea and vomiting. Present illness. Twenty-four hours previously, when in good health, the patient felt while chopping wood a sudden sharp cramp-like pain in the left loin, this remained localized and was soon followed by nausea and vomiting. Several hours before admission to hospital, which was the following day, he noticed a gradual swelling in the left flank. On admission, he appeared acutely ill, though the color of his skin and mucous membranes was good. His pulse was 108, respirations 25 and the temperature was 98.2°. The general physical examination apart from the genito-urinary system was normal. The blood pressure at this time was 140/100. The abdomen was asymmetrical, due to a uniform fullness in the left flank extending from the costal margin to the iliac crest on that side. The overlying rectus muscle was rigid and the mass gave a dull note on percussion. It was only slightly tender to palpation. There was no costo-lumbar tenderness on the right side, and the lower pole of that kidney was just palpable. Urinalysis at this time of catheterized specimen showed the urine to be, clear amber, acid, 1.035, albumin++, sugar none, with microscopically, an occasional red blood cell and white blood cell, and some scattered epithelium. The leucocytosis was 20,600. Cystoscopy. Shortly after admission showed a normal bladder. The ureters were easily catheterized and normal urine obtained from each side. A pyelogram on the left side showed a large irregular renal pelvis, displaced downwards and laterally, as if compressed from without (fig. 1). The patient was observed for four hours during which time the blood pressure rose from 140/100 on admission to 155/115, and the pulse rate increased from 108 to 160. The mass in the loin became larger and firmer, while the patient's general condition grew rapidly worse. The color of the skin all the while was good, though his general condition, the rising pulse and the rapidly enlarging tumor indicated a retroperitoneal hemorrhage. The high blood pressure was a feature we could
PERIRENAL HEMATOMA
537
not explain, and several conditions were mentioned such as tumor of the adrenal, or stimulation of the adrenal gland due to the increased retroperitoneal pressure.
FIG.
1.
PYELOGRAM OF LEFT RENAL PELVIS SHOWING DOWNWARD DISPLACEMENT FROM EXTERNAL COMPRESSION
Four and a half hours after admission an operation was performed: Through a curved left loin incision, the muscles were incised and underneath was found a tense shining black cystic mass which was very
538
DAYID W, MACKENZIE
large and firm, filling the entire loin and left flank. The peritoneum was pushed forward by the mass, which was freed as quickly as possible and delivered. At this time it ruptured as the wall was very thin, and a very large quantity, roughly a quart of old blood clot escaped. At this point the blood pressure fell to 68 systolic. Hoping to be able to find the source of the hemorrhage, we isolated the renal pedicle, beyond the fatty capsule, which we clamped, then removed the mass as a whole. The pedicle was then tied with three strong ligatures and the clamps removed. A small hole in the peritoneum was sutured. The peritoneal cavity did not appear to contain any blood. The surrounding tissues were engorged and dark in color but there were no bleeding points apparent and the cavity in the loin appeared to be quite dry. The wound was closed as quickly as possible with a large cigarette drain leading down to the bottom of the cavity. Grossly the wall of this mass seemed to be formed by thinned-out perirenal capsule, and the extravasated blood was held between this and the kidney itself. The kidney was split but appeared perfectly normal. The pathological report is as follows: A rather large kidney 13 by 6 cm. with its enclosing perirenal fatty capsule. Both this capsule and the kidney have been opened. The perirenal fatty capsule is enormously thickened and infiltrated with clotted blood forming a diffuse hematoma throughout this capsule. Renal capsule proper is intact and strips with difficulty exposing a smooth cortex which is mottled with pin-point yellowish spots. Cortex is 7 mm. thick and well differentiated from medulla. Pelvis is free. On dissecting out ureter and blood vessels at the hilus the tissue between these vessels was infiltrated with clotted blood, but though the vessels were dissected as far as possible into renal substance, no rupture or point of hemorrhage could be demonstrated. Several sections through hilus were taken, including all blood vessels. Microscopic examination. Sections taken across vessels at hilus show extensive hemorrhagic extravasation throughout surrounding tissue. The arteries appear thickened with some degeneration in the media. There is nothing however to explain positively the hemorrhagic extravasation. The glomeruli of the kidney appear for the most part hemorrhagic and there is a certain amount of degenerative change in the epithelium of the tubules which may be due to lack of immediate fixation. Anatomical summary. Perirenal hematoma. Special laboratory findings were: Blood Wassermann negative.
PERIRENAL HEMATOMA
Fundi were normal. Blood urea, 0.774 gram per liter. Blood urea nitrogen, 36.12 mgm. per 100 cc. Creatinine, 1.93 mgm. per 100 cc, A.C. blood sugar, 0.086 gram per cent. P.C. blood sugar, 0.114 gram per cent. Following operation the patient's condition rapidly improved. The blood pressure rose to 90/30, five hours after operation, and gradually
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:reached 120/60 as will be seen on the accompanying chart. The pulse reached its normal level on the third day (fig. 2). Following operation for several days the patient's skin and mucous membranes were pale; but ten days later he had quite a healthy ruddy colour and his red cell count at this time was 6,630,000 per centimeter. On questioning, the patient stated that since 1923 he had noticed a THE JOURNAL OF 'GROLOGY, VOL,
xxnr,
NO.
5
540
DAVID W. MACKENZIE
gradual enlargement of the superficial veins. His complexion had become a ruddier hue and the conjunctivae were constantly injected. Three months before his hemorrhage he had acted as donor for blood transfusion on three different occasions, and had felt much improved from the loss of blood. Following the finding of his high red cell count, a periodic check up was made, as seen in the accompanying chart (fig. 3). It will be seen that seventy days after his hemorrhage, his red cell count had risen to 7,800,000.
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The morphological examination of the blood ten days after operation was as follows: Red blood cells, 6,500,000. White blood cells, 13,000. Hemoglobin; 98 per cent (13.7 gram/100 cc. Color index, 0.75. Red blood cells: Stain rather poorly. Moderate anisocytosis. Slight poikilocytosis and polychromatophilia. No punctuate basophilia or nucleated reds. Reticulated reds, 1 per cent. Fragility: normal. Corpuscle volume: 52 per cent. Average corpuscle volume: 80 cubic microns. Hemoglobin concentration: 0.83. Sedimentation velocity: slow. Viscosity: increased. White blood cells (400 examined): Polys. Eosin. Mast. Mono. Lymph. 82.25 1.25 0.75 4.75 11 percent 10693 162 98 617 1430 per cmm. No pathological forms. No immature elements.
PERIRENAL HEMATOMA
541
Platelets (400,000, usual size and shape): Bleeding time: Not prolonged. Coagulation: Fibrin congealing with calcium retraction 4. 5 min. 7 min. 4 min. poor Serum: Rather pale yellow with faint greenish tinge. Van den Bergh: Direct, prompt, negative: direct, delayed, faint. Indirect,-less than 0.3 unit. Refraction-52. Low. Conclusions: The lack of immature myeloid elements and bilirubinemia suggest we are dealing with a symptomatic polyglobuli rather than a polycythemia vera. It seemed at first as if we were dealing with a case of symptomatic polyglobuli, which could be explained in the light of the severe hemorrhage which had taken place. A second morphological examination at a later date showed us to be dealing probably, with a true polycythemia. Red blood cells, 7,800,000. White blood cells, 15,000. Hemoglobin 119 per cent (16.6 grams per 100 cc.). Color index, 0.76. Red blood cells: Stain rather poorly. Slight anisocytosis and polychromatophilia. No poikilocytosis, punctate basophilia or nucleated reds. Reticulated reds: Less than 1 per cent. Fragility: Moderately increased resistance Corpuscle volume: 59 per cent. Average corpuscle volume: 76 cubic microns. Hemoglobin concentration: 0.89. Viscosity: Very high. Sedimentation velocity: Very slow. White blood cells (400 examined): Lymph. Polys. Eosin. Mast. Mono. 12 per cent. 77 3 1 7 1800 per cmm 450 1050 11550 150 Increase in myeloid elements. Platelets (370,000, usual size and shape): Bleeding time: Not prolonged. Coagulation: Fibrin congealing with calcium retraction, 4. 5 min. 3 min. 2.5 min. poor Serum: Yellow with faint greenish tinge. Refractometry: 5L Van den Bergh: Direct, prompt, negative; delayed, faint. lndirect,-less than 0.3 unit. Conclusions: There has been a definite rise in the erythrocytes and hemoglobin since the last examination, otherwise the findings are essentially the same. The persistence of the high red count speaks definitely for polycythemia vera, although there is still lacking the usual immaturity in the leucocytes.
542
DAVID W. MACKENZIE
The red cell count since this last report has fallen somewhat, but is still beyond normal limits. vVe have been unable to satisfy ourselves as to the relation of the hemorrhage to the polycythemia-which of the two conditions was the etiological factor? It is possible that the condition of polycythemia brought about a series of factors underlying the perirenal hemorrhage. It is also possible that the severe hemorrhage induced a marked reaction on the part of the red blood cell formation. Taking the cases of perirenal hemorrhage as a group regardless of whether primary or s,econdary cause, the statistics of the 66 cases reviewed, show that a correct preoperative diagnosis was only made in five of the cases, and that with immediate operation there is a 50 per cent mortality. On the other hand, those cases not operated on all died. In the majority of cases of the primary or essential group, the source of the hemorrhage, or the etiological factor underlying it, was not demonstrated. CONCLUSIONS
1. Spontaneous perirenal hemorrhage is a comparatively rare lesion. 2. It has been classified according to the source, such as primary, or of unknown etiology; and secondary, those due to some discoverable lesion. 3. The case just reported is the only one in association with the condition of polycythemia. 4. The question still persists, of the two factors, hemorrhage and polycythemia, which is the cause and which the effect? REFERENCES (1) WUNDERLICH, C. A.: Handbuch der Pathologie und Therapie, 1846, iii, 1197. (2) HERS KY, P.: Medizinische Klinik, Berlin, May 8, 1925, 700. (3) RAPIN: Les hematomes perinephretiques non traumatiques. Paris Medical, 1919, xxxiii, 31. (4) MAYER AND SINGER: Spontaneous perirenal haematoma. Jour. Surg., Gynecol. and Obstet., September, 1927, 300-306. (5) ISRAEL; Chirurgie der niere und des Harnleiters. 1925, Leipsig. (6) VoGELER: Das Nierenaneurysma. Deutsche Ztschr. Chir., 1922, 297-324.
PERIRENAL HEMATOMA
543
(7) CAENAK: Das Perirenal Haematom. Beitr. Zklin Chir., 1910, 494-538. (8) DoLL: Die Apoplexie des Nierenlagers. Muenchen Med.. Wchnschr., 1907, 2417-2420. (9) LAEWE'J, A.: vVeber das sogenannte perirenale hematom und andere spontane retroperitoneale Massenblutungen. Deutsche Zysche Chir.,, 1912, cxiii, 367-388. (10) RICKER: Uber die haemorrhagische Infarzierung des Nierenlagers und and.ere kapillare Diapedesis Blutungen grofsen Umfanges an und. in Or. ganen der Bauch Hohle. Beitr. pathol. anat. Bell., 1911. (11) LiPPEKs, A.: L'hematome perirenal spontane. Jour. de Chir., t. 1913, N. 20, p. 1. (12) MAYER, K. A.: Spontaneous perirenal haemorrhage. Jour. Amer. Med. Assoc., 1919, xxii, 1451-2. (13) ScHLoss, VV.: Weiner Klinische, W ochenschrift. Uber einen Full von Massenbluntung ins Nierenlager, October 21, 1926. (14) ErGLER: Munchener Medizinische Wochenschrift, March, 1928. Uber Retroperitoneale Massenbluntungen. (15) BAGGARD: Zur Kenntnis der Massenblutingen ins Nierenlager. Beitr. z. klin. Chir., 1914, xci, 454-474. (16) GRECO, F.: L'ematoma perirenale non traumatico. Archivio Italiano di Chirurgia, 1915, xi, 1-40. (17) BoLLAG: Ein Fall von Massenblutung in das Nierenlager bei Hemophilie. Dent. Zeitscher f. Chir., 1920, 152--155. (18) SAINT-CE NE: Un nouveau cas d'hematome perinephretique non traumatique. Jour. d.'Urologie, t. ix, 1921, 25. (19) SoHN, A.: Die Spontanen Massenblutungen ins Nierenlager. Deutsche Ztschr. f. Chir., 1921, clxiv, 48-92. (20) ErsENDRATH, D. N.: Text Book of Urology, 1928, p. 621-623. J.B. Lippin .. cott Company. (21) CHAUVEKE1', A.: Jour. Med. de Bordeaux, March 25, 1928, lviii, 228. (22) PINEY, A.: Recent Advances in Haematology, 162-167.
The case which we wish to bring to your attention ls one of spontaneous perirenal hemorrhage, occurring in a male suffering from polycythemia. So far we have been unable to find a similar case reported in the literature. Spontaneous or non-traumatic perirenal hematoma itself has been described by Rayer as far back as 1839, and also by Willis in 1841. Since then many writers, among them Doll, Richer, Laewen, Baggard, Koch, Greco, Schloss, Eigler, Chauvent, J\Iyeres and Singer have reported similar cases. Caenan has given us a classification of these hematomata, dividing them mainly into t,, o grours. 1. Primary non-traumatic or essential type. 2. Secondary type or those due to known causes, such as tuberculosis, tumor, aneurysm or perinephritic abscess.
It is in the first group into which our case falls, and with which we are mainly interested. Richer ha.s suggested that the lesion occurs by means of diapedesis due to a pathological lesion of the vasomotor system. Baggard believes that alterations in compression as found in hydronephrosis may be the cause, while others think that a degenerative inflammation of the veins is the etiological factor. While some 66 cases such as these have been reported, not one has occurred jn a patient suffering from polycythemia. Four have occurred in patients who were hemophilics as reported by Caenan, Laewen, Bollag and Saint Cene. The question naturally arises was the polycythemia the cause or the result of the perirenal hemorrhage. 1 Read at the annual meeting of the American Association of Genito-urinary Surgeons, Manchester, Vermont, June 13, 1929. 535
536
DAVID W. MACKENZIE
The resume of the case report is as follows : J. D., male, thirty-five years of age, admitted to the Urological Service of the Royal Victoria Hospital at 1 p.m., December 18, 1928. Complaints on admission were: (1) Severe sharp pain in the left loin and left upper quadrant; (2) mass in the left loin. (3) nausea and vomiting. Present illness. Twenty-four hours previously, when in good health, the patient felt while chopping wood a sudden sharp cramp-like pain in the left loin, this remained localized and was soon followed by nausea and vomiting. Several hours before admission to hospital, which was the following day, he noticed a gradual swelling in the left flank. On admission, he appeared acutely ill, though the color of his skin and mucous membranes was good. His pulse was 108, respirations 25 and the temperature was 98.2°. The general physical examination apart from the genito-urinary system was normal. The blood pressure at this time was 140/100. The abdomen was asymmetrical, due to a uniform fullness in the left flank extending from the costal margin to the iliac crest on that side. The overlying rectus muscle was rigid and the mass gave a dull note on percussion. It was only slightly tender to palpation. There was no costo-lumbar tenderness on the right side, and the lower pole of that kidney was just palpable. Urinalysis at this time of catheterized specimen showed the urine to be, clear amber, acid, 1.035, albumin++, sugar none, with microscopically, an occasional red blood cell and white blood cell, and some scattered epithelium. The leucocytosis was 20,600. Cystoscopy. Shortly after admission showed a normal bladder. The ureters were easily catheterized and normal urine obtained from each side. A pyelogram on the left side showed a large irregular renal pelvis, displaced downwards and laterally, as if compressed from without (fig. 1). The patient was observed for four hours during which time the blood pressure rose from 140/100 on admission to 155/115, and the pulse rate increased from 108 to 160. The mass in the loin became larger and firmer, while the patient's general condition grew rapidly worse. The color of the skin all the while was good, though his general condition, the rising pulse and the rapidly enlarging tumor indicated a retroperitoneal hemorrhage. The high blood pressure was a feature we could
PERIRENAL HEMATOMA
537
not explain, and several conditions were mentioned such as tumor of the adrenal, or stimulation of the adrenal gland due to the increased retroperitoneal pressure.
FIG.
1.
PYELOGRAM OF LEFT RENAL PELVIS SHOWING DOWNWARD DISPLACEMENT FROM EXTERNAL COMPRESSION
Four and a half hours after admission an operation was performed: Through a curved left loin incision, the muscles were incised and underneath was found a tense shining black cystic mass which was very
538
DAYID W, MACKENZIE
large and firm, filling the entire loin and left flank. The peritoneum was pushed forward by the mass, which was freed as quickly as possible and delivered. At this time it ruptured as the wall was very thin, and a very large quantity, roughly a quart of old blood clot escaped. At this point the blood pressure fell to 68 systolic. Hoping to be able to find the source of the hemorrhage, we isolated the renal pedicle, beyond the fatty capsule, which we clamped, then removed the mass as a whole. The pedicle was then tied with three strong ligatures and the clamps removed. A small hole in the peritoneum was sutured. The peritoneal cavity did not appear to contain any blood. The surrounding tissues were engorged and dark in color but there were no bleeding points apparent and the cavity in the loin appeared to be quite dry. The wound was closed as quickly as possible with a large cigarette drain leading down to the bottom of the cavity. Grossly the wall of this mass seemed to be formed by thinned-out perirenal capsule, and the extravasated blood was held between this and the kidney itself. The kidney was split but appeared perfectly normal. The pathological report is as follows: A rather large kidney 13 by 6 cm. with its enclosing perirenal fatty capsule. Both this capsule and the kidney have been opened. The perirenal fatty capsule is enormously thickened and infiltrated with clotted blood forming a diffuse hematoma throughout this capsule. Renal capsule proper is intact and strips with difficulty exposing a smooth cortex which is mottled with pin-point yellowish spots. Cortex is 7 mm. thick and well differentiated from medulla. Pelvis is free. On dissecting out ureter and blood vessels at the hilus the tissue between these vessels was infiltrated with clotted blood, but though the vessels were dissected as far as possible into renal substance, no rupture or point of hemorrhage could be demonstrated. Several sections through hilus were taken, including all blood vessels. Microscopic examination. Sections taken across vessels at hilus show extensive hemorrhagic extravasation throughout surrounding tissue. The arteries appear thickened with some degeneration in the media. There is nothing however to explain positively the hemorrhagic extravasation. The glomeruli of the kidney appear for the most part hemorrhagic and there is a certain amount of degenerative change in the epithelium of the tubules which may be due to lack of immediate fixation. Anatomical summary. Perirenal hematoma. Special laboratory findings were: Blood Wassermann negative.
PERIRENAL HEMATOMA
Fundi were normal. Blood urea, 0.774 gram per liter. Blood urea nitrogen, 36.12 mgm. per 100 cc. Creatinine, 1.93 mgm. per 100 cc, A.C. blood sugar, 0.086 gram per cent. P.C. blood sugar, 0.114 gram per cent. Following operation the patient's condition rapidly improved. The blood pressure rose to 90/30, five hours after operation, and gradually
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AND JvIARKED
FALL DURING OPERATIO:'-r,
WITH GRADUAL
RISE TO NORMAL
:reached 120/60 as will be seen on the accompanying chart. The pulse reached its normal level on the third day (fig. 2). Following operation for several days the patient's skin and mucous membranes were pale; but ten days later he had quite a healthy ruddy colour and his red cell count at this time was 6,630,000 per centimeter. On questioning, the patient stated that since 1923 he had noticed a THE JOURNAL OF 'GROLOGY, VOL,
xxnr,
NO.
5
540
DAVID W. MACKENZIE
gradual enlargement of the superficial veins. His complexion had become a ruddier hue and the conjunctivae were constantly injected. Three months before his hemorrhage he had acted as donor for blood transfusion on three different occasions, and had felt much improved from the loss of blood. Following the finding of his high red cell count, a periodic check up was made, as seen in the accompanying chart (fig. 3). It will be seen that seventy days after his hemorrhage, his red cell count had risen to 7,800,000.
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75
DAYS FOLLOWING HEMORRHAGE
The morphological examination of the blood ten days after operation was as follows: Red blood cells, 6,500,000. White blood cells, 13,000. Hemoglobin; 98 per cent (13.7 gram/100 cc. Color index, 0.75. Red blood cells: Stain rather poorly. Moderate anisocytosis. Slight poikilocytosis and polychromatophilia. No punctuate basophilia or nucleated reds. Reticulated reds, 1 per cent. Fragility: normal. Corpuscle volume: 52 per cent. Average corpuscle volume: 80 cubic microns. Hemoglobin concentration: 0.83. Sedimentation velocity: slow. Viscosity: increased. White blood cells (400 examined): Polys. Eosin. Mast. Mono. Lymph. 82.25 1.25 0.75 4.75 11 percent 10693 162 98 617 1430 per cmm. No pathological forms. No immature elements.
PERIRENAL HEMATOMA
541
Platelets (400,000, usual size and shape): Bleeding time: Not prolonged. Coagulation: Fibrin congealing with calcium retraction 4. 5 min. 7 min. 4 min. poor Serum: Rather pale yellow with faint greenish tinge. Van den Bergh: Direct, prompt, negative: direct, delayed, faint. Indirect,-less than 0.3 unit. Refraction-52. Low. Conclusions: The lack of immature myeloid elements and bilirubinemia suggest we are dealing with a symptomatic polyglobuli rather than a polycythemia vera. It seemed at first as if we were dealing with a case of symptomatic polyglobuli, which could be explained in the light of the severe hemorrhage which had taken place. A second morphological examination at a later date showed us to be dealing probably, with a true polycythemia. Red blood cells, 7,800,000. White blood cells, 15,000. Hemoglobin 119 per cent (16.6 grams per 100 cc.). Color index, 0.76. Red blood cells: Stain rather poorly. Slight anisocytosis and polychromatophilia. No poikilocytosis, punctate basophilia or nucleated reds. Reticulated reds: Less than 1 per cent. Fragility: Moderately increased resistance Corpuscle volume: 59 per cent. Average corpuscle volume: 76 cubic microns. Hemoglobin concentration: 0.89. Viscosity: Very high. Sedimentation velocity: Very slow. White blood cells (400 examined): Lymph. Polys. Eosin. Mast. Mono. 12 per cent. 77 3 1 7 1800 per cmm 450 1050 11550 150 Increase in myeloid elements. Platelets (370,000, usual size and shape): Bleeding time: Not prolonged. Coagulation: Fibrin congealing with calcium retraction, 4. 5 min. 3 min. 2.5 min. poor Serum: Yellow with faint greenish tinge. Refractometry: 5L Van den Bergh: Direct, prompt, negative; delayed, faint. lndirect,-less than 0.3 unit. Conclusions: There has been a definite rise in the erythrocytes and hemoglobin since the last examination, otherwise the findings are essentially the same. The persistence of the high red count speaks definitely for polycythemia vera, although there is still lacking the usual immaturity in the leucocytes.
542
DAVID W. MACKENZIE
The red cell count since this last report has fallen somewhat, but is still beyond normal limits. vVe have been unable to satisfy ourselves as to the relation of the hemorrhage to the polycythemia-which of the two conditions was the etiological factor? It is possible that the condition of polycythemia brought about a series of factors underlying the perirenal hemorrhage. It is also possible that the severe hemorrhage induced a marked reaction on the part of the red blood cell formation. Taking the cases of perirenal hemorrhage as a group regardless of whether primary or s,econdary cause, the statistics of the 66 cases reviewed, show that a correct preoperative diagnosis was only made in five of the cases, and that with immediate operation there is a 50 per cent mortality. On the other hand, those cases not operated on all died. In the majority of cases of the primary or essential group, the source of the hemorrhage, or the etiological factor underlying it, was not demonstrated. CONCLUSIONS
1. Spontaneous perirenal hemorrhage is a comparatively rare lesion. 2. It has been classified according to the source, such as primary, or of unknown etiology; and secondary, those due to some discoverable lesion. 3. The case just reported is the only one in association with the condition of polycythemia. 4. The question still persists, of the two factors, hemorrhage and polycythemia, which is the cause and which the effect? REFERENCES (1) WUNDERLICH, C. A.: Handbuch der Pathologie und Therapie, 1846, iii, 1197. (2) HERS KY, P.: Medizinische Klinik, Berlin, May 8, 1925, 700. (3) RAPIN: Les hematomes perinephretiques non traumatiques. Paris Medical, 1919, xxxiii, 31. (4) MAYER AND SINGER: Spontaneous perirenal haematoma. Jour. Surg., Gynecol. and Obstet., September, 1927, 300-306. (5) ISRAEL; Chirurgie der niere und des Harnleiters. 1925, Leipsig. (6) VoGELER: Das Nierenaneurysma. Deutsche Ztschr. Chir., 1922, 297-324.
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(7) CAENAK: Das Perirenal Haematom. Beitr. Zklin Chir., 1910, 494-538. (8) DoLL: Die Apoplexie des Nierenlagers. Muenchen Med.. Wchnschr., 1907, 2417-2420. (9) LAEWE'J, A.: vVeber das sogenannte perirenale hematom und andere spontane retroperitoneale Massenblutungen. Deutsche Zysche Chir.,, 1912, cxiii, 367-388. (10) RICKER: Uber die haemorrhagische Infarzierung des Nierenlagers und and.ere kapillare Diapedesis Blutungen grofsen Umfanges an und. in Or. ganen der Bauch Hohle. Beitr. pathol. anat. Bell., 1911. (11) LiPPEKs, A.: L'hematome perirenal spontane. Jour. de Chir., t. 1913, N. 20, p. 1. (12) MAYER, K. A.: Spontaneous perirenal haemorrhage. Jour. Amer. Med. Assoc., 1919, xxii, 1451-2. (13) ScHLoss, VV.: Weiner Klinische, W ochenschrift. Uber einen Full von Massenbluntung ins Nierenlager, October 21, 1926. (14) ErGLER: Munchener Medizinische Wochenschrift, March, 1928. Uber Retroperitoneale Massenbluntungen. (15) BAGGARD: Zur Kenntnis der Massenblutingen ins Nierenlager. Beitr. z. klin. Chir., 1914, xci, 454-474. (16) GRECO, F.: L'ematoma perirenale non traumatico. Archivio Italiano di Chirurgia, 1915, xi, 1-40. (17) BoLLAG: Ein Fall von Massenblutung in das Nierenlager bei Hemophilie. Dent. Zeitscher f. Chir., 1920, 152--155. (18) SAINT-CE NE: Un nouveau cas d'hematome perinephretique non traumatique. Jour. d.'Urologie, t. ix, 1921, 25. (19) SoHN, A.: Die Spontanen Massenblutungen ins Nierenlager. Deutsche Ztschr. f. Chir., 1921, clxiv, 48-92. (20) ErsENDRATH, D. N.: Text Book of Urology, 1928, p. 621-623. J.B. Lippin .. cott Company. (21) CHAUVEKE1', A.: Jour. Med. de Bordeaux, March 25, 1928, lviii, 228. (22) PINEY, A.: Recent Advances in Haematology, 162-167.