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Thomas Kiefer
Editor

Chest Drains in
Daily Clinical Practice

123
Chest Drains in Daily Clinical
Practice
Thomas Kiefer
Editor

Chest Drains in Daily

Clinical Practice
Editor
Thomas Kiefer
Lungenzentrum Bodensee
Klinikum Konstanz
Konstanz
Germany

ISBN 978-3-319-32338-1    ISBN 978-3-319-32339-8 (eBook)

DOI 10.1007/978-3-319-32339-8

Library of Congress Control Number: 2016958757

© Springer International Publishing Switzerland 2017

This work is subject to copyright. All rights are reserved by the Publisher,
whether the whole or part of the material is concerned, specifically the rights of
translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduc-
tion on microfilms or in any other physical way, and transmission or information
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The use of general descriptive names, registered names, trademarks, service
marks, etc. in this publication does not imply, even in the absence of a specific
statement, that such names are exempt from the relevant protective laws and
regulations and therefore free for general use.
The publisher, the authors and the editors are safe to assume that the advice and
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lication. Neither the publisher nor the authors or the editors give a warranty,
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Printed on acid-free paper

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The registered company is Springer International Publishing AG
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To Gerlinde and Julia
Preface

This book is addressed to all professions who have to deal

with chest drains – not only physicians of any specialisation
but also nurses. It is my strong conviction that – with the
exception of very few – all who work in somatic acute and
emergency medicine should be able to manage chest drains
and chest drain systems properly!
This is so important because a chest drain managed in the
wrong way can be truly dangerous or even life threatening for
the patient.
According to my knowledge, so far there is no such an
elaborated book dealing with chest drains and chest drain
systems covering all issues – beginning with anatomy and
ending up with pain management and physiotherapy. That’s
why I am very grateful that the publishing company Springer
made this project possible. I also want to thank my co-­
authors, who made it happened and helped publish this book
just on schedule due to their tremendous work. My special
thanks concerning this English edition of the text book go to
Dr. Sarah Counts from Yale University who transformed my
“school English” into a readable textbook!
Those who will read the entire book will mention that
there are some reiterations concerning one or more chapters.
This is intended! On the one hand it may make sense to
repeat important aspects from a didactic point of view. On
the other hand, the more experienced reader will pick just the
chapter they are interested in.
I am open to critics and would appreciate to receive critics
because this is the only way to improve and which hopefully
may lead to a second edition!
Konstanz, September 2016

vii
Contents

1 Anatomy of the Chest Wall and the Pleura . . . . . . 1

Peter Ehrhardt

2 Physiology and Pathophysiology of the Pleura . . . 17

Stefano Cafarotti, Adalgisa Condoluci,
and Rolf Inderbitzi

3 Indications for Draining the Chest . . . . . . . . . . . . . . 29

Christian Kugler

4 Different Kinds of Drains (−Catheters) . . . . . . . . . 61

Erich Hecker

5 Different Drainage Systems and Philosophies . . . . 75

Thomas Kiefer

6 Inserting a Chest Drain: How to Do . . . . . . . . . . . . 93

Thomas Kiefer

7 Complications of Chest Drain Insertion

and Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . 107
Jan Volmerig

8 Care of Patients Having a Chest Drain . . . . . . . . . . 133

Fabian Graeb

9 Management of the Pleural Space: Handling

of Chest Tubes and Drainage Systems . . . . . . . . . . . 153
Thomas Kiefer

ix
x Contents

10 Pain Management in Patients

with a Chest Drain . . . . . . . . . . . . . . . . . . . . . . . . . . . 171
Dana Mergner

11 Physiotherapy in Patients with Chest Drains . . . . . 181

Kathrin Süss

12 Removal of the Chest Drain: How to Do It . . . . . . 189

Thomas Kiefer

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 195
Contributors

Stefano Cafarotti Chirurgia toracica EOC, Ospedale San

Giovanni, Bellinzona, Switzerland
Adalgisa Condoluci Chirurgia toracica EOC, Ospedale San
Giovanni, Bellinzona, Switzerland
Sarah Counts Cardiothoracic Surgery, Yale School Medicine,
New Haven, CT, USA
Peter Ehrhardt Klinik für Unfallchirurgie, Orthopädie und
Handchirurgie, Klinikum Konstanz, Gesundheitsverbund
Landkreis Konstanz, Konstanz, Germany
Fabian Graeb Karl-Olga-Krankenhaus ICU, Stuttgart,
Germany
Erich Hecker Klinik für Thoraxchirurgie, Ev. Kranken­
hausgemeinschaft Herne, Castrop-Rauxel gGmbH, Herne,
Germany
Rolf Inderbitzi Chirurgia toracica EOC, Ospedale San
Giovanni, Bellinzona, Switzerland
Thomas Kiefer Klinik für Thoraxchirurgie, Lungenzentrum
Bodensee, Klinikum Konstanz, Konstanz, Germany
Christian Kugler Klinik für Thoraxchirurgie, Lungen Clinic
Grosshansdorf GmbH, Großhansdorf, Germany
Dana Mergner Sektionsleiterin Schmerztherapie, Klinikum
Konstanz, Konstanz, Germany

xi
xii Contributors

Kathrin Süss Asklepios Fachkliniken München-Gauting,

Gauting, Germany
Jan Volmerig Klinik für Thoraxchirurgie, Ev. Kranken­
hausgemeins chaft Herne, Castrop-Rauxel gGmbH, Herne,
Germany
Chapter 1
Anatomy of the Chest Wall
and the Pleura
Peter Ehrhardt

1.1 Introduction
The chest wall represents the outer covering of the chest and
shelters the organs inside the thorax. Due to its mobility and
the wall structure, which is comparable to a cage, it plays an
active role in the function of breathing when the intrathoracic
volume is changed. During inspiration the volume increases
and during expiration it decreases, therefore generating a
negative or a positive pressure respectively. According to the
law of Boyle-Mariotte, gases move constantly as a result of
pressure and volume.
The chest wall is construced as a cage with variable rods.
The spaces within the rods are the intercostal spaces. This
space has to be air tight, robust in regards to pressure, while
also being adequately mobile for ventilation. This is possible
with the help of the pleural space which is created by two
sheets of pleura, the parietal and visceral layers. The pleural
space allows the lung to slide during inspiration and expira-
tion, keeping the lung expanded due to adhesive forces.

P. Ehrhardt
Klinik für Unfallchirurgie, Orthopädie und Handchirurgie,
Klinikum Konstanz, Gesundheitsverbund Landkreis Konstanz,
Luisenstr. 7, 78464 Konstanz, Germany
e-mail: Peter.Ehrhardt@glkn.de

© Springer International Publishing Switzerland 2017 1

T. Kiefer (ed.), Chest Drains in Daily Clinical Practice,
DOI 10.1007/978-3-319-32339-8_1
2 P. Ehrhardt

1.2 The Compostion and Margins

of the Chest Wall
The sternum and cartilage of ribs 1–10 represent the anterior
chest wall. The posterior part consists of 12 thoracic vertebrae
and the posterior aspects of ribs 1–12. Laterally the chest cav-
ity consists of ribs 1–12.
The thoracic aperture is created by the first ribs, the first
thoracic vertebra, the upper edge of the sternum, the nerves,
and the blood vessels, which together with the trachea and
esophagus compose the upper opening of the chest.
The lower chest aperture is much wider and is formed by
the costal arch, the free ribs (11th and 12th), and the sternum.
The costal arches form an angle called the Angulus infraster-
nalis (epigastric angle) that opens caudally. This varies
according to age, sex, and body compostion. In infants and
women it is typically wider as compared to men (70°).
The diaphragm seals the lower chest aperture. Due to the
negative pressure inside the pleural space, it is sucked crani-
ally creating a dome.
The space between two ribs is called the intercostal space.
The space is strengthened with muscles and ligaments which
prevent sinking during inspiration. This whole construction is
called the chest wall.
Anatomical regions are defined by the chest wall’s surface:
Ventral: Regio pectoralis / mammaria, Regio infraclavicu-
laris, Regio parasternalis, Regio hypchondriaca
Lateral: Regio axillaris
Dorsal: Regio suprascapularis, Regios scapularis, Regio
infrascapularis
Orientation during a clinical examination and/or thera-
peutic procedure can be done with the assistance of anatomi-
cal lines: (Figs. 1.1 and 1.8)
– Linea sternalis
– Linea parasternalis
– Linea medioclavicularis (MCL)
– Linea axillaris anterior, media, posterior
– Linea scapularis
– Linea paravertebralis
 Chapter 1. Anatomy of the Chest Wall and the Pleura 3

Linea mediana anterior

Linea sternalis
Linea parasternalis
Linea medioclavicularis

Figure 1.1 Anatomical lines of the anterior chest wall (Tilmann BN

(2010), Ventrale Rumpfwand. In: Anatomie, Springer-Verlag Berlin
Heidelberg, S. 816, Abb. 21.1)

Certain ribs and intercostal spaces can be located by pal-

pating these structures.
The margin between the corpus and manubrium sterni is
called the angulus sterni (Ludovici or sternal angle) which is
visible and located next to the second rib. The first ribs cannot
4 P. Ehrhardt

be palpated as they are covered by the clavicles. The second

ribs and below can be identified.

1.3 Bony Components and Joints

The sternum consists of the manubrium sterni, the corpus
sterni, and the processus xiphoideus. The manubrium is
linked with the clavicles on each side and also with the first
ribs with the help of cartilagenous joints, called synchondro-
ses. Ribs 2–7 articulate laterally at the corpus sterni. The
xiphoid is not attached to any ribs.
In general, the ribs in humans are numbered the same as
their corresponding vertebral bodies. There are 12 pairs of
ribs with some of them rudimentary and fused with the ver-
tebral bodies in so called rib stumps.
The ribs are divided into real ribs (costae verae, 1–7) that
have sternal joints, false ribs (costae spuriae, 8–10) with
cartilagenous joints to the costal arch (arcus costalis), and
free ribs (costae fluctuantes, 11–12) that end in the soft tissue
of the lateral chest wall. The 12th rib is not always present.
The head of the rib (caput costae) articulates laterally with
the vertebral body and there is a second articulation between
the transverse process and the vertebral body. The rib neck is
located between these articulations and acts as the longitudinal
axis for rib movement. The neck of the rib is followed by the
body of the rib (collum costae), turning anteriorly at an angle
(angulus costae). Anteriorly all bony tissue is followed by carti-
lage which represents the elastic link with the sternum (Fig. 1.2).
The ribs move upwards during inspiration around their rib
neck and downwards during expiration. This volume increase
and decrease is due to changes in both the sagital and trans-
verse directions. The mobility of the chest is guaranteed by the
joints between the vertebral bodies and ribs as well as by the
interactions between the cartilage, sternum, and costal arch.
The costosternal complex moves cranially and ventrally
(sagittal extension). The lower ribs move towards cranially
and laterally to increase the diameter of the chest in the
transverse direction (Fig. 1.3).
 Chapter 1. Anatomy of the Chest Wall and the Pleura 5

Figure 1.2 Bony chest (a) view from anterior, (b) view from poste-
rior (Tilmann BN (2005), Rumpfskelett In: Atlas der Anatomie,
Springer-Verlag Berlin Heidelberg, S. 187/188, Abb. 4.1, 4.2. (jeweils
oberer Abschnitt ohne Becken))
6 P. Ehrhardt

a b

Figure 1.3 Movement of the ribs during inspiration and expiration

(van Gestel A et al. (2010), Atembewegungsapparat. In:
Physiotherapie bei chronischenAtemwegs- und Lungenerkrankungen,
Springer-Verlag Berlin Heidelberg, S. 17, Abb. 2.2)

At the lower edge of the rib, the sulcus costaeis is located

where the intercostal vessels and the intercostal nerve run. The
intercostal muscles are attached to the edges of the ribs (Fig. 1.9).

1.4 Muscles of the Chest Wall

The lung itself does not have any muscles and therefore the
muscles of the chest wall and diaphragm are responsible for
the movements that let us breathe. Some of the chest wall
muscles can be used as helpful anatomical landmarks.
At the neck, the chest is attached by the three scalene
muscles, the intercostal muscles, and the muscles eminating
from ribs 1 and 2 to the vertebral bodies (1–7). They are
responsible for the flexion of the upper spine anteriorly and
for lifting the ribs during inspiration (Fig. 1.4).
The Pectoralis major muscle covers the upper and lateral
part of the chestwall like a shelf and creates the outline of the
 Chapter 1. Anatomy of the Chest Wall and the Pleura 7

Figure 1.4 Chestwall muscles, view from anterolateral (Tilmann

BN (2005), Muskeln der Brustwand. In: Atlas der Anatomie,
Springer-Verlag Berlin Heidelberg, S. 204, Abb. 4.30 (jeweils oberer
Abschnitt ohne Becken))

chestwall. It originates from the medial clavicle, the sternum,

the cartilages of ribs 5–7, as well as from the rectus sheath,
and inserts at the tuberculum majus humeri. The lower edge
of the muscle creates the anterior axillary plication. This
muscle causes a strong adduction and rotation of the arm and
its lower portion acts as an auxillary breathing muscle.
8 P. Ehrhardt

Figure 1.5 Muscles of the anterior chestwall (Tilmann BN (2005),

Muskeln der Brustwand. In: Atlas der Anatomie, Springer-Verlag
Berlin Heidelberg, S. 207, Abb. 4.33 (oberer Abschnitt))

The Pectoralis minor muscle is completely covered by the

Pectoralis major muscle. It derives from the ribs 3–5 and con-
nects to the processus coracoideus of the shoulder. This
muscle pulls the shoulder anteriorly and downwards and also
lifts the chest as an auxillary breathing muscle (Fig. 1.5).
The intercostal muscles consist of two layers of short
muscles between the ribs oriented in different directions. The
more external layer is made of the intercostales externi muscle
which is oriented craniolaterally to mediocaudally from the
lower edge of the upper rib to the upper edge of the rib
below. The intercostales interni muscle is located underneath
oriented opposite of the externi and therefore from cranio-
medial to laterocaudal. Both muscles help to maintain the
appropriate tension of the rib cage. The outer muscles lift the
chest up (inspiration) and the inner ones lower it and
strengthen expiration.
A soft tissue layer allows room for the intercostal vessels
and nerve and separates the intercostales interni muscles from
the intercostales intimi muscles. These muscle fibers are
oriented in the same direction. The intercostales interni
 Chapter 1. Anatomy of the Chest Wall and the Pleura 9

Figure 1.6 Muscles of the anterior chest wall – view from behind
(Tilmann BN (2005), Muskeln der Brustwand. In: Atlas der
Anatomie, Springer-Verlag Berlin Heidelberg, S. 205, Abb. 4.31)

muscles that create a longer layer of muscle going over the

first and second rib are called Subcostales muscles.
Muscles running transversely from the inner surface of the
sternum towards the ribs are called the transversus thoracis
muscles (Fig. 1.6).
The lower border of the chest cavity made up of the
diaphragm which originates from the lower chest aperture
and the vertebral bodies 1–4 of the lumbar column. The
10 P. Ehrhardt

Figure 1.7 Diaphragm, view from above (Tilmann BN (2005),

Hintere Rumpfwand. In: Atlas der Anatomie, Springer-Verlag
Berlin Heidelberg, S. 212, Abb. 4.40b)

diaphragm is a muscle measuring 3–5 mm thick which creates

a dome with a tendon in the center. In regard to surface area
it is the largest muscle in the human body. Due to the elastic
recoil of the lung which is transferred throughout the pleural
cavity, the diaphragm lifts upwards creating the diaphrag-
matic dome which is slightly higher on the right side. The top
of the dome can vary about 6–7 cm from inspiration to expi-
ration respectively. Contraction of the diaphragmatic muscle
causes it to flatten and thus increases the volume of the chest
cavity (Fig. 1.7).

1.5 Topography of the Chest Cavity

The pleura is a serous skin that consists of mesothelium, a
squamous epithelium (one layer), and the lamina propria.
The pleura covers the lung and chest wall. There are two lay-
ers called the visceral pleura and the parietal pleura which
are separated by a capillary gap filled up with 2–4 ml of fluid.
This configuration allows the lung to slide up and down and,
despite the elastic recoil, keeps the lung expanded.
 Chapter 1. Anatomy of the Chest Wall and the Pleura 11

In the pleural cavity there is a negative pressure due to the

elastic recoil of the lung fighting against the adhesive forces
generated by the pleural fluid. These forces during inspira-
tion pull the lung to follow the chest wall.
The visceral pleura covers the entire lung with the excep-
tion of the hilar region. The parietal pleura covers the inner
chest wall similar to wallpaper. The regions where the parietal
pleura covers the mediastinum, chest wall, or diaphragm are
correspondingly named Pars mediastinalis, Pars costalis and
Pars diaphragmatica. Both of the pleural cavities are closed
spaces completely filled with the lungs without any connection
to each other, the atmosphere, or the other lung. The shape of
the pleural cavity is determined by the lordosis of the vertebral
column. The domes of the diaphragm create an optimal shape
for expansion of the volume of the chest cavity during inspira-
tion. In the middle, the two pleural cavities are separated by
the mediastinum anteriorly and vertebral collum posteriorly.
At the middle aspect of the sternum, the two pleural cavities
are separated by the parietal pleura which are separated by the
parietal pleura and are in contact with each other.
Cranially the pleural cavity extends for 2–3 cm above the
upper chest aperture (Cupula pleurae).
The pleura cavities have narrow spaces called Recessus
pleurales where the lung can expand which are located ante-
riorly between the chest wall and sternum and laterally
between diaphragm and chest wall. The recessus costomedias-
tinalis on the left side between pericardium and chestwall is
somewhat wider as compared to the right side. The recessus
costodiaphragmaticus creates an additional deep semicircular
space reaching nearly to the origin of the diaphragm (Fig. 1.8).
In the back, the recessus may extend up to 2 cm below the
12th rib therefore putting it in the neighborhood of the right
lobe of the liver and on the left towards the stomach, spleen,
and upper pole of the kidney (Fig. 1.8, Table 1.1). The margins
of the lung shift during inspiration and expiration anteriorly
for 1–2 cm and in the back for 5–6 cm. Normally the lower
margin of the right lung is 1–2 cm above the lung margin on
the left side.
12 P. Ehrhardt

Figure 1.8 Margins of the lung and the pleura (Larsen R et al.
(2004), Anatomie der Atmungsorgane. In: Beatmung, Springer-
Verlag Berlin Heidelberg, S. 16, Abb. 1.9)

Table 1.1 Margins of the lung and pleura as projected on the chest-
wall during resting expiratory position [2]
Mid Mid Paravertebral
Sternal clavicular axillary line
line line lini
Margin of 6th rib 7th rib 9th rib 12th rib ≙ 12th
the plaura DP
Margin of 6th rib 6th rib 8th rib 11th rib ≙ 10th
the lung DP
a
DP = dorsal process

There are projections on the bony chest wall of the fissures

(in resting expiratory position):
The fissure between left upper and lower lobe (Fissura
obliqua) is at the level of the fourth rib posteriorly and the
third dorsal process respectively and sinks down anteriorly to
the cartilagenous junction of the sixth rib with the sternum.
On the right side, the horizontal fissure between the upper
and lower lobe is located above the fourth rib in the axillary
line heading towards the sternum and the oblique fissure
 Chapter 1. Anatomy of the Chest Wall and the Pleura 13

Fascia thoracica

M. serratus anterior

V. intercostalis
M. intercostalis intimus
A. intercostalis
N. intercostalis M. intercostalis internus Mm.intercostales
M. intercostalis externus
Punktionskanüle
Pulmo

Costa
Pleura visceralis
Pleuraspalt
Pleura parietalis
Fascia endothoracica

Figure 1.9 Upright section through the posterior chest wall at the
level of the posterior axillary line (Christ B. (2003) Skelett- und
Muskelsystem. In: Drenckhahn D (Hrsg) Anatomie Band 1, 16. Aufl.
Urban & Fischer Verlag München Jena with permission from
Drenckhahn, Benninghoff, Anatomie Band 1, 17.Auflage 2008 ©
Elsevier GmbH, Urban & Fischer, München)

going down to the sixth rib. In between these two is the loca-
tion of the middle lobe [3].
The innervation of the costal pleura is provided by the cor-
responding intercostsal nerve and the mediastinal and dia-
phragmatic pleurae by the phrenic nerve. These nerves have
a lot of pain fibers. Pain is noticed as an acute stabbing pain
and can be localized precisely.

1.6 Layers of the Chest wall

The anterior and lateral parts of the chestwall in particular
are easily accessible for invasive procedures. Therefore a
deep knowledge the anatomy is mandatory. Three layers can
be described:
• Superficial layer consisting of skin, subcutaneous soft and
fatty tissue (including the mammary gland, which is attached
via the membrana sterni with the sternum. Fig. 1.9).
14 P. Ehrhardt

• Middle layer consisting of muscles of the chest and the

abdomen including their fascias
• Deep layer consisting of the skeleton, intercostal muscles,
blood vessels/nerves, fascia endothoracica (covers the
inner surface of the chest wall), and parietal pleura.
The Fascia endothoracica lies in between the inner muscles
of the chest wall and the pars costalis of the parietal pleura
which both are very strongly combined. In a cranial direction
it continues as the fascia of the neck and caudally it covers
the diaphragm.

1.7 Nerve and Blood Supply

Innervation of the chest wall is mainly supplied by the inter-
costal nerves (intercostales nerves) which derive from the
spinal cord at each segmental level as rami anteriores. They
run along the lower edge of the ribs. They supply the intercos-
tal muscles as well as the skin. In addition there are fibers that
go to the perspiratory glands.
Blood supply of the chest wall is caried out by the
intercostal arteries (intercostales arteries) and by the
internal mammary artery (thoracica interna artery) which
create a ring of vasculature in the region of the anterior
chest wall.
Intercostal arteries 3–11 are directly derive from the aorta
whereas arteries 1–2 derive from the truncus costocervicales.
They all run along the lower edge of the ribs and anastomose
with the Rr. intercostales anteriores anteriores which derive
from the internal mammary artery.
Intercostal veins run together with the arteries and drain
into the azygos vein posteriorly and anteriorly into internal
mammary vein into the subclavian vein.
At the lower edge of the ribs, the structures are found in
the following order: vein, artery, and nerve (Fig. 1.10).
 Chapter 1. Anatomy of the Chest Wall and the Pleura 15

Figure 1.10 Arterial blood supply of the chestwall (Tilmann BN

(2005), Rücken- und Nackenmuskeln. In: Atlas der Anatomie,
Springer-Verlag Berlin Heidelberg, S. 218, Abb. 4.49)

Literature
1. Drenckhahn D, Benninghoff WJ (HRSG). Anatomie Band 1, 17.
Aufl. Elevier GmbH, Urban & Fischer, München; 2008.
2. Duncker HR, Kummer W. Atemsystem. In: Drenckhahn D
(Editor) Anatomie Band 1, 16. Aufl. Urban & Fischer Verlag
München Jena; 2003.
3. Larsen B. et al. Anatomie der Atmungsorgane. In: Larsen B
(Editor) Beatmung. Berlin Heidelberg: Springer; 2004.
4. Roberts KP, Weinhaus AJ. Vessels oft he thoracic wall. In: Iaizzo
PA (Editor) Handbook of cardiac anatomy, physiology and
devices. Totowa: Humana Press Inc; 2005.
5. Tillmann BN. Atlas der Anatomie, Springer Heidelberg; 2005.
6. Tillmann BN. Ventrale Rumpfwand. In: Zilles K, Tillmann BN
(Editor), Anatomie, Springer Heidelberg, Berlin; 2010.
7. Van Gestel AJR, Teschler H. Physiotherapie bei chronischen
Atemwegserkrankungen. Springer Berlin, Heidelberg; 2010.
Chapter 2
Physiology
and Pathophysiology
of the Pleura
Stefano Cafarotti, Adalgisa Condoluci, and Rolf Inderbitzi

2.1 Introduction
The physiology and pathophysiology of the pleural space can
be explained simply and reasonable by reviewing the
functional and anatomic composition of the pleura. The
­
pleura represents the connection between the lung and chest
wall and acts as a crucial component for breathing mechanics.
The pressure present in between the two pleura sheets is also
important for the physiology and pathophysiology of the pleu-
ral space and its organs. The pressure ratio from the outer side
of the lung and heart on one side to the inner side of the chest
wall on the other side is regulated by the intrapleural pressure.
The lungs, heart, and chest wall are expandable. The volume of
an expandable object depends on it elasticity and the differ-
ence in pressure from the inner to the outer side of the object.
In the pleural cavity, the intrapleural pressure plays an impor-
tant role concerning the volume of these three very important
structures. The lymph located in the parietal pleura together
with the intra pleural pressure are responsible for the produc-
tion of the pleural fluid and its consistency.

S. Cafarotti • A. Condoluci • R. Inderbitzi (*)

Chirurgia toracica EOC, Ospedale San Giovanni,
6500 Bellinzona, Switzerland
e-mail: Rolf.Inderbitzi@eoc.ch

© Springer International Publishing Switzerland 2017 17

T. Kiefer (ed.), Chest Drains in Daily Clinical Practice,
DOI 10.1007/978-3-319-32339-8_2
18 S. Cafarotti et al.

The pleural fluid creates a film of fluid between the pari-

etal and visceral pleural sheets which is of functional impor-
tance. The quality and quantity of the pleural fluid represents
the physiological or pathophysiological condition of the
pleural space. The pleural fluid is also accessible for diagnos-
tic procedures.

2.2 Functional Anatomy and Biology

2.2.1 Pleura

The pleura consists of two sheets (parietal and visceral pleura)

which meet at the hilum and distally create a plication called
the pulmonary ligament. The reflective surfaces of the healthy
pleura (Fig. 2.1) are separated by the pleural space which is a
capillary space filled with pleural fluid (5–15 ml). The fluid
allows the pleural sheets to slide along each other. This fluid
film, under healthy conditions, is free from air and gas. This
allows for intrapleural pressure modulation according to posi-
tioning of the chest and for the sliding of the intrathoracic
organs along the chest wall. The visceral pleura is 100–200 μm
thick and is strongly adherent to the lung. The superficial
mesothelium (covering cell layer) is made up of mesothelial
cells which are connected to each other by desmosomes and
have surface microvilli. There are three layers of soft tissue
limited by a basal membrane. The main layer of the pleura
consists of soft tissue covered by inner and outer boundary
lamella. Between these two lamellas are where the vessels are
found (Fig. 2.2). The inner lamella is located next to the alveo-
lar walls and is connected with the interstitial soft tissue of the
lung in the fissures. The parietal pleura is located via the endo-
thoracic fascia next to the intercostal muscle and the ribs.

2.2.2 Vessels

The pleural vessels run in the soft tissue main layer. The
blood supply of the visceral pleura is located in the area of
 Chapter 2. Physiology and Pathophysiology of the Pleura 19

Figure 2.1 Normal, transparent Pleura: Left subclavian artery and

phrenic nerve are visible

the ribs and the diaphragm via the pulmonary arteries and
bronchial arterial branches which create anastomoses with
the pulmonary arteries in all other areas. The parietal pleura
is fed by the intercostal arteries in the regions of the ribs and
by the rami intercostales of the internal mammary arteries.

2.2.3 Lymph Vessels

The lymphatics of the visceral pleura are located close to the

lung in the soft tissue main layer of the pleura. Of special
importance are lymphatic stomata which are 2–8 μm in diam-
eter in the parietal pleura. In these areas the pleural space is
directly connected to the draining lymphatic system [1]. The
20 S. Cafarotti et al.

Figure 2.2 Layer with arterial and venous capillaries

pleural fluid circulates at a speed of 0.2 ml/kg/h, which allows

for a total exchange of the fluid within one hour.

2.2.4 Mesothelium

The mesothelium is a tissue with a high metabolism that is

able to produce different mediators and soluble factors for
chemotactic activity and phagocytic activity. Mesothelial cells
not only play an active roll in inflammatory processes but
also participate in tissue repair as they synthesize collagen
types I, II, and IV. Under physiologic circumstances, the pleu-
ral cell surfaces have mononuclear phagocytes that produce
cytokines IL-1P, TNF-a, IL-8, and LTB-4 [3].
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 CONGESTION OF THE LIVER IN THE
HORSE.
Causes. Beside the general causes above mentioned, may be
specially named, musty, decomposed, and irritant fodders: those
which like green legumes, are easily fermented; and those which
contain stimulating volatile oils or carminative principles. They are
also especially exposed to such causes as severe and prolonged work
under a hot sun, the nervous atony which causes vaso-dilatation in a
hot climate, and such traumatisms as come from falls, kicks, goring,
and blows by shafts, poles and clubs. These especially induce active
congestion. The passive forms come mainly from obstruction in the
lungs, or heart (dilatation, right valvular insufficiency, pericarditis,
hydropericardium, myocarditis, fatty degeneration, endocarditis), or
in the posterior vena cava.
Lesions. The congested liver is enlarged and deeply colored with
blood. The weight of twenty to thirty pounds is often attained. While
the color is of a deep red throughout, there are spots of a still darker
hue indicating the seat of subcapsular or deeper seated hemorrhages.
The color varies according as the congestion is passive or active. In
the former the coloration is deeper in the centre of the acinus
(nutmeg liver) indicating congestion of the hepatic veins, while in the
latter the periphery of the acinus may be most deeply stained
implying congestion of the portal vein. The consistency of the organ
is diminished, and the more acute the attack the greater the friability.
In such cases there is a parboiled appearance indicating granular and
commencing fatty degeneration. Under the microscope the relative
distension of the intralobular, and interlobular veins and the hepatic
capillaries becomes more distinctly marked and the presence of
pigment and fatty granules and the lack of protoplasm and nuclei in
the hepatic cells indicate their progressive changes. When the
peripheral cells are pale from fatty granules the contrast between the
light margin and dark centre of the acinus, makes the mottled or
nutmeg aspect of the liver much more pronounced.
 In old standing cases of passive congestion the liver may be the
seat of fibroid degeneration, extending from the capsule inward in
bands or trabeculæ, and giving to the organ a firm resistant character
(sclerosis, cirrhosis).
Symptoms. The symptoms are general and suggestive rather than
pathognomonic. There are dullness, prostration, unsteady walk,
pendent head, with occasional jerking, semi-closed eyes, redness of
the conjunctiva, slight colicy pains, arching of the loins, muscular
tremblings and decubitus on the left side rather than the right. The
more definite symptoms are tenderness on percussion with the
closed fist over the last ribs (the liver) especially on the right side,
increase of the area of hepatic percussion dullness (which may be
rendered valueless by a loaded colon), the presence of a slight icterus
in the conjunctiva and urine, and an increase of the urine secreted
and an excess of the contained urea.
In passive cases however the obstruction to the escape of blood
from the liver prevents the development of icteric symptoms, of
uræmia and of polyuria. In all such cases however there follows a
general congestion of the portal system and if it persists for any
length of time gastro-intestinal congestion and catarrh and even
ascites may develop.
In all cases alike the history of the attack will help towards a
satisfactory diagnosis.
Prevention. A rational hygiene embracing daily work or exercise,
moderate laxative diet, green food in its season, pure cool air are
important precautions.
Treatment. A moderate supply of green or laxative food, the
withholding for the time of grain, and especially of maize, wheat or
buckwheat, saline laxatives daily, and a stimulating embrocation or
blister to the tender hypochondrium are the most important
measures. Exercise in a box stall, or still better in a yard or paddock
in the intervals between more systematic work forms an important
adjunct to medicine. As a laxative sulphate of soda is to be preferred
at first in a full cathartic dose and later in a daily amount sufficient to
relax the bowels. Given in a bucket of water every morning before the
first meal a very small dose will be effective.
 CONGESTION OF THE LIVER IN THE DOG.
Active congestion is very rare excepting in over-fed and indolent
family pets. Passive congestion induced by diseases of the lungs and
heart is however far from uncommon.
Lesions. True to their origin these usually appear as the spotted
nutmeg liver with the deep congestion in the centre of the acini. For
the same reason the fibroid degenerations shown in chronic cases,
show the firm fibroid neoplasm chiefly around the hepatic veins.
Granular, fatty and pigmentary degeneration of the cells are found as
in the solipeds.
Symptoms. These are as obscure as in the horse. There is always a
history of a sluggish, gourmandizing life, and in the early stages, a
manifestation of embonpoint which suggests a torpid liver. Further
suggestions may also be obtained from coexisting diseases of the
lungs, or heart, from gastro-intestinal catarrh, from piles, or ascites.
Then there is at times a slight icterus of the conjunctiva and urine.
Finally tenderness on percussion on the right hypochondrium,
decubitus on the left side, and an increased area of dullness on
percussion may afford useful hints for diagnosis.
Treatment. In the rare cases due to infection from the intestine, an
active saline purgative followed by antiseptics (salol, naphthalin,
naphthol, etc.,) daily will be of value. It is also desirable to keep up
the action of the bowels by morning doses of salines. In cases
consequent on chest disease attention must be given to such primary
trouble. In all cases a restricted laxative diet, and graduated but
increasing exercise in the open air are demanded.
 HEPATIC HÆMORRHAGE OR RUPTURE.
Causes: Mechanical injuries, falls, blows, kicks, degenerations, amyloid, fatty,
granular, congestion, neoplasms, glanders, tuberculous, myomatous, microbian
infection. In the horse, disease of liver, heart, lungs, hepatic artery, portal vein,
degenerations following overfeeding, idleness, foreign bodies, arsenic, phosphorus,
parasites, violent movements in colic, running, draught, leaping. In the dog,
pampering and traumatism. In cattle forced feeding, emaciation, microbian
infection. In birds, tubercle, tæniasis, microbian infection. Lesions: extravasation,
intracapsular, or through capsule into the peritoneal cavity. The extravasation
bulges of a deep black, covering a dark softened, pulpy, hepatic tissue, with light
colored fatty tissue around. Clots may be stratified from successive bleedings. Liver
usually enlarged. Symptoms: onset sudden, or preceded by stiffness, soreness and
other signs of hepatic trouble. Extensive rupture, entails weakness, unsteady gait,
perspiration, pallor of mucosæ, small weak rapid pulse, palpitations, dilated
pupils, rolling eyes, amaurosis, tremors, convulsion in case of survival, coldness,
œdemas. Death in five hours to five days. Risk of relapse in recovering cases.
Treatment: rather hopeless, rest, laxative, ergot, ferric chloride, tannic acid, witch
hazel, cold water, snow or ice to right side. In meat producing animals fatten.
Causes. Hemorrhage and rupture of the liver are closely correlated
to each other, the accumulation of extravasated blood in the
parenchyma in the one case leading to over distension of the capsule,
and the laceration of this capsule and of the adjacent substance of
the liver occurring in the other as a mere extension of the first. They
usually occur as the direct result of mechanical injury (falls, blows,
kicks) acting on a liver already softened and friable through disease.
These predisposing degenerations may be amyloid (Caparini, Johne,
Rabe), fatty (Julien, Gowing, Adam, Siedamgrotzky), granular
softening, hepatitis or congestion (Zundel), glander neoplasms
(Mathis), tubercles, angiomata (Trasbot), microbian infection
(Stubbe), tumors (Brückmüller).
In the horse predisposing conditions may be found in diseases of
the liver, heart or lungs, in embolism of the hepatic artery (Wright),
in obstruction of the portal vein (Pierre), in infarction of the liver, in
degeneration with softening, in sarcomatous, melanotic, glanderous
or cancerous deposits in its substance, in degenerations consequent
on over feeding, idleness, congestions, on the penetration of husks of
grains into the liver substance, on arsenical or phosphorus
poisoning. The presence of flukes, echinococci and other parasites
may also cause congestion and softening. To the immediate or
traumatic causes above named may be added the violent movements
attendant on a severe attack of colic, and violent exertions in
running, draught, leaping, etc. (Friend).
In the dog we must recognize all the pampering conditions which
predispose to congestion and degeneration, together with more
direct operation of kicks, blows, falls, fights, over exertion, etc.
In cattle a forcing regimen is especially predisposing, and yet the
loss of vigor resulting from a diametrically opposite treatment, must
be accepted as an occasional cause. Stubbe found in emaciated cows
miliary hemorrhagic infarcts of a dark red color which gradually
extended to an inch or more in diameter. These he traced to
microbian infection coming by way of the chronic intestinal lesions
which are common in old cows. The final result of such infarctions
was loss of hepatic substance and the formation of cicatricial tissue
with a marked depression on the surface of the organ.
In birds fatal hepatic hemorrhages occur in connection with local
tubercle (Cadiot), tæniasis of the liver, or microbian infection.
Lesions. The hemorrhage may take place into the substance of the
liver only, or the capsule may be lacerated so that the blood escapes
into the peritoneal cavity in considerable quantity.
In the horse it usually occurs in the right or middle lobe, rarely in
the left. There may be one or more hemorrhagic effusions varying in
size from a cherry to a duck’s egg, or even an infants’ head (Lorge).
This projects from the surface of the organ and its deep black
contrasts strongly with the white of the adjacent capsule. When laid
open the hepatic tissue is seen to be softened and pulpy, and its dark
color forms a striking contrast with any surrounding fatty liver. Any
form of degeneration may be revealed on microscopic or chemical
examination. Not unfrequently small clots of blood form under the
capsule raising it in the form of little sacs. Such clots are usually
stratified indicating a succession of small hemorrhages.
When the capsule is torn, the lesion may extend from one surface
of the organ to the other, and the edges, smooth, uneven or fringed,
are united together by a blood clot.
 In case of hemorrhagic infarcts the lesion usually has a distinctly
conical outline corresponding to the vascular distribution. These are
especially characteristic of cases supervening on heart disease.
The volume of the liver is usually increased and the weight may
reach 30 lbs. (Schmeltz), 34 lbs. (Lorge), or even 66 lbs. (Trasbot).
In other domestic animals analogous lesions are found modified
largely according to the size of the subject.
Symptoms. These may develop instantaneously without any
marked premonitory indication. In other cases tenderness on
percussion over the liver, stiffness or groaning under sudden
movements or turning, arching of the back, hanging of the head,
slowness in rising, costiveness, slight transient colics, and even
icterus may have been detected on close observation. The symptoms
of actual rupture are essentially those of internal hemorrhage. The
animal becomes weak, or unsteady upon its limbs, perspires, arches
the back, and shows a marked pallor of the visible mucosæ. The
pulse is small, thready, weak and accelerated, and the heart beats
violent or palpitating. The percussion dullness over the liver is
extended (Weber), the loins become insensible to pinching, and
there may be some distension of the abdomen. Dilatation of the
pupils, retraction or rolling of the eyes, amaurosis, tremors of the
muscles of the neck, lying down, or falling, and general convulsions
may precede death. This may occur in a few hours or it may be
delayed if the lesions are restricted. In case of survival, coldness and
œdema of the extremities and sheath have been observed. The lesser
hemorrhages may terminate in recovery if there is no attendant
incurable disease. In anthrax, glanders, cancer, tuberculosis,
septicæmia, etc., a favorable issue is not to be looked for.
Duration. Termination. In severe cases a fatal issue may be
expected in from five hours to five days. In the milder cases which
make a temporary recovery there is great danger of a second
hemorrhage from the new vessels in the tissue undergoing
organization or from the adjacent degenerate liver tissue. The course
of the affection may be altered by such complications as arthritis
(Dieckerhoff), pneumonia, pulmonary thrombosis (Leblanc),
enteritis or peritonitis (Cadeac).
Treatment is usually of no avail. Rest, and the administration of
laxatives and hæmostatics, have been especially recommended. Of
the latter, ergot by the mouth or ergotin subcutem, tends to
contraction of the blood-vessels and to check the flow. Ferric
chloride is also used, though apt to interfere with hepatic function.
Tannic acid, hamamelis, and other astringents may be used instead.
Cold water, snow or ice applied to the right hypochondrium may act
as a check to the hemorrhage. Unless in purely traumatic cases in an
otherwise healthy liver, a recovery is at best temporary, and the
already degenerate liver is liable to relapse at any moment. In horses
and dogs, therefore, recovery is by no means an unmixed good. Meat
producing animals that recover should be prepared for the butcher.
 HEPATITIS.
Forms of hepatitis: Parenchymatous hepatitis. Definition: Degeneration of
hepatic cells. Relation to enteritis and nephritis. In horse—causes:—as in
congestion, pampering, spoiled fodder, malt, inundated meadows, chill,
overfeeding, hot moist climate, hæmoglobinæmia, infection. In cattle—causes:—
forcing ration, hot weather, overwork, infection. In dog—causes:—infection from
alimentary canal. Lesions: Enlarged, softened liver, round edges, a week later
yellow atrophy, granular on section, bloodless. Acini with indefinite margins, cells
granular, nuclei lost. In dog centres of softening. Symptoms:—in horse: Attack
sudden, rigor, fever, dullness, prostration, yellowish red mucosæ, unsteady gait,
slight colic, anorexia, urine decreased, glairy, brownish red, groaning in defecation,
excited circulation and breathing, increased icterus by third day, fœtid, colorless
diarrhœa. Diagnosis: Coincidence of fever, prostration, icterus, painful defecation,
fœtid diarrhœa, light color of stools, tenderness and flatness on percussing hepatic
area. From influenza by absence of watering eyes and contagion. Prognosis in
horse: Very grave unless urine is free. Treatment in horse: Portal depletion,
calomel, ipecacuan, salines, diuretics, fomentation of loins, antiseptics, derivatives,
mineral acids, bitters. Careful laxative diet in convalescence. Symptoms in cattle:
Slower onset, anorexia, dullness, depression, drivelling saliva, grinding teeth,
icterus, constipation, later fœtid diarrhœa, pale colored stools, recumbency, groans
on rising, arching back, tender right hypochondrium, fever. Prognosis grave. Death
in five to six days. Treatment as in horse: Only saline laxatives. Symptoms in dog:
Muscular tremors, staring coat, hyperthermia, icterus, fœtid breath, ventral
decubitus, extreme prostration, anorexia, tender right hypochondrium, diminished
urine, death in two or three days. Treatment in dog: Calomel and jalap, diuretics,
laxatives, derivatives, germicides, in convalescence, mineral acids, bitters, careful
diet.
The different forms of inflammation of the liver are distinguished
according as they affect, especially the hepatic cells and tissue of the
acini (parenchymatous), as they result in suppuration (suppurative,
catarrhal, abscess), as they cause necrobiosis in nodular masses
(infectious or necrotic), as they lead to fibroid thickening under the
peritoneum and proper capsule (perihepatitis); or as they cause
general fibroid induration of the organ by increase of its connective
tissue (cirrhosis).
 PARENCHYMATOUS HEPATITIS, ACUTE
YELLOW ATROPHY OE THE LIVER.
The characteristic morbid lesion in this disease is the degeneration
of the liver cells, loss of their protoplasm and nuclei and of their
normal functions. It may be circumscribed to limited areas, or may
affect the liver, generally. As the hepatic functions, are so intimately
related to those of the bowels and kidney, the affection is usually
accompanied by inflammations of these organs as well.
Causes in horses. The same general causes which produce
congestion, may also determine the further morbid stage of
inflammation. Cadeac mentions a case which developed in a horse
kept alone and idle in the stable. He makes no mention of condition,
food, cleanliness nor ventilation. Haubner and Franzen have traced it
to a diet of malt or of hay harvested from inundated meadows.
Zundel records a case following exposure to extreme cold. More
commonly the disease is secondary to the overtaxing of the liver, by
heavy feeding in warm moist climates, or in hæmoglobinæmia, or to
the arrest of the micro-organisms of the food, or of infectious
diseases.
Causes in Cattle. These suffer rarely, but from essentially the same
conditions. It has followed aphthous fever (Eletti), and arisen under
a forcing ration, in hot weather (Callot, Cruzel), or under overwork
(Cruzel).
Causes in Dogs. Most cases result from infection by way of the
stomach and intestines, or by the transfer to the liver of the
ptomaines and toxins of such infections. It is thus related in its origin
to catarrhal jaundice and hyperæmia.
Lesions. In the earliest stage with albuminoid exudation into its
substance the liver may be greatly enlarged, its sharp edges rounded,
and its consistency softened. After a week’s illness atrophy may have
set in and the organ appears shrunken and of ocherous yellow. In the
early stages there may be sanguineous engorgement, the cut surface
may bleed freely, and small extravasations may show throughout the
liver substance, later the clay yellow hue, the granular aspect and the
absence of blood on the cut surface are characteristic. The margins of
the adjacent acini are indefinite or lost, and under the microscope
the hepatic cells are charged with granules (albuminoid, fatty and
pigmentary), while the nuclei are no longer demonstrable.
In cattle the liver may be double the normal size and at first of a
deep purple red, which may change later to the earthy yellow.
In dogs the liver is tumid and yellow, and marked by small pea-
like centres of softening. There is marked softening and the
microscope reveals the characteristic degeneration of the hepatic
cells.
Symptoms in the Horse. These resemble those of congestion
rendered more intense and therefore somewhat less obscure. The
attack is usually sudden, there may be rigor followed by
hyperthermia, dullness, pendent head, drooping eyelids, injected
conjunctiva with a yellowish tinge, unsteady gait and slight
indications of colic. There is anorexia, partial suppression of urine,
and what is passed is thick, glairy and brownish red, fæces are passed
with pain, and groaning, probably from compression of the liver, the
heart beats violently, while the pulse is small, breathing accelerated
and perspiration abundant. The temperature rises (101° to 106°) and
remains high throughout unless lowered through biliary intoxication.
Percussion over the liver and especially on the right side shows
increased area of dullness and marked tenderness. On the second or
third day the icterus usually increases, and a slight fœtid diarrhœa
may set in with marked fœtor of the pale or colorless discharges. The
jaundice is not, however, a criterion of the danger, as it may become
less marked or entirely disappear because of the extensive
degeneration of the hepatic cells and the arrest of the formation of
bile.
Diagnosis in the horse. The disease is recognized by the
coincidence of fever, with great depression, icterus, painful
defecation, constipation followed by a fœtid diarrhœa with lack of
color in the stools and by increased area of dullness and tenderness
in the region of the liver and especially on the right side. From
influenza which it resembles in many respects, it is distinguished by
the absence of watery discharge from the eyes, and by the entire
absence of all indication of contagion. The cases occur one at a time.
 Prognosis in the horse. The disease is exceedingly fatal. When the
kidneys remain active, the poisons are eliminated and there may be
hope of recovery, but when urine is suppressed an early death by
poisoning is to be expected.
Treatment in the horse. A most important indication is to secure
depletion from the portal system. Calomel 1 dr., aloes 4 drs.,
ipecacuan 1 dr. may be given in bolus, and followed by small daily
doses of sulphate and nitrate of soda with bitters, with or without the
ipecacuan. Action on the kidneys is essential to secure elimination of
the poisons which threaten a fatal poisoning if retained. To favor the
same action fomentations may be applied to the loins. The frequent
presence of pathogenic microörganisms either in the bowels or liver
suggests the use of germicides (salol, salicylic acid, salicylate of soda,
naphthalin, naphthol, beta-naphthol, etc.) as in catarrhal jaundice.
Sinapisms or blisters applied to the right side of the chest and over
the short ribs may be useful, and after the subsidence of the more
violent symptoms, dilute mineral acids and especially nitro-muriatic
acid may be resorted to in combination with diuretics and bitters.
When appetite returns succulent, laxative, non-stimulating food in
small quantity should be given. Wheat bran mashes, carrots, turnips,
potatoes, apples, fresh grass, ensilage may be adduced as examples.
Throughout the disease the ingestion of an abundance of pure water
should be encouraged.
Symptoms in the ox. These may appear more tardily than in the
horse, loss of appetite, staring coat, dullness, pendent head and ears,
unsteady movements, rigors, drivelling of saliva from the mouth and
grinding the teeth are usually noted. To these are added the more
diagnostic symptoms of slight (or severe) jaundice, constipation
followed by a fœtid light colored diarrhœa, a strong disposition to
remain recumbent, marked suffering attendant on rising, arching of
the back when up, and tenderness on percussion over the right
hypochondrium. The temperature gradually rises, though more
slowly than in the horse, and may again descend under a profound
poisoning.
Course. The disease reaches its acme in four to six days, and
generally has a fatal issue.
Treatment, is on the same lines as for the horse only as a
purgative, sulphate of soda may advantageously replace the aloes.
 Symptoms in the dog. The symptoms are those of congestion in an
exaggerated form. There are muscular tremors, erection of the hair,
followed by rising temperature up to 105° or 106°, an icteric hue of
the mucosæ, the pulse is accelerated, strong, irregular, respiration
rapid, panting, fœtid breath, ventral decubitus, and prostration
extreme. Appetite is completely lost, the bowels become relaxed, the
stools fœtid, the right hypochondrium painful on pressure or
percussion, and the urine greatly reduced and icteric or suppressed.
This feature of urinary suppression, determines a rapid poisoning
and death in two or three days.
Treatment must follow the same lines as in other animals, a
purgative of calomel and jalap, followed by diuretics, laxatives,
derivatives, and above all germicides. In case of survival mineral
acids, aqua regia, bitters, and a carefully regulated diet will be in
order.
 SUPPURATIVE HEPATITIS. HEPATIC
ABSCESS.
Causes in horse: pyæmia, omphalitis, thrombosis, infection, biliary calculi,
concretions or parasites, foreign bodies, hot, damp climates, strangles,
brustseuche, glanders, endocarditis. Lesions in horse: from parasites and
mechanical irritants, pea-like or hazelnut; embolic abscess, pin head to hen’s egg;
infection from strangles, foreign bodies, etc., may be of large size, and burst into
adjacent organs, the peritoneum or externally. Symptoms in horse: of pre-existent
malady, remitting fever, successive chills, intermittent icterus, hypochondriac
tenderness. Spontaneous recovery, aspiration, opening, antiseptics locally and
generally. Lesions in ruminants; secondary multiple abscesses, bean-like or (with
foreign body) very large, may extend into adjacent parts. Symptoms in cattle: fever,
chills, jaundice, tympany, diarrhœa, dysentery, wasting, tender right
hypochondrium. Treatment: as in horse. Causes in dog: foreign bodies, tumors,
infections, blows, traumas. Lesions: traumatic abscesses, single, large, infectious
abscesses multiple, small. Former fœtid. Symptoms in dog: hepatic congestion or
colic, then chills, prostration, irritability, tenderness of right hypochondrium,
nausea, vomiting. Treatment in dog: antiseptic aspiration, laparotomy.
Causes in the Horse. Hepatic abscess arises from a great many
primary morbid conditions. As a secondary abscess it is seen in the
different forms of pyæmia and especially in suppurative omphalitis
in young animals. It may start in thrombosis determined by clots or
septic matters carried from a distance through the portal vein or
hepatic artery, in biliary calculi or concretions, in parasites
introduced from the duodenum, in barbs or husks of the cereals that
have penetrated through the biliary ducts, or in bacteria or their
toxins which have been carried from the bowels, spleen or pancreas.
The government veterinarians have found it a comparatively
common lesion in the hot damp climate of Hindoostan, and a similar
frequency has been noticed in west Africa. Among general affections
it is liable to occur in strangles, contagious pneumonia, glanders,
endocarditis of the left heart and phlebitis with the formation of
thrombi in the lungs. In the two last named disorders, the affection
takes place by the simple transference of detached clots to the liver to
block its arteries or capillaries. Or it may be that micro-organisms
are transferred in the same way. With modern views of suppuration
the presence of the pyogenic organisms must be conceded.
Lesions in the horse. Cadeac distinguishes the different types of
hepatic abscess as: 1st biliary abscess in which suppuration
commences in the interior of the biliary ducts and usually from
parasites or mechanical irritants introduced or from calculi or
concretions formed within them: these rare abscesses contain biliary
salts, pigments, and epithelium and acquire the size of a pea or
hazelnut: 2d Metastatic abscesses which start in the arterial, portal,
or capillary vessels, by the arrest of infecting clots, which determine
a further clotting, the obstruction of the vessel, the accumulation of
leucocytes and the formation of abscess of the size of a pin head or
larger up to a hen’s egg, surrounded by a hæmorrhagic infarct
softening in the centre: these are numerously disseminated through
the liver: 3d Mechanical Abscess due to the penetration of foreign
bodies or parasites: 4th Infection as in strangles. These may attain a
large size, cause adhesion to adjacent organs, and rupture into the
chest, the colon, stomach or peritoneum. The pus may even escape
externally through the right hypochondrium.
Symptoms in the horse. These are always obscure and vary much
with the source of the malady. If there has been a pre-existing
hepatic malady the symptoms of that will be in evidence; if an
omphalitis its existence may still be recognizable; if pulmonary or
cardiac disease, that may be detected; if parasites, evidence of their
existence may perchance be found; if gall stone, a previous violent
hepatic colic with icterus may have occurred; and if intestinal septic
disorder, there may be the testimony of intestinal troubles. The more
diagnostic symptoms are a fever of a remittent type, one or several
violent shivering fits, a marked jaundice which like the fever shows
exacerbations, and a similar irregularity of the condition of the urine
which may be successively of a dark brown, a deep yellow, and a
transparent amber color. Tenderness and grunting on percussion of
the right hypochondrium would be an additional aid in diagnosis.
Treatment. Death has been hitherto considered as the inevitable
result, yet recoveries may ensue after rupture into the colon or
through the abdominal walls. If the seat of the abscess can be
ascertained its evacuation through an aspirator and the subsequent
injection of an antiseptic would be appropriate. The concurrent use
of antisuppurants like hyposulphite of soda, or sulphide of calcium
would also be in order.
Causes in Cattle. Hepatic abscess is much more frequent in cattle,
and is commonly a result of perforation by sharp pointed bodies
(needles, pins, nails, wires, etc.) from the reticulum and rumen, or of
parasites, or biliary calculi. Other cases are occasioned by the
presence of tubercles, actinomycosis, or omphalitis.
Lesions in Cattle and Sheep. Secondary abscesses are usually
multiple and disseminated through the organ, though Cadeac says
they are more common in the left half. They vary in size from a bean
to a pigeon’s egg, project often from the surface, and contain a viscid,
creamy, yellowish or greenish pus. Abscesses dependent on foreign
bodies often attain a great size, so as to contain a pint or quart of pus
(Landel). They may make their way through the diaphragm, rumen,
or abdominal wall leaving a thick cicatrix in the liver, or they may
become slowly absorbed and dry up into a putty-like or cretaceous
mass. Brusaferro found hepatic abscesses in lambs twenty to thirty
days old—probably of omphalic origin.
Symptoms in Cattle are usually very obscure. Fever, shivering fits,
jaundice, indigestion, diarrhœa or dysentery, emaciation, colics,
tender right hypochondrium, and peritonitis may all be in evidence
but the diagnosis is little better than a guess.
Treatment when possible at all would be on the same lines as for
the horse.
Causes in the dog. According to Cadeac these are mostly foreign
bodies (needles, pins, etc.) which have been swallowed, tumors of the
liver or adjacent organs, phlebitis and thrombosis of the portal vein,
pyæmia, septicæmia, and external injuries (kicks, blows, contusions,
falls, etc.)
Lesions in the dog. As in the other animals traumatic abscess is
usually solitary and large, secondary abscess multiple and small. The
pus developed around a foreign body is reddish, greenish and fœtid,
that of the metastatic abscess is usually whitish or yellowish and with
a sweet odor.
Symptoms in the dog are those of hepatic congestion, or violent
gall stone colic, followed by severe rigor, great depression, or
irritability, and tenderness over the right hypochondrium. Nausea
and vomiting is a marked symptom though not a diagnostic one.
Treatment. If the flaccid abdominal walls will allow of the locating
of the abscess it should be treated by aspiration and antiseptic
injections. It would even be admissible to perform laparotomy, stitch
the wall of the abscess to the external wound, and empty it under due
antiseptic precautions.
 INFECTED HEPATITIS. NODULAR
NECROBIOSIS OF THE LIVER.
In ox, sheep, pig, dog, horse. Necrotic areas projecting on surface of liver.
Causes: bacteria, toxins, from bowels, womb, navel. Lesions: In cattle dirty gray
nodules in brownish red liver, nodules firm, granular, necrotic, elements do not
stain, later leucocytes and fibro-plastic growth in periphery. In lambs the nodules
are white, common to the lungs and pleura, pathogenic to rabbit. In pigs nutmeg
liver, cells without nuclei, fatty, granular, pathogenic to rabbits, guinea pigs, rats
and young pigs. In dog, nutmeg liver, with violet areas, and white spots, 1–2 lines,
having granular, fatty cells without nuclei. Symptoms: fever, constant lying, tarry
fæces, icterus, tender right hypochondrium, and those of the primary disease.
Treatment: antisepsis of primary seat, and bowels, elimination by kidneys, general
antisepsis, stimulants, etc. Case usually hopeless. Prevention.
This has been observed particularly in cattle, but also in sheep, pig,
dog and horse. It is characterized by the formation of circumscribed
areas of gangrene, becoming hard, dry, yellowish and usually slightly
projecting beyond the adjacent surface. Its infected character is
shown by the presence in the lesion and adjacent parts of the hepatic
tissue of an abundance of bacteria, which, from the varied
description, appear to differ in different cases. The cause may
however be safely stated as one of the bacteria of gangrene. It is
alleged with some show of reason, that the lesion may be determined
by the action of toxins and ptomaines produced by bacteria in the
alimentary canal and carried to the liver with the portal blood
(Cadeac). The bacteria themselves commonly come from the same
source, (Stubbe), but also from the uterus (Berndt), the mammæ
(LeBlanc), and above all from the suppurating or septic umbilicus.
McFadyean in five cases found a long slender bacillus, Hamilton in a
single case in the horse found cocci, Rivolta in an infectious hepatitis
in sheep found bacterium subtilis agnorum, and Semmer found the
same condition in young pigs from micrococci introduced through
the diseased umbilicus.
Lesions. In cattle the liver has a general brownish red, or greenish
white color, and shows projecting, hard nodules of a dirty gray color
more or less tinged with yellowish brown. The margins of these hard
nodules are very sharply defined, and on section show a
homogeneous granular surface, devoid of areas of softening or of
connective tissue, and formed of the hepatic parenchyma in a state of
necrobiosis. The granules and nuclear elements do not stain like
those of healthy liver. As the disease advances the periphery of the
nodule may be invaded by leucocytes and become the seat of a fibro-
plastic hypertrophy (McFadyean) with the ultimate formation of
cicatricial tissue (Stubbe).
In lambs Rivolta found the necrosed nodules standing out as white
patches under the capsule of the liver, but similar lesions were met
with in the lungs and pleuræ, an observation which has been
confirmed by Hanbold. The affection was conveyed by inoculation to
the rabbit.
In pigs Semmer found nutmeg liver, deep red or grayish yellow,
hypertrophied, the hepatic cells swollen and divested of nuclei but
containing fatty and pigmentary granules. It was inoculable on
rabbits, guinea pigs, white rats and on young pigs.
In the dog, Courmont and Doyon found congested liver (portal
congestion) with projecting patches of a deep violet color and sharply
defined borders, and one to two lines in diameter, also salient white
spots with distinct outlines. In the white spots the hepatic cells had
lost their nuclei and were charged with fatty granules.
Symptoms. These are indications of hepatic disease. In parturient
cows, Berndt noted fever (102° to 104°), anorexia, stiffness, cough,
labored breathing, intense thirst, constant decubitus, and
constipation followed by lowering temperature, tarry fæces and
icterus. The region of the liver was very sensitive to pressure or
percussion. In the other animals the symptoms appear to be largely
over-shadowed by those of the primary disease, but the same general
indications of jaundice, hepatic tenderness and digestive disorder are
superadded.
Treatment when it can be intelligently adopted, consists largely in
evacuation and antisepsis of the seat of primary infection, and of the
prima viœ, and in maintaining elimination by the kidneys. In this
way, as in congestion and hepatitis, the concentration of the poison
is as far as possible counteracted, and an opportunity may
sometimes be furnished for the recuperation of the liver cells. As a
rule, however, the case is hopeless, and thus preventive measures, by
cleanliness, disinfection and antisepsis of the ascertained sources of
the infection are indicated.
 PERIHEPATITIS.
Inflammation of capsule of liver (external and Glisson’s). Causes: Traumas,
infective diseases, phlebitis of the portal vein, chill, distomatosis. Lesions:
Peritonitis and inflammation of the capsule in patches, yellowish gray exudate,
fibroid thickening or pus. Adhesions to adjacent objects. Thickening of trabeculæ.
Symptoms, tardy respiration and circulation, tender hypochondrium, colics,
diarrhœa, painful defecation, moan with expiration. Slight cases recover. Sequelæ:
compression of portal vein or bile duct, gastric catarrh, piles, etc. Treatment:
Salines, alkaline diuretics, mineral tonics, bitters.
This is inflammation of the external capsule of the liver and
Glisson’s capsule. It may arise from direct mechanical injury, or by
extension of inflammation from adjacent structures, such as the
peritoneum. It may also complicate contagious pneumonia in the
horse, tuberculosis in the ox, pneumoenteritis in pigs, and also
phlebitis of the vena portæ (Cadeac, Morot). It may follow a chill, or
distomatosis.
Lesions. These are essentially peritonitis circumscribed by the
liver, and extending to the proper capsule, and its vaginal
investments of the hepatic vessels. It is usually limited to certain
spots which become the seats of a yellowish gray exudation, with a
tendency to fibroid development and thickening, but sometimes
degenerating into pus. The deposits on the outer side of the hepatic
peritoneum may develop false membranes and fibrous adhesions to
surrounding objects, the diaphragm, omentum, stomach or intestine.
The deposits under the peritoneum lead to similar fibrous
development with hypertrophy or thickening of the capsule, the
trabeculæ extending thence into the liver and the vaginal sheaths of
the vessels. Such areas of thickening are revealed as depressed spots
or patches of a white color, and showing a firm fibrous, pearly
appearance when incised. Such lesions are not uncommon in the
livers of horses, cattle and swine. In the pig they may have a violet, or
brownish red color, but with spots of other colors—grayish or
brownish (Kitt).
Symptoms. Dopheïde, who has studied the disease in cows and to
a less extent in horses, found a reduction in pulsations (26 per