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258
publication of his sign, coauthored with J.Marchand who was former substitute
intern at Lyon Hospitals [89].
Lesieur and Marchand described a pulmonary percussion nding in patients with
typhoid fever caused by liver hypertrophy (Table7.1):
In two previous communications, one at the Congress of the French Association for the
Advancement of Science in Dijon (August 1911) and the other at the National Society of
Medicine of Lyon (meeting December 11, 1911), one of us was attracted the attention to a
“very clear and frequent” sign of typhoid fever, of which he gave the description and
showed the value while trying to explain its pathogenic mechanisms. During ordinary clas-
sic fever, he wrote, if one supercially percusses the right base of the thorax, one notices
almost always a noticeable dullness, which we do not nd at the left base, which is gener-
ally not explained by pleuro-pulmonary lesion and whose observation appears to have a real
value in diagnosis, prognosis, and treatment [89, p.625]. Hypertrophy of the liver seemed
capable of explaining the existence of a zone of sub-dullness at the right base of the thorax
in typhoid patients [89, p.626].
Thus, Lesieur sign refers to decreased auscultatory breath sounds at the right base
in typhoid fever caused by hepatic hypertrophy.
7.2.17 Frank Sign
Alfred Erich Frank (1884–1957) was born in Berlin, Germany, and studied medi-
cine in Breslau (Wroclaw, Poland). He passed his state examination in 1907, com-
pleted his internship at the Wiesbaden Municipal Hospital, and received his
doctorate from the University of Strasbourg in 1908 [90]. He was involved in diabe-
tes and metabolic research under the aegis of Wilhelm Weintraud (1866–1920) at
the medical clinic at the Wiesbaden Municipal Hospital from 1908 to 1911 [90].
Frank was an assistant in Oskar Minkowski’s (1858–1931) Clinic for Internal
Diseases at the University of Breslau beginning in 1911, habilitated in 1913, and an
extraordinary professor in internal medicine in 1919 [90]. He was a senior physician
at the University of Breslau in 1918 and, in 1926, was chief physician in the medical
department of the Municipal Wenzel-Hancke Hospital, Breslau. Among his many
accomplishments, he was the rst to recognize the association between the posterior
pituitary gland and diabetes insipidus [90].
He ed during National Socialism to Turkey in 1934 and was granted a position
at the University of Istanbul, where he was director of the second chair of the inter-
nal department of the Faculty of Medicine at Gureba Hospital [90]. He founded
Istanbuler Zeitschrift für klinische Medizin (Istanbul Journal for Clinical Medicine)
in 1951 [90].
Frank coined the term pseudohemophilia to describe the clinical features that
distinguish true hemophilia from other causes that resemble this condition
(Table7.1):
There is no doubt that acute and chronic liver disease, if sufciently advanced, results in a
signicant prolongation of blood coagulation. However, it must be emphasized that it is not
found in all cases of severe hepatic insufciency [91, p.457]. (…) The cause of hypocoagu-
lability is the disappearance of the brinogen, through lack of formation and increased
7 Liver andBiliary Signs
259
destruction [91, p.457]. (…) I now imagine that even in severe hepatic insufciency, the
delay in coagulation is merely an indicator of a process that prevents platelet thrombus
formation. (…) The mechanism of hemorrhage in hepatic pseudohemophilia is, therefore,
similar to that in thrombocytopenia: it is based on the absence or the excessively loose
structure of the platelet thrombus. It is, therefore, a question of thrombocytopenia in the
truest sense of the word; but since the name thrombocytopenia has already been assigned, I
would prefer to refer to the absence of thrombus formation when there is a numerically suf-
cient number of platelets as athrombia [91, p.458].
Frank recognized the nding of hypocoagulability in patients with chronic liver
disease is caused by hypobrinogenemia and platelets thatmay be normal in num-
ber but fail to cause blood clotting—a condition he referred to as athrombia, cur-
rently known as thrombasthenia.
7.2.18 Ortner Sign
Ritter Norbert Ortner von Rodenstätt (1865–1935) was born in Linz, Austria, and
received his medical degree from the University of Vienna in 1888 [92]. He was a
physician at the Crown Prince Rudolf Children’s Hospital and, subsequently, the
Rudolf Foundation Hospital until 1893 [90]. He was appointed assistant to Edmund
von Neusser (1852–1912) at the second medical clinic in 1893. Ortner was primaries
at the Kaiser-Franz-Josef Hospital in 1900 and a full professor of internal medicine at
the University of Innsbruck in 1907 [92]. He returned to the University of Vienna in
1911 as a professor of special medicine and pathology, and therapy at the third medi-
cal clinic and the second medical clinic (a position previously held by Neusser) [92].
Ortner described two signs. One involves hoarseness due to vocal cord paralysis
caused by compression of the recurrent laryngeal nerve in patients with an enlarged
left atrium. He also described the physical examination ndings in patients with
biliary colic (Table7.1):
Objectively, we nd tenderness in the region of the incisura, at least on deep inspiration,
pressure against the liver during inspiration, and on bimanual palpation of the liver with one
hand on the incisura and the other pressing against it from the lumbar region. There is
hyperesthesia of the skin over the gallbladder region and posteriorly between the lower
border of the right lung and posterior costal arch. The lowest part of the thorax and right
hypochondrium is tender on rapid, sharp percussion of these regions with the ulnar part of
the hand. (…) Not uncommonly, the patient complains of increased pains which last several
hours after palpation of the gallbladder [93, p.164–165].
Thus, Ortner sign refers to the (1) palpable technique for detecting cutaneous hyper-
esthesia over the gallbladder region and posteriorly between the lower right lung
and posterior costal arch and (2) percussion tenderness using the ulnar aspect of the
hand located over the lower thorax and right hypochondrium in patients with acute
cholecystitis.
7.2 Liver andBiliary Eponymous Signs
260
7.2.19 Riesman Sign
David Riesman (1867–1940) was born in Thuringia, Germany, received his medical
training at the University of Michigan and the University of Pennsylvania, and earned
his medical degree from the latter in 1892 [94]. He completed an internship at the
Philadelphia General Hospital and was appointed demonstrator in pathology until
1901. He held subsequent positions as instructor in clinical medicine in 1901, assistant
professor of clinical medicine in 1905, and professor of clinical medicine from 1912 to
1933 at the University of Pennsylvania [94]. He also held teaching posts from 1901 to
1918 as a professor of clinical medicine in the Polyclinic Hospital and at the College
for Graduates in Medicine. He was appointed the rst professor of medical history in
the Graduate School of Medicine at the University of Pennsylvania [94].
As to a description of his character and teaching:
He was kindly and wise, forceful and stimulating, tolerant, versatile, cultivated and amaz-
ingly industrious. (…) His life and teaching will always stand as an inspiration to all of us
who had the rare privilege of knowing David Riesman personally, and to those countless
members of the profession who knew him only through his works [94, p.303].
Riesman described ulnar percussion as a method for diagnosing cholecystitis
where conventional examination methods for eliciting tenderness remain obscure
(Table7.1) (Fig.7.5):
The method of employing it simple: The patient is asked to take as deep a breath as possible and
to hold it. The suddenly one strikes a quick but not hard blow over the upper part of the right
rectus muscle, with the ulnar side of the hand. If there is any disease of the gallbladder, the blow
will cause a sharp pain. If one is in doubt as to whether this pain is supercial and due to the
blow on the integument, all that is necessary is to perform the test on the left side [95, p.1963].
Fig. 7.5 Riesman sign (by Ryan Yale)
7 Liver andBiliary Signs
261
Thus, Riesman sign refers to the pain located along the upper portion of the right
rectus muscle while the patient holds their breath after deep inspiration and strikes
this region using the ulnar aspect of the hand.
7.2.20 Carmalt-Jones Sign
Dudley William Carmalt-Jones (1874–1957) was born in London, England, and
received his Bachelor of Medicine degree from St. Mary’s Hospital, London, in
1903 [96, 97]. He continued as house surgeon and house physician at St. Mary’s
Hospital and subsequently was appointed senior house physician at the National
Hospital for the Paralyzed at Maida Vale [94]. He returned to St. Mary’s and worked
as an assistant in Sir Almroth Wright’s (1861–1947) Laboratory of Therapeutic
Inoculation [97]. Carmalt-Jones was an assistant physician at the Seamen’s Hospital,
Greenwich, in 1907 and Westminster Hospital, London, and honorary director of
the department of bacterio-therapeutics from 1910 to 1913, where he later was full
physician and dean of the Westminster Hospital Medical School in 1912 [96, 97].
He received his Doctorate of Medicine degree from Oxford in 1911 [94]. During
World War I, he served in the Royal Army Medical Corps, where he was stationed
in France from 1914 to 1918, and as a temporary colonel and a consulting physician
of the expeditionary forces to Egypt from 1918 to 1919 [96, 97].
Carmalt-Jones was the Mary Glendinning professor and chair of systemic medi-
cine at the University of Otago School of Medicine, New Zealand, in 1920, whose
primary responsibility was teaching medical students at Dunedin Hospital [96–98].
He was a member of the Royal College of Physicians, London, in 1907 and a fellow
in 1914 [96]. Carmalt-Jones was editor of the Proceedings of the University of
Otago Medical School [96, 98]. He served as president of the New Zealand Branch
of the British Medical Association in 1935 [96]. He was appointed foundation fel-
low, vice-president, and member of the rst council of the Royal Australian College
of Physicians [96].
As articulated by his former student regarding Carmalt-Jones character:
Carmalt-Jones was beloved by all, who recognized him the scholar and gentleman in addi-
tion to the physician. Maybe he was a little “old school,” but he strove to keep us abreast of
developments. He was ne company, and lost no chance of introducing us to Plato and the
Greeks through Sir Richard Livingstone’s little books. His own history of the Otago School
is a valued bequest. Those who were fortunate to meet him latterly in his retirement near
London found him the same kindly interested “C.J.” of thirty years ago in Dunedin [99,
p.661].
Carmalt-Jones identied in patients with cholecystitis a sharp pain involving the rib
cartilage in the right hypochondrium (Table7.1):
I found a tender spot upon the eight right costal cartilage, on its lower edge (not its anterior
surface), which could have been found by approaching the patient from behind and hooking
one’s right-hand ngers round the costal margin. (…) The sign is sought for with the hand
at on the upper abdomen; the third nger-tip is brought into rm contact with the costal
7.2 Liver andBiliary Eponymous Signs
262
margin, inch by inch along its whole length from without inwards, beginning on the left
side, saying nothing and watching the patient’s face. (…) On the right, in a case of chole-
cystitis, a single tender spot, indicated by the patient’s expression, is found, generally on the
eight rib edge, sometimes a little higher or lower, and just covered by the nger-tip.
Occasionally, but by no means always, the skin of the whole eight dorsal segment on the
same side is hyperalgesia to pin-prick [100, p.615].
He postulated that the etiology was due to:
I would suggest that spasm of the sphincter of Oddi, which is believed to be controlled by
the sympathetic, induces this tender spot on the body wall, and sometimes hyperalgesia of
a whole segment in the areas of corresponding somatic innervation [100, p.616].
Thus, Carmalt-Jones sign refers to a tender spot located on the eighth right costal
cartilage below the costal margin elicited by hooking the ngers of the right hand
around the costal margin.
7.2.21 Kenawy Sign
There is limited historical information available on Mohammed Radwan Kenawy.
He served in the medical unit as a medical tutor at the Qasr al-Aini Hospital,
University of Cairo, Egypt, in 1939 and in the Faculty of Medicine at Fuad
I.University, Cairo, in 1947 [101, 102].
Kenawy described in 1939 an auscultatory nding, the continuous venous hum,
in patients with cirrhosis (Table7.1):
The venous hum is usually heard over a localized area over just below the xiphoid process
of the sternum. It is continuous and is accentuated by deep inspiration. (…) i) Over the site
of the hum and in a strictly localized area a continuous thrill could be felt, especially on
applying very lightly the tip of one nger; ii) careful inspect of the site of the thrill showed
an elevation of the skin, which is probably due to an underlying vein; iii) when light pres-
sure was applied over the elevation, the thrill disappeared; and iv) when the stethoscope was
applied to the xiphoid process and the hum listened to, the application of light pressure over
the site of the thrill caused the hum to disappear. When the pressure was released, the hum
returned [102, p.821–822].
Thus, Kenawy sign refers to a continuous venous hum in patients with hepatic
cirrhosis.
7.2.22 Čičovački Sign
We were unable to identify any historical information on Danilo Čičovački. At the
time of his publication, he held an appointment under Professor Nikolaus V.Jagié
(1875–1956) at the Second Medical University Clinic in Vienna.
Čičovački further expanded upon the cutaneous condition found in patients with
cirrhosis (Table7.1):
7 Liver andBiliary Signs
263
Star-shaped skin telangiectasias in cirrhosis of the liver, rst described by Eppinger, were
reported in 23 out of 41 cases. They are predominantly located on the skin of the upper half of
the body and increase in number and size as the disease progresses. Their presence has been
found exclusively in liver cirrhosis, although not in every case, and their diagnostic impor-
tance is emphasized accordingly. As far as the development of vasodilatation is concerned, a
common signicant constitutional cause is assumed for both liver cirrhosis and telangiectasia.
Liver disease signicantly inuences their shape, size, and appearance [103, p.483].
Thus, Čičovački sign refers to the star-shaped cutaneous telangiectasis in patients
with hepatic cirrhosis.
7.2.23 Gruenwald Sign
Peter Gruenwald (Grünwald) (1912–1979) was born in Schoenwald, Bohemia
(Czech Republic), and received his medical degree from the University of Vienna in
1936 [104, 105]. He was appointed demonstrator and instructor of histology and
embryology at the University of Vienna from 1936 to 1938 [102]. During World
War II, he immigrated to the USA, where he was a research fellow at the Cook
County Hospital in Chicago [104, 105]. He was an instructor of anatomy at the
Chicago Medical School from 1939 to 1942; assistant professor of histology and
embryology at Middlesex University at Waltham, Massachusetts from 1942 to
1944; NewYork State fellow in pathology Mount Sinai Hospital from 1944 to 1945;
assistant professor of pathology at Long Island College of Medicine from 1945 to
1951; and assistant professor Department of Obstetrics and Gynecology (pathol-
ogy) State University of NewYork College of Medicine from 1951 to 1954 [104,
105]. He was appointed pathologist and director of laboratories Margaret Hague
Maternity Hospital, New Jersey, in 1955 and in the Department of Obstetrics and
Gynecology at Johns Hopkins School of Medicine, Baltimore, Maryland, in 1958.
He was named assistant professor in 1961 and associate professor in 1964in the
Department of Pathology at Johns Hopkins University [104, 105].
His academic interests included placental development, developmental and com-
parative anatomy, placental and fetal pathology, fetal malnutrition, and respiratory
distress syndrome [105]. He served as an associate professor of pathology at the
University of Pennsylvania and Veterans Administration Hospital in 1969. His nal
appointment was at Hahnemann Medical College and Hospital in Philadelphia,
where he accepted the associate professor of pathologist position in 1970 [104].
He was a member of the American Association of Anatomists, American Society
of Human Genetics, and a fellow of the NewYork Academy of Science, Teratology
Society, and American Association for the Advancement of Science [104].
Gruenwald reported eight cases of hepatic rupture with associated hemoperito-
neum occurring during vaginal delivery. He proposed a mechanism for this phe-
nomenon (Table7.1):
Pressure on the thorax is an important factor in the production of these lesions. By such
pressure, the organs of the upper abdomen are squeezed out of the hollow of the diaphragm,
and undue tension on the ligaments of the liver and spleen then produce part of the lesions.
Others are the result of direct pressure of the costal margin on the anterior surface of the
7.2 Liver andBiliary Eponymous Signs
264
liver. A minority of the lesions of the liver in the present group of cases are not obviously
related to these mechanisms and are probably due to direct trauma [106, p.201].
This mechanism was proposed to account for the locations of the lacerations of the
spleen at the phrenicolienale, liver at the coronary and hepatoduodenal ligaments,
and umbilical vein in infants.
7.2.24 Tanyol Sign
7.2.24.1 Hasib Tanyol
Hasib (Hasip) Tanyol (1916–1999) was born in Eskisehir, Turkey, and received his
medical degree from the University of Istanbul Faculty of Science [107, 108]. He
completed his internship at the Universities of Vienna and Freiburg [107]. He was a
research fellow at Jefferson Medical College and an assistant professor of anatomy
at Hahnemann Medical College in 1951 [107]. He was a private practitioner in
Lafayette Hill and subsequently Fort Washington in the mid-1960s and was
appointed to the medical staff at Germantown Hospital, Philadelphia, and
Montgomery Hospital, Norristown, Pennsylvania [107].
His primary areas of interest were hypertension and vascular aspects of liver cir-
rhosis. He was a founding member of the American Society of Hypertension. He
received the Honors Achievement Award from the Angiology Research Foundation
[107, 108].
7.2.24.2 Hyman Menduke
Hyman Menduke (1921–1999) received his Ph.D. in economic statistics at the
University of Pennsylvania in 1952 [109]. He was appointed assistant professor of
biostatistics at Thomas Jefferson University in 1953 and professor of preventive
medicine (biostatistics) in 1963 [109]. Menduke served as professor of pharmacol-
ogy (biostatistics) in the Faculty of Medicine at Thomas Jefferson University in
1978 [109].
Among his other appointments, Menduke was an adjunct professor of statistical
evaluation of clinical data at Philadelphia College of Pharmacy and Science. He
also served as past president of the Philadelphia Chapter of the American Statistical
Association [109]. The Hyman Menduke Research Prize is awarded annually to the
graduating senior for excellence in research [110].
Tanyol and Menduke measured the distance between the lower edge of the
xiphoid and umbilicus and umbilicus and upper edge of the pubic symphysis in
patients with cirrhosis without ascites or obesity and age and race match controls
without liver disease and found that (Fig.7.6):
In noncirrhotic individuals the distance from the umbilicus to the xiphoid process is almost
equal to the distance from the umbilicus to the symphysis. In cirrhotic patients, however,
the upper distance is much greater than the lower [111, p.422–423].
7 Liver andBiliary Signs
265
Fig. 7.6 Tanyol sign (by Ryan Yale)
They coined the term “umbilical ptosis” to signify the lengthening of the distance
between the xiphoid process and the umbilicus in patients with portal cirrhosis
(Table7.1).
7.2.25 Coronel Sign
Armando Pareja Coronel (1896–1965) was born in Guayaquil, Ecuador, and
received his medical degree from the Faculty of Medicine of the University of
Guayaquil in 1920 [112, 113]. He was head of the women’s tuberculosis service at
Guayaquil Hospital in 1924 and appointed professor of internal medicine at the
University of Guayaquil in 1929 [112]. Coronel was chief physician of the women’s
service at Santa Elena Hospital in 1931 [112]. He was elected president of the
Municipality of Guayaquil in 1908, appointed governor of Guays in 1922, and the
province of Guayaquil in 1926 [112, 114]. Coronel was president of the Surgical
Medical Society of Guayas, the Ecuadorian Anti-tuberculous League in 1940, a
member of the council in 1946, and the Sports Federation of Guays and the National
Federation of Ecuador [112, 113]. He received the Medal of Civic Merit from the
Municipality of Guayaquil in 1956 [112].
The phrenic nerve pressure point of sensitivity described by Coronel is: [a] pain-
ful spot in front of the scalenus muscle corresponding to the area of the phrenic
nerve [115, p.119]. Coronel believed that the phrenic nerve pressure point was
diagnostic of acute malaria and that the pain was due to hepatosplenic syndrome
(Table7.1).
7.2 Liver andBiliary Eponymous Signs
266
Table 7.1 Liver and biliary signs
Name Year Description of sign Signicance
Hanot [15] 1876 Jaundice and hepatic pain are accompanied initially by anorexia, constipation, general malaise, fatigue, and
fever. Fever was present initially, during ares, and throughout the disease course. Several times, the pain
was accompanied by a high fever of 39.5–39.8° and a pulse of 110 or 120. This fever did not last as long as
the pain, but the episode was more intense and prolonged. At other times the painful episodes were
completely afebrile. This initial crisis lasts from one to several weeks. Then, the disease enters a quiescent
period, characterized by chronic jaundice and enlarged liver. Jaundice is one of the major manifestations of
the disease and, in some cases, the initial symptom. Jaundice, once present, persists throughout the disease
course. However, there is a variable intensity of jaundice during its long duration. Even though it may be
minimum, it is generalized and apparent and always more intense than the subicteric hue encountered in
other conditions
Primary biliary
cirrhosis
Rosenbach [22] 1878 Pulsatile liver in aortic insufciency Aortic insufciency
Courvoisier [27] 1890 A stone obstructing the common bile duct leads to contraction of the cystic duct and gallbladder, while a
normal complaint gallbladder is found in other causes of obstruction (e.g., tumor)
Gallstones
Rovighi [32] 1894 A distinct resonant sound is heard at a site on a hydrogenic cyst of the liver using digital or pleximetric
percussion. When moderate pressure is applied with the stethoscope on the cystic mass, resonance on
percussion acquires a higher pitch. The sonority remains distinct if a solid body is interposed between
the stethoscope and the mass, while the hydrogenic thrill is no longer palpable. In cases where the thrill
is not apparent, it can be elicited by placing the palm of the left hand rmly on the mass and striking it
with the right hand’s middle nger on the left hand’s rst phalanges. Thus a kind of vibratory tremor is
felt, which cannot in any way be confused with uctuation or other tactile sensations
Echinococcal cyst
Boas [37] 1894 1. Pressure points are present to the left of the 12th thoracic vertebral body in gastric ulcers. The painful
area can be higher on the 10th or 11th thoracic vertebra or lower at the level of the rst lumbar vertebra.
Occasionally there is a corresponding soreness on the right side, but in this case, the pressure point on the
left is the more sensitive
Gastric ulcer
2. The pressure area in cholelithiasis is also found 2–3 nger widths from the 12th thoracic vertebra,
often extending to the right, and sometimes to the posterior axillary line
Cholelithiasis
Naunyn [50] 1896 Pain occurs during deep inspiration when pressure is applied with the hand direct superiorly beneath the
right costal border. When the liver impinges upon the tips of the ngers, the patient experiences
deep-seated pain, which sometimes radiates over the entire hepatic region and epigastrium. The liver
tenderness is associated with tension involving the right rectus abdominis muscle
Acute gallstone
cholecystitis
7 Liver andBiliary Signs
267
(continued)
Name Year Description of sign Signicance
Lennhoff [54] 1898 On inspection of the abdomen, a moderate bulging of the hepatic region is seen, projecting beyond the
midline to the right. During deep inspiration, two smaller protrusions are seen on the right. They are
found within the liver during palpation. The lower left edge of the liver is sharp and rough, with the right
edge slightly harder and thicker. The entire surface of the organ, including the protrusions, is smooth,
with the latter feeling rmer. With the patient supine, the furrow formed between the rib wall and the
protrusion is perceived as soon as the liver descends during deep inspiration
Echinococcal cyst
Mayo- Robson
[55]
1900 Tenderness at a point midway between the ninth costal cartilage and the umbilicus. A transference of
pain takes place from the right to the left side. The left-sided pain is associated with adhesions between
the pylorus and gallbladder or bile ducts
Cholecystitis with
adhesions
Gilbert [62] 1901 In patients with cirrhosis, the urine becomes scarce after a meal and more abundant after fasting. This
disorder in urinary excretion is an early sign of portal hypertension and may precede the development of
ascites
Cirrhosis
Kayser [64] 1902 The cornea, clear and transparent in its central parts, shows a ring-shaped opacity in the periphery,
resembling gerontoxon. The cornea appears opaque with a dark green-brown ring color widest above,
less wide below, and very narrow laterally and medially so that the area of the clear cornea is oval. The
opacity begins immediately at the limbus and has no sharp border at the clear center of the cornea. On
binocular microscopic examination in the peripheral ring zone described above, there is a signicant
accumulation of ne yellow spots in the deeper layer close to the posterior wall so that the underlying
iris and chamber angle cannot be seen. The yellow spots are apparently in an area parallel to the corneal
surface. This accumulation of yellow spots begins in the periphery, where their arrangement is densest,
and the individual spots are the largest. In general, they are smaller and less dense in the middle portion
of the ring and ne in the portion nearer the corneal center so that their turbidity no longer appears
patchy but diffuse, allowing more light to reach the underlying surface of the iris. While the above dense
patches of turbidity give a yellow appearance, the color at the center of the cornea is different. The
yellow hue changes into a yellowish-green, proceeding gradually into the black of the pupil. The
arrangement of the spots is completely random. The individual spots appear under the binocular
microscope as at bodies without sharp boundaries that are quite irregular, at least the coarser ones in
the periphery. The corneal tissue does not reveal any abnormal abnormalities. There is no sign of
vascular formation. The central part of the cornea is completely normal
Ocular nding in
Wilson disease
7.2 Liver andBiliary Eponymous Signs