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268
Table 7.1 (continued)
Name Year Description of sign Signicance
Fleischer [66] 1903 Greenish discoloration of the cornea is ring-shaped in the periphery, approximately 1mm wide, and
consists of small brownish-greenish dots and spots merging into one another, which become ner toward
the center of the cornea and very gradually merge into the clear cornea. Fine, lighter stripes run through
the discolored area irregularly. The supercial layers of the cornea are translucent; the discoloration
resides in the deepest layers, in an area concentric to the surface, and is quite similar in both eyes
Ocular nding in
Wilson disease
Murphy [72] 1903 Hypersensitiveness of the gallbladder is elicited by deep palpation just below the right ninth costal
cartilage or in a line from that point to the middle of the inguinal ligament. Deep percussion along the
same line, with the patient in forced inspiration, gives pronounced pain
Acute cholecystitis
Maneuver 1
The most characteristic and constant sign of gallbladder hypersensitiveness is the inability of the patient
to take a full, deep inspiration when the physician’s ngers are hooked up deep beneath the right costal
arch below the hepatic margin. The diaphragm forces the liver down until the sensitive gallbladder
reaches the examining ngers, which causes inspiration to cease suddenly
Maneuver 2
The right hand is elevated with the middle nger of the left hand exed perpendicularly at the tip of the
ninth costal cartilage. The nger is struck with the right hand when the patient is in deep inspiration,
causing severe pain if the gallbladder is distended or inamed
Abrahams [76] 1910 A painful point is located midway between the umbilicus and the costal cartilage of the ninth rib in the
right hypochondriac. Place the patient in a recumbent position with the arms and legs extended—a point
is located midway between the umbilicus and the ninth costal cartilage. Press the index and middle
ngers using the right hand into that point, applying a sudden thrust. This causes either a grimace on the
face or a quick involuntary jump of the abdomen. In an acute attack with a diffuse area of hyperesthesia,
the midway point is the point of maximum pain
Cholelithiasis
Finsterer [80] 1910 Bradycardia Liver injury
Milkó [82] 1911 In severe abdominal injuries or general peritonitis, the pulse may be normal. In severe intestinal injury,
marked bradycardia lasts 8–10h
Intestinal injury
7 Liver andBiliary Signs
269
Name Year Description of sign Signicance
Grocco [87] 1911 Percussion should extend from the last dorsal vertebral and left paravertebral zone to determine whether
there is an enlargement of the left lobe of the liver. Percuss with sufcient force in a systematic manner
moving from the top to bottom, rst along the right paravertebral line a, then along the spine b, and to
the left of it, corresponding to lines c, d, e, etc., so that each time where the thoracic sound ends and
liver dullness begins is marked. In this way, one nally arrives at line f, which delimits the almost
horizontal section of liver dullness to the left of the spinal column. Once line f is reached, it is advisable
to percuss from left to right, along the horizontal line i–g, in the direction of arrow 1, to pinpoint point g,
the outer limit of the left portion of the hepatic dullness
Hepatomegaly
Lesieur [89] 1913 Dullness on supercial percussion at the right base of the thorax is caused by liver hypertrophy Typhoid fever
Frank [91] 1915 Acute and chronic advanced liver disease results in impaired blood coagulation. The cause is
hypobrinogenemia, due to either the lack of its formation or increased destruction. Even in severe
hepatic insufciency, the delay in coagulation is merely an indicator of a process that prevents platelet
thrombus formation. Sometimes, a coagulation abnormality is not detectable, and there is no platelet
aggregate. The mechanism of hemorrhage in hepatic pseudohemophilia is similar to that in
thrombocytopenia—the absence or the excessively loose structure of the platelet thrombus
Liver disease
Ortner [93] 1922 Maneuver 1 Biliary colic
Tenderness is present in the region of the hepatic incisura during deep inspiration, with pressure against
the liver during inspiration and on bimanual palpation of the liver while applying one hand on the
incisura and the other pressing against it from the lumbar region
Maneuver 2
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 using the ulnar aspect of the hand in these regions. The patient complains of
increased pains which last several hours after palpation of the gallbladder
Riesman [95] 1922 Ask the patient to take a deep breath and hold it. Using the ulnar side of the hand, apply a quick but not
hard blow over the upper part of the right rectus muscle. If there is disease involving the gallbladder, the
blow causes sharp pain. If in doubt as to whether this pain is supercial and caused by the blow, perform
the same maneuver on the left side
Cholecystitis
(continued)
7.2 Liver andBiliary Eponymous Signs
270
Table 7.1 (continued)
Name Year Description of sign Signicance
Carmalt-Jones
[100]
1932 While approaching the patient posteriorly, hook the ngers of the right hand around the costal margin; a
tender spot is present on the inferior edge of the eighth right costal cartilage. The hand is at on the
upper abdomen. The third ngertip is brought into rm contact with the costal margin, inching along its
whole length, beginning laterally on the left side and moving medially while observing the patient’s
facial expression. In cholecystitis, a single tender spot over the ngertip on the right eighth rib edge,
sometimes slightly superiorly or inferiorly, is conrmed by the patient’s expression of the pain.
Occasionally, the skin of the eighth dorsal segment on the same side is hyperalgesia to pinprick
Cholecystitis
Kenawy [102] 1939 The venous hum is usually heard over a localized area over just below the xiphoid process of the
sternum. It is continuous and accentuated by deep inspiration. Over the site of the hum and in a strictly
localized area, a continuous thrill could be felt, especially on applying the tip of one nger very lightly.
Inspection of the thrill site showed an elevation of the skin, probably due to an underlying vein.
Applying light pressure over the elevation causes the thrill to disappear. The venous hum also disappears
when light pressure of the stethoscope is applied over the site of the thrill at the xiphoid process. The
venous hum returned when the pressure was released
Hepatic cirrhosis
Čičovački [103] 1940 Star-shaped skin telangiectasias are located predominately over the skin of the upper half of the body
and increase in number and size as the disease progresses
Liver cirrhosis
Gruenwald [106] 1948 Hepatic rupture and hemoperitoneum occur in newborns during vaginal delivery Hepatic rupture
Tanyol [111] 1956 In patients with cirrhosis without ascites or obesity, the distance from the umbilicus to the xiphoid
process is greater than that from the umbilicus to the pubic symphysis. In noncirrhotic, the distance from
the umbilicus to the xiphoid process is nearly equal to the distance from the umbilicus to the symphysis
in cirrhotic patients
Hepatic cirrhosis
Coronel [115] [n.a.] A painful spot in front of the scalenus muscle corresponds to the phrenic nerve Hepatosplenic
syndrome and acute
malaria
7 Liver andBiliary Signs
271
7.3 Conclusion
Murphy sign is the most highly recognized sign involving the liver and biliary tract.
Even today, clinicians still use it as a bedside maneuver despite its wide sensitivity
and specicity in diagnosis. For the remainder of the signs, their sensitivity and
specicity have yet to be studied, and their utility in clinical practice remains to be
discovered. They are important to recognize and further study to better understand
their role, if any, in clinical practice.
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277© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
S. H. Yale et al., Gastrointestinal Eponymic Signs,
https://doi.org/10.1007/978-3-031-33673-7_8
Chapter 8
Spleen Signs
8.1 Introduction
The word spleen—σπλήν (splín) in Ancient Greek and splen in Middle English—
dates back to Hippocrates in the fourth century BC [1]. Marcello Malpighi
(1628–1694), in 1659, was the rst to describe the white pulp, later eponymously
named Malpighian corpuscles in his book De Viscerum Structura Exercitatio
Anatomica (An Anatomical Study on Structure of the Viscera) [2]. Rudolf Albert
Kölliker (1817–1905), in A Manual of Human Microscopic Anatomy, proposed the
concept of the normal phagocytic destruction of nascent red blood cells in the
spleen [3]:
For these considerations, I was forced (as early as 1854) to abandon the view, that the
changes of the blood discs in the splenic pulp belonged to the series of physiological
appearances; I conceived that such changes, to be normal, must occur in the interior of ves-
sels, and in this opinion I nd myself supported by the great majority of physiologists. I am
still of opinion that a solution of blood-cells actually does go on within the spleen, and in
this organ much more than in the liver. But I have conclusively given up the grounds on
which I originally regard the occurrence of decomposed blood-cells in the pulp as establish-
ing such a view [3, p.367].
Eponymous signs related to the spleen were rst reported in the late nineteenth
century by Georges Maurice Debove, who described splenomegaly and its associ-
ated clinical features. It was in the mid-twentieth century that Robert K. Nixon and
Donald O. Castell reported percussion methods to determine splenic dimensions
and enlargement. Other signs described during the physical examination by Pitts,
Ballance, Saegesser, and Hedri were involved in devising methods for detecting
splenic injury. This chapter contains brief biographical information of physicians
who reported splenic signs and the sign as initially described.
278
8.2 Splenic Eponyms
8.2.1 Debove Sign
Georges Maurice Debove (1845–1920) was born in Paris, France, was a hospital
intern in 1869, and received his medical degree from the Faculty of Medicine, Paris,
in 1873 [4–6]. He was head of the Germain Sée Clinic, a hospital doctor in 1877,
and agrégé of the Faculty of Medicine in 1878 [4–6]. Debove was professor of the
second chair of medical pathology in the Faculty of Medicine from 1890 to 1900;
appointed the second chair at Charité; taught medicine at the Beaujon Hospital,
Paris, from 1901 to 1908; and was dean of the Faculty of Medicine, Paris, in
1906 [5–7].
He was president of the French National League against Alcoholism and was a
staunch critic of alcohol and its adverse effect on human health [7]. Debove was
elected member of the French National Academy of Medicine, member of the sec-
tion of therapeutics in 1893, later permanent secretary from 1913 to 1920, and titu-
lar of the Anatomical Society of Paris in 1873 [4, 6]. He was honorary president of
the National Council of Hygiene and presided over the Medical Society of Hospitals
in 1897 [4]. In collaboration with Charcot, they wrote Bibliothèque Médicale
Charcot-Debove in 1892 and with Achard, Manuel de Médecine in eight volumes
and Manuel de Thérapeutique in three volumes [7].
Debove described the entity, primary splenomegaly, a condition previously rec-
ognized by Gaucher in 1882 (Table8.1):
Primary splenomegaly, which I believe should be separated from other splenic hypertro-
phies, is characterized by hypertrophy or an increase in spleen volume and progressive
anemia without an increase in the number of leukocytes or alteration of the lymph nodes.
The onset is sometimes insidious, and hypertrophy of the spleen is present during the initial
examination. At other times the disease is announced by local phenomena, including weight
loss, uneasiness, and pain in the left side, sometimes even by painful crises analogous to
visceral colic, which is probably the expression of an attack of localized peritonitis. Finally,
the disease begins at other times with general phenomena: weakness, pallor, apathy, asthe-
nia, and weight loss. After a variable time, the spleen becomes greatly enlarged, to the point
of sometimes occupying the entire left half of the abdomen. Its shape is preserved, but its
consistency is increased, assuming a woody hardness on palpation. The liver protrudes one
to two ngerbreadths from the false ribs. However, there is neither ascites, jaundice, or dila-
tion of veins on the abdominal wall. The spleen, thus hypertrophied, may cause heaviness,
tightness, and soreness in the region. Sometimes the pain resembles intercostal neuralgia
and is so severe as to recommend a splenectomy. There is no relationship between the size
of the spleen and the degree of anemia. The examination of the blood reveals marked hypo-
globulism with decreased hemoglobin. There are variable digestive disorders. Hematemesis
is often observed, most likely due to congestion of the portal vein. This hematemesis recurs,
in some cases, several times and, if frequent enough, can be life-threatening [8, p.506].
Thus, Debove described the condition splenomegaly. Although he classied this as
primary splenomegaly, hepatomegaly with splenomegaly is consistent with portal
hypertension (secondary splenomegaly).
8 Spleen Signs