Intrahepatic hematoma resulting in obstructive jaundice

99165065/79/9974-9991992.9910 GAWRIOENTEBOLOOY 74124127,1978 Copyright0 1978by the AmericanGastroenterological Association

INTRAHEPATIC JAUNDICE

Vol. 74, No. 1

Printed in USA.

HEMATOMA RESULTING IN OBSTRUCTIVE

An unusual complication of liver biopsy ROBERTO 0. CHIPRUT, M.D., RICHARD A. GREENWALD, M.D., M.D., ROBERT ZEPPA, M.D., AND EUGENE R. SCHIFF, M.D. Departments of Medicine and Surgery, of Medicine, Miami, Florida

Veterans Administmtion

STEVEN J. MORRIS,

Hospital, and University of Miami School

A patient who developed obstructive jaundice as a complication of a liver biopsy is presented. The jaundice was found to be attributable to obstruction of the biliary tree at the level of the bifurcation by an intrahepatic hematoma. The patient had a complete and spontaneous recovery. Percutaneous liver biopsy -is a relatively safe but invasive diagnostic procedure. Although infrequent, a wide variety of local and general complications have been reported. 1- l5 Post-liver biopsy intrahepatic and subcapsular hematomas have been recently evaluated by pre- and post-liver biopsy scanning.‘+14 This complication appears to occur more often than is clinically apparent. In the patient described in this report, a post-biopsy hematoma resulted in a clinical picture of mechanical obstruction of the biliary tree.

The prothrombin time was 13 set with a control of 13 sec. The partial thromboplastin time was 41 set (normal 45 set). Monospot test was negative and the HBsAg was positive. A diagnosis of acute type B viral hepatitis was made. The patient was treated with bed rest and a high carbohydrate diet. On day 13 significant clinical and laboratory improvement was noted (fig. 1). On day 14 a liver biopsy using the Menghini technique was performed. Following the procedure the patient developed pain at the biopsy site. The patient did not adhere to absolute bed rest after the procedure. One day later she developed a moderately severe epigastric pain which was continuous and radiated to the back. Oral and parenteral Case Report analgesics were required and the pain persisted to varying This was the first Jackson Memorial Hospital admission degrees for the next week. On day 19 her hemoglobin was for this 17-year-old white female transferred from another 11.9 g per dl, her hematocrit was 34 volumes per cent, and hospital on December 10, 1976 for treatment of “surgical she had 9500 leukocytes per mm3 with a normal differential jaundice.” The patient had been well until the 1st week in count. Stool specimens for occult blood were negative. The October when she developed malaise, easy fatiguability, nau- liver biopsy was indicative of acute hepatitis. The patient continued experiencing epigastric discomfort sea, and anorexia which was followed 10 days later by dark urine and the development of scleral icterus. She denied for the next 10 days but then noted recurrence of tiredness, parenteral drug abuse and exposure to toxins but she had anorexia, and jaundice. She was readmitted on day 36 with a been on oral contraceptives for 6 months. One year before presumed diagnosis of recurrent hapatitis. Her physical exadmission the patient underwent surgical exploration for amination disclosed icterus, hepatomegaly, and epigastric mesenteric lymphadenitis, and 3 months before admission tenderness without signs of peritoneal irritation. The laborashe had a tonsillectomy. No blood transfusions were adminis- tory studies revealed a hemoglobin of 11.6 g, hematocrit of 34 tered for either procedure. The patient was hospitalized at volumes per cent, and leukocyte count of 8300. The serum her local community hospital (day 1) where she was noted to glutamic oxaloacetic transaminase was 107 mU per ml, total have scleral icterus and moderate tender hepatomegaly. No bilirubin, 12.1 mg per dl; alkaline phosphatase, 250 mU per splenomegaly, lymphadenopathy, or peripheral manifesta- ml; serum cholesterol, 386 mg per dl; and lactic dehydrogentions of chronic liver disease were noted. An initial laboratory ase, 158 mU per ml. The total protein, albumin, calcium, and evaluation demonstrated a hemoglobin of 12.6 g, hematocrit the roentgenograms of abdomen and chest were reported as of 36 volumes per cent, leukocytes 13,300, platelet count normal. An upper gastrointestinal series was normal. A ggmTc 150,000. The serum glutamic oxaloacetic transaminase was sulfur colloid liver scan revealed a large filling defect (fig. 2). 1,500 mU per ml; total bilirubin, 11.0 mg per dl; alkaline Ultrasonography of the liver was compatible with a dilated phosphatase, 100 mU per ml; lactic dehydrogenase, 411 mU biliary tree without visualization of a definitive mass. The per ml; total protein 6.7 g per dl; and albumin, 3.7 g per dl. gallbladder appeared normal in size without evidence of calculi. A “skinny” needle percutaneous transhepatic cholanUrinalysis was normal except for the presence of bilirubin. giogram (fig. 3) demonstrated a dilated right hepatic duct system with apparent blockage at the level of the bifurcation. ReceivedJune 24, 1977. Accepted Agust 17, 1977. The left hepatic biliary system was incompletely visualized. Address requests for reprints to: Eugene R. Schiff, M.D., Hepa- The diagnosis of bifurcation cholangiocarcinoma was entertology Section, Veterans Administration Hospital, 1201 N.W. 16th tained and the patient was transferred to Jackson Memorial Street, Miami, Florida 33125. Hospital for further evaluation and surgery was anticipated. 124

January 1978

CASE REPORTS

125

On her arrival at Jackson Memorial Hospital on day 40 she was a thin girl in no distress, markedly icteric, afebrile, and with normal blood pressure and pulse. There was mild epigastric tenderness, and a palpable liver with an over-all span of 14 cm without bruit or rubs. The hemoglobin was 11.8 g per dl with a hematocrit of 33 volumes per cent, total bilirubin of 18.6 mg per dl with 18 mg per dl direct reaction. An alkaline phosphatase test was 238 mU per ml. The serum glutamic oxaloacetic transaminase was 58 mU per ml and serum STEROIDS -

19 1 iI8

: :: :: . .

:

I-

g

;

550

In 500 0

E

i . . ...-?

450

/ . ...*-

\:

j

.. ..

LlVPl7 BIOPSY ,

:

14

;

ee

I3 p

:

:

lZz

\

.. ..

i 11,

t IO,' 95 .- Bm .. 7 .. 6 .. 5

O’AYS

7

14

21

2.3

35

42

49

79

swl N.w.IIR ?noSPluTASL------~IL*IIoBI” . . . . . . . . . . . . . . . . . . . . . .

FIG. 1. Laboratory findings during course of illness. SGOT, serum glutamic oxaloacetic transaminase.

FIG. 3. This percutaneous transhepatic cholangiogram demonstrates a dilated right hepatic biliary tree with obstruction at the level of the bifurcation. There is some contrast faintly visible in the dilated left duct system.

FIG. 2. A -Tc sulfur colloid liver scan demonstrating a large central filling defect.

FIG. 4. The repeat ge”Tc sulfur colloid liver seen shows resolution of the previously detectable filline defect.

126

CASE REPORTS

glutamic pyruvic transaminase was 71 mU per ml. The lactic dehydrogenase was 150 mU per ml, the platelet count was 368,000with a normal prothrombin time and partial thromboplastin time. The HBsAg was positive. Antinuclear antibody, smooth muscle antibody, and antimitochondrial antibody were negative. A carcinoembryonic antigen was normal and an cr-fetoprotein was negative. Stool specimen for occult blood was negative. A hepatic arteriogram was attempted but was terminated when the patient developed wheezing with the test injection. In order to prevent an allergic reaction to iodinated contrast material in a second attempt to perform this procedure, the patient received a brief course of antihistamines and corticosteroids. During the second dose test of iodinated material the patient developed a diffuse rash and recurrent wheezing. She was given several doses of intermittent parenteral hydrocortisone for the following 6 days. Twenty-four hours after this regimen was initiated the rash disappeared and the serum bilirubin began to decrease. A gallium scan was negative. On day 46 the serum bilirubin was 4.6 mU per ml, the alkaline phosphatase was 128 mU per ml, and the serum glutamic oxaloacetic was 25 mU per ml. A Rose Bengal scan showed normal excretion of the material into the duodenum. A repeat 99mTcsulfur colloid liver scan showed resolution of the defect (fig. 4). At the time of discharge on day 49 the bilirubin was 3.2 mU per ml, alkaline phosphatase, 103 mU per ml, serum glutamic oxaloacetic transaminase, 28 mU per ml, and the patient was asymptomatic. One month later (day 79) the patient remained symptomfree. A total bilirubin was 1.0 mU per ml, alkaline phosphatase, 50 mU per ml, and serum glutamic oxaloacetic transaminase, 28 mU per ml. The HBsAg remained positive. Throughout the course of her illness the patient continued the use of oral contraceptives.

Discussion Although percutaneous liver biopsy is a relatively benign procedure of proven safety and efficacy a wide variety of complications have been reported. These include: fracture of the needle,’ local pain and infection,2 pneumothorax,3 perforation of an intercostal art~ry,~bile pleuritis,5 damage of intrahepatic and extrahepatic biliary ducts with biliary peritonitis,6 hematobilia,’ secondary arteriovenous f%tulae,* unexpected biopsy of other organs,s neurogenic hepatic hypotension, lo immediate and delayed hemorrhages,“, l2 intrahepatic hematomas,13*l4 bacteremia,15 and tumor seeding.*’ The patient in the case report developed a previously undescribed complication of liver biopsy, that of jaundice secondary to obstruction at the level of the bifurcation of the right and left hepatic biliary radicles. Her original diagnosis of acute type B viral hepatitis was well established on chemical and histological grounds; this was apparently resolving when the liver biopsy was performed. The onset of pain at the biopsy site followed by epigastric pain are highly suggestive of the development of an intrahepatic hematoma. It is likely that an expansion of this lesion caused compression of the biliary tree. Definitive con&nation of the latter was established by the onset of obstructive jaundice with a filling defect on liver scan, dilated biliary tree by hepatic ultrasonography, and finally the demonstra-

Vol.74,No.l

tion of the obstruction by skinny needle cholangiography. Hematobilia with clots obstructing the biliary tree is possible but unlikely without a falling hematocrit or blood in the stool. The complete resolution of the jaundice, the disappearance of the defect on the ssmTc sulfur colloid liver scan, and subsequent normal Rose Bengal scan indicates an acute reversible process. Intrahepatic hematoma after percutaneous liver biopsy is a well-described clinical entity. In a prospective study intrahepatic hematomas occurred in 3 of 40 cases.14 These lesions were confirmed by serial liver scans, hepatic angiography, and peritoneoscopy. Conn retrospectively was able to recognize only one instance in 2400 biopsies. l3 Furthermore, he did not encounter this complication after 50 consecutive bi0psies.l” Clinically this lesion may be asymptomatic or may present as right upper quadrant pain, hypotension, abdominal rigidity, or hepatomegaly. l4The laboratory studies usually reveal a significant drop in the hematocrit and elevation of the serum glutamic oxaloacetic transaminase.14 Liver scan demonstrates a defect that may be confused with other space-occupying lesions, resulting in otherwise unnecessary invasive or noninvasive diagnostic and therapeutic procedures. l4 In this patient there was a close relationship between her clinical improvement and the initiation of corticosteroid therapy. Although it is probable that the resolution of the serum bilirubin was spontaneous, it is known that steroids frequently reduce serum bilirubin concentration in patients with mechanical obstruction of the biliary tree. I6The exact mechanism is unknown. It is possible that some improvement of the inllammatory reaction surrounding the hematoma occurred in our patient, explaining the relief of the biliary tree compression and improvement of jaundice. This patient’s course indicates that the diagnosis of intrahepatic biliary tree obstruction secondary to an iatrogenic hematoma should be considered in patients who develop obstructive jaundice after liver biopsy, particularly if the biopsy is complicated by pain or a falling hematocrit. Recognition of this problem may save the patient unnecessary surgical intervention. REFERENCES 1. Peters RS Fracture of Menghini needle in liver biopsy. JAMA 206:1575-1576, 1968 2. Baron E: Aspiration for removal of biopsy material from the liver. Arch Intern Med 63:276-289, 1939 3.Cogswell RC, Schiff L, Safdi SA: Needle biopsy of the liver. JAMA 140:385-390, 1949 4.Mangold R: Risiko der Leber Biopsie. Helv Med Acta 30:552555, 1963 5.Dosik MH: Bile pleuritis: another complication of percutaneous liver biopsy. Am J Dig Dis 20:91-93, 1975 6.Kelley ML, Mosenthal WT, Milne J: Bile leakage following Menghini needle liver biopsy. JAMA 216333, 1971 7.Cox EF: Hematobilia following percutaneous needle biopsy of the liver. Arch Surg 95198-201, 1967 8.Preger L: Hepatic arteriovenous fistulae after percutaneous liver biopsy. Am J Roentgen01 Radium Ther Nucl Med 101:619620, 1967

January 1978

CASE REPORTS

127

terology 67:375-381, 1974 9. Linder H: Grensen und Gefahren der perkutanen Leber Biopsie mit der Menghini Nadel. Dtsch Med Wochenschr 92:1751-17X& 14. Raines DR, Van Heertum RL, Johnson LF: Intrahepatic hematoma: a complication of percutaneous liver biopsy. Gastroenter1967 ology 67:2&I-289, 1974 10. Sullivan S, Watson WC: Acute transient hypotension as compli15. McCloskey RV, Gold M, Weser E: Bacteremia after liver biopsy. cation of percutaneous liver biopsy. Lancet 1:389-390, 1974 Arch Intern Med 132:213-215, 1973 11. Snapper I: Discussion of Rappoport EM: Liver biopsy Review. 16. Lewis C, Mahoney P, Arias MI: Jaundice: clinical and pathoRev Gastroenterol 18:642-650, 1951 physiologic features. In Gastroenterology. Edited by HL Bockus. 12. Kottlors W, Brugel H: Spatblutung nach Leberblindpunktion. Philadelphia, London, Toronto, WB Saunders Co, 1976, p 182Munch Med Wochenschr 112:1238-1240, 1970 202 13. Conn HO: Intrahepatic hematoma after liver biopsy. Gastroen-