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Tumours
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Christopher Watson
Learning objectives
✓ To know the pathology and clinical features of tumours, as well as the
ways in which a tumour might present and the histological features that
inuence prognosis.
✓ To understand the principles of tumour staging.
✓ To know the treatment options, including the principles of cytotoxic
chemotherapy and the broad classes of agents available.
7
Cancers are so common and widespread that their consideration must at least pass through the mind in most
clinical situations. It, therefore, behoves the student,
both for examinations and, still more importantly, for
the future practice of medicine, to have a standard
scheme with which to tabulate the pathology, diagnosis, treatment and prognosis of neoplastic disease.
Pathology
When considering the tumours affecting any organ,
this simple classification should be used.
Benign
1
2 Malignant:
a primary;
b secondary.
For each particular tumour, the following headings
should be used:
• Incidence.
• Age distribution.
• Sex distribution.
Ellis and Calne’s Lecture Notes in General Surgery, Fourteenth Edition.
Edited by Christopher Watson and Justin Davies.
© 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd.
Companion website: www.wiley.com/go/Watson/GeneralSurgery14
• Geographical distribution (where relevant).
• Predisposing factors.
•
Macroscopic appearances.
• Microscopic appearances.
• Pathways of spread of the tumour.
• Treatment options.
•
Prognosis.
Clinical features
anddiagnosis
A malignant tumour may manifest itself in any or all
of four ways:
The effects of the primary tumour itself.
1
2 The effects produced by secondary deposits
(metastases).
3 The general effects of malignant disease.
4 Paraneoplastic syndromes. These are remote
effects caused by hormones or other tumour cell
products, which are most common in carcinoma
of the lung, particularly small cell tumours. For
example, production of ectopic adrenocorticotrophic hormone (ACTH) may present like
Cushing’s syndrome, and production of ectopic
parathormone (PTH) may present with hypercalcaemia and its symptoms.
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Table7.1 The 10most common cancer killers inthe UK in2018
Cancers in males Cancers in females
Cancer site
1 Lung 65.9 Lung 47.0
2 Prostate 45.9 Breast 33.3
3 Colorectal 32.8 Colorectal 21.4
4 Oesophagus 19.6 Pancreas 13.3
5 Pancreas 17.5 Ovary 12.5
6 Bladder 14.0 Brain, other CNS and
7 Liver 12.6 Uterus 7.3
8 Brain, other CNS and
9 Kidney 10.5 Liver 6.3
10 Non-
Data for 2018 obtained from Cancer Research UK, January 2022.
CNS, central nervous system.
The only common exceptions to this scheme are
primary tumours of the central nervous system
(CNS), which seldom produce secondary deposits.
Diagnosis is always made by history, clinical examination and, where necessary, special investigations.
Let us now, as an example, apply this scheme to
carcinoma of the lung– the most common lethal cancer in the UK, accounting for 21% of all deaths from
cancer; bowel (10%), breast (7%), prostate (7%), pancreas (6%) and oesophagus (5%) follow lung cancer in
this comparison of cancer frequency by site
(Table7.1).
intracranial tumours
Hodgkin’s lymphoma 10.1 Non- Hodgkin’s lymphoma 6.2
Mortality
per 100,000 Cancer site
intracranial tumours
10.5 Oesophagus 7.1
• General effects of malignant disease: the patient
may present with malaise, lassitude, poor appetite
or loss of weight.
•
Paraneoplastic syndromes, such as:
– ectopic hormone production (e.g. PTH, ACTH);
– myasthenia- like syndrome (Eaton–Lambert
syndrome
– hypertrophic pulmonary osteoarthropathy
(HPOA) and finger clubbing.
1
);
Examination
Mortality
per 100,000
7.3
History
• The primary tumour may present with cough,
haemoptysis, dyspnoea and pneumonia (sometimes recurrent pneumonia due to partial bronchial obstruction).
• Secondary deposits in bone may produce pathological fracture or bone pains; cerebral metastases
may produce headaches or drowsiness; liver
metastases may result in jaundice.
• The primary tumour may produce signs in the chest.
• Secondary deposits may produce cervical lymph
node enlargement hepatomegaly or obvious bony
deposits (e.g. in the skull).
• The general effects of malignancy may be suggested by pallor or weight loss.
1
Lealdes M Eaton (1905–1958), Professor of Neurology,
Mayo Clinic, Rochester, MN, USA. Edward Lambert
(1915–2003), Professor of Physiology and Neurology, Mayo
Clinic, Rochester, MN, USA.
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Special investigations
• The primary tumour: chest X- ray, computed
tomography (CT) scan, bronchoscopy, cytology of
sputum and needle core biopsy.
•
Secondary deposits: CT scan and isotope bone
scan.
General manifestations of malignancy: a blood
•
count may reveal anaemia. The erythrocyte sedimentation rate (ESR) may be raised.
•
Paraneoplastic hormone production: hormone
assay.
Tumour markers
These are blood chemicals (often fetal proteins) produced by the malignant cells. Some tumours have a
characteristic marker associated with them, such as
α-
fetoprotein (AFP) in hepatoma and teratoma and
prostateprostate (Table 7.2). Tumour markers may indicate
malignant change in a benign condition and are useful in postoperative monitoring. If a marker was raised
before treatment, it should fall when the disease is
controlled but will rise again if recurrence occurs.
specific antigen (PSA) in carcinoma of the
Some tumours produce excess amounts of the appro-
This simple scheme applied to any of the principal
malignant tumours will enable presentation of a full
clinical picture of the disease.
priate hormone, such as medullary carcinoma of the
thyroid producing calcitonin, in which case hormone
assay may be used to detect tumour activity.
Table7.2 Tumour markers
Malignant disease
associated with rise in
Marker Nature of marker
Fetoprotein (AFP) Protein secreted by
α-
β- Human chorionic
gonadotrophin (β- HCG)
Ca 15.3 Oncofetal antigen Breast carcinoma Hepatitis, cirrhosis,
Ca 27.29 Glycoprotein mucin 1
Ca 19.9 Intracellular adhesion
Ca 125 Glycoprotein on
Carcinoembryonic
antigen (CEA)
Prostate- specific
antigen (PSA)
fetal liver
Protein normally
produced by placenta
(MUC1) on epithelial
cells
molecule related to
Lewis blood group
coelomic epithelium
during fetal
development
Oncofetal protein
(protein secreted by
fetal gut)
Glycoprotein produced
by epithelium of
prostatic duct
marker
Hepatocellular carcinoma
and testicular teratoma
Testicular teratoma and
chorion carcinoma
Breast carcinoma Benign breast disease,
Hepatocellular and
cholangiocarcinoma.
Also colorectal and
ovarian carcinoma
Ovarian carcinoma Pregnancy, ovarian cysts,
Advanced colorectal,
breast and lung
carcinomas
Prostatic carcinoma Prostatitis, benign
Benign disease
associated with rise in
marker
Viral hepatitis (e.g.
hepatitis C) and cirrhosis;
pregnancy esp. if spinal
cord abnormality
Pregnancy
autoimmune diseases,
benign lung disease
ovarian cysts, liver and
kidney disease
Pancreatitis, cholestasis,
cholangitis, cirrhosis
pelvic inflammation,
ascites, cirrhosis,
hepatitis, pancreatitis
Peptic ulcer, inflammatory
bowel disease,
pancreatitis
prostatic hypertrophy
and prostatic trauma
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Prognosis
The prognosis of any tumour depends on four main
features:
1
Extent of spread.
Microscopic appearance.
2
3
Anatomical situation.
General condition of the patient.
4
Extent ofspread (staging)
The extent of the tumour (its staging) on clinical
examination, on radiological imaging, at operation
and on studying the excised surgical specimen is of
great prognostic importance. Obviously, the clinical
findings of palpable distant secondaries or gross fixation of the primary tumour are serious. Similarly, the
local invasiveness of the tumour at operation and evidence of distant spread are of great significance.
Finally, histological study may reveal involvement of
the lymph nodes that had not been detected clinically
or radiologically, or microscopic extension of the
growth to (and by inference beyond) the edges of
theresected specimen with consequent worsening of
the outlook for the patient.
The TNM classication
The TNM classification is an international system for
tumour staging. Tumours are staged by scoring them
according to the following.
•
Tumour characteristics – size and degree of
invasion.
•
Node involvement – regional nodes and distant
nodes.
• Metastases– presence or absence.
An example of TNM staging as it relates to breast
cancer is illustrated in Table37.2. Tumours are most
accurately staged by pathological criteria (i.e. measurement of size, invasion and nodal involvement on
the excised specimen) rather than based on clinical
examination, although the latter gives an immediate
idea of spread. Use of pathological criteria when
referring to tumour stage is denoted by the prefix ‘p’,
hence pT1 for a pathologically proven T1 tumour.
Some tumours have additional classifications that
are more familiar to the clinician. Examples are
Breslow’s staging of local invasion of malignant melanoma (Table11.2) and Dukes’ staging of rectal carcinoma (Figure28.4).
Microscopic appearance
(histological differentiation)
As a general principle, the prognosis of a tumour is
related to its degree of histological differentiation (its
grading) on the spectrum between well differentiated
(low grade) and poorly differentiated (anaplastic).
The spread of the tumour and its histological differentiation should be considered in conjunction
with each other. A small tumour with no apparent
spread at the time of operation may still have a poor
prognosis if it is poorly differentiated, whereas an
extensive tumour is not incompatible with long survival of the patient after operation if the microscopic
examination reveals a high degree of differentiation.
Anatomical situation
The site of the tumour may preclude its adequate removal
and thus seriously affect the prognosis. For example, a
tumour at the lower end of the oesophagus may be easily
removable, whereas an exactly similar tumour situated
behind the arch of the aorta may be technically inoperable; a brain tumour located in the frontal lobe may be
resected, whereas a similar tumour in the brain stem will
be a desperate surgical proposition.
General condition ofthe patient
A patient apparently curable from the point of view of
the local condition may be inoperable because of
poor general health. For example, gross congestive
cardiac failure may convert what is technically an
operable carcinoma of the rectum into an unacceptable anaesthetic risk.
Treatment
The treatment of malignant disease should be discussed in a multidisciplinary team setting, involving
review of histopathology and radiology, with surgical
and oncological expertise. Treatment options should
then be discussed with the patient before a treatment
plan is pursued. Treatment could be considered
under two headings.
1
Curative: an attempt is made to ablate the disease
completely.
2 Best supportive/palliative: although the disease is
incurable or has recurred after treatment,
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m easures can still be taken to ease the symptoms
of the patient and provide best supportive care.
In this section, we will summarize the possible
lines of treatment for malignant disease in general; in
subsequent chapters, the management of specific
tumours will be considered in more detail. Treatment
given after surgery to reduce the risk of recurrence is
often referred to as adjuvant therapy (Latin adiuvare,
to help); treatment given before surgery with the
intention of shrinking a tumour and making it easier
to resect is known as neoadjuvant therapy.
Curative treatment
1 Surgical resection (e.g. carcinoma of the lung or
colon).
Radiotherapy alone (e.g. tumours of the mouth
2
and pharynx).
3
Cytotoxic chemotherapy when the tumour is espe-
cially sensitive to particular agents, such as teratoma of the testis to platinum compounds.
A combination of treatment modalities including
4
surgery and/or radiotherapy and/or cytotoxic
chemotherapy.
Best Supportive/Palliative
treatment
1 Operative intervention
a Surgical resection. The palliative excision of a
primary lesion may be indicated, although secondary deposits may be present. For example,
a carcinoma of the ascending colon may be
excised to prevent recurrent bleeding and
pain, although secondary deposits may already
be present in the liver.
b Prevent obstruction: Obstructing cancers in the
large bowel may be stented. Inoperable
obstructing tumours of the oesophagus or cardia of the stomach may also be stented so that
dysphagia can be relieved. The bile duct may
be stented endoscopically via the duodenal
papilla for the relief of jaundice and pruritus in
patients with inoperable carcinomas of the
head of pancreas.
2 Radiotherapy. Palliative treatment may be given to
localized secondary deposits in bone, irremovable
breast tumours, inoperable lymph node deposits
and some symptomatic primary tumours, for
example. It is particularly indicated for localized
irremovable disease, such as bleeding, pain and
mucus from a low rectal cancer.
Hormone therapy. Applicable in carcinoma of the
3
breast and prostate.
Radiofrequency ablation is a treatment for primary
4
or secondary tumours of the liver, lung and kidney. It involves a needlepercutaneously into the tumour through which a
radiofrequency current is passed, causing a thermal injury that destroys the tumour cells
Tumour embolization (TAE): Some tumours, such
5
as small primary or secondary cancers in the liver,
may be treated by embolizing the feeding artery
with a chemotherapy agent, or beads coated with
a slow- release chemotherapy agent, to reduce
growth (transarterial chemoembolization, TACE),
or simply embolizing the tumour deposit to
deprive it of its blood supply completely.
Radioactive beads, typically yttrium- 90, may also
be used which cause local irradiation to tissue
around the bead.
Cytotoxic chemotherapy. A wide range of drugs
6
have anticific; all the drugs damage normal dividing cells,
especially those of the bone marrow, gut, skin and
gonads.
7 Non- chemotherapy drugs. These are administered
for pain relief (e.g. non- steroidal analgesics, opiates), hypnotics, tranquillizers and anti- emetics
(e.g. chlorpromazine).
8
Nerve blocks, with phenol or alcohol for relief of
pain.
Psychological support. This is often impossible but
9
might be improved by a cheerful and kindly attitude of medical and nursing staff, and sometimes
with formal psychological input. The surgeon
must also deal with the psychological effect of not
being able to cure the patient, or that their treatment has failed, and not lose sight of the patient in
need of psychological support.
cancer action, but this action is not spe-
like probe being passed
Anti- neoplastic agents
The chemical therapy of cancer can be divided into
four classes of agent:
Cell cycle chemotherapy, typically targeting cell
•
proliferation pathways. Cancers with very rapid
growth are particularly susceptible.
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• Targeted chemotherapy, utilizing specific
operties of cancer.
pr
•
Hormone therapy, used commonly for the treat-
ment of hormone sensitive prostate, breast, ovarian and uterine cancer.
•
Immunotherapy, utilizing immune system com-
ponents to fight cancer.
Some drugs may fall into more than one class, such
as the CD20monoclonal antibody rituximab, which
targets the CD20 epitope on B cells and is used for the
treatment of B cell lymphoma.
Cell cycle chemotherapy
classication
Chemotherapy agents that target the cell cycle are
particularly suited to the treatment of rapidly dividing tumours, which are, therefore, affected more
than nonover rapidly may be affected and manifest with side
effects, such as bone marrow suppression and
mucositis.
but a useful classification is as follows:
•
Alkylating agents bind to DNA or RNA, interrupt-
• Antimetabolites. Structural analogues of sub-
• Anti- microtubule agents. Inhibit mitosis by inter-
•
Topoisomerase inhibitors. Cause DNA strand
• Cytotoxic antibiotics. Interfere at different points of
cancer cells. Non- cancer cells that turn
There is no standard classification of such agents,
ing synthesis of DNA, RNA or proteins, e.g. cyclophosphamide, chlorambucil, busulphan, and the
platinum compounds cisplatin, carboplatin and
oxaliplatin.
strates of DNA and RNA synthesis, which they
interrupt:
– Pyrimidine analogues: 5- fluorouracil, cytara-
bine and gemcitabine;
– Purine analogues, e.g. 6- mercaptopurine,
thioguanine;
– Folate analogues, e.g. methotrexate.
fering with microtubule formation or function:
– Plant alkaloids, e.g. vincristine and vinblastine
– Taxanes, e.g. paclitaxel, docetaxel
breaks by disrupting action of topoisomerase
enzymes:
– Topoisomerase I inhibitors, e.g. irinotecan,
topotecan;
– Topoisomerase II inhibitors, e.g. etoposide;
anthracyclines (e.g. daunorubicin).
cell cycle division: e.g. bleomycin and mitomycin.
Immunotherapy
Immunotherapy involves harnessing elements of the
immune system for antibelow gives some examples, although there may be
overlap between them; for example, some monoclonal antibodies may act as checkpoint inhibitors.
•
Monoclonal antibodies – targeting specific cell
surface protein or cytokine
•
Checkpoint inhibitors – molecules on the cell
s
urface that keep the immune response in check,
preventing immune activation against self.
Checkpoint molecules are highly expressed on
some tumour cell types.
Cytokines, such as interferon, used to enhance an
•
immune response, although less commonly used
nowadays.
Vaccine therapy, which can utilize a historic vac-
•
cine response. For example, using an immune
response to Bacille Calmette-
immunized individuals to stimulate a local
immune response in bladder cancer. Alternatively,
the vaccine may be a protein or nucleic acid fragment of the cancer cell, stimulating an immune
response to the cancer.
Chimeric antigen receptor (CAR)- T cell therapy– T
•
cells are removed from the patient’s blood, then
engineered to express a receptor for a protein
expressed by the cancer, after which they are cultured in volume before reinfusing into the patient.
cancer therapy. The list
Guérin (BCG) in
Targeted drugs
Some tumours have characteristic metabolic pathways
that can be targeted, or histological or genetic analysis
of individual tumours may identify such pathways or
pathological cell surface protein expression. Targeting
may be either with small molecules, which usually act
within the tumour cell, or monoclonal antibodies to
cell surface proteins or products. Examples are:
1
Checkpoint inhibitors block the mechanisms by
which cancer cells evade the immune response,
by targeting specific cell surface proteins/receptors on leucocytes
Programme cell death- 1 receptor, blocked by
a
pembrolizumab and nivolumab, for example.
b Programme cell death- 1 ligand, blocked by
atezolizumab and avelumab.
c Cytotoxic T- lymphocyte–associated antigen 4
(CTLA4), such as ipilimumab.
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2 Angiogenesis inhibitors, targeting tumour- produced
vascular endothelial growth factor (VEGF)
VEGF inhibition: monoclonal antibodies to
a
VEGF, e.g. bevacizumab.
VEGF receptor blockade: monoclonals in
b
development.
c
VEGF receptor signal transduction: small mol-
ecule tyrosine kinase inhibition by sorafenib
and sunitinib.
VEGF signal translation: mTOR inhibitors, e.g.
d
everolimus and temsirolimus.
3
Proliferation signal inhibition
a Blockade of epidermal growth factor receptor
(EGFR), e.g. cetuximab and panitumumab.
b
Blockade of human epidermal growth factor recep-
tor 2 (HER2), which is overexpressed on the cells of
some cancers, especially breast, e.g. trastuzumab.
Combination chemotherapy
Multiple drugs with different modes of action and different toxicity profiles may be used to increase the efficacy of
treatment. A balance must be made between the chances
of regression of the tumour in relatively fit patients with
tumours likely to be sensitive (e.g. breast, ovary and testis)
and the toxic effects of the drug regimen.
Radiotherapy
Radiotherapy involves administering ionizing radiation that causes DNA damage and thus prevents
tumour cell proliferation. It can be divided into:
External radiotherapy, where the irradiating
•
source is outside of the body.
•
Internal radiotherapy:
Systemic radioisotope therapy where the radio-
a
active source is within the body and is taken up
preferentially by the tumour cells, such as
iodine-
131 for thyroid cancer.
Selective internal radioisotope therapy, such as
b
yttriuminto the arteries feeding liver metastases.
Brachytherapy where the irradiation is from an
c
implanted radioactive source placed inside or
adjacent the tumour, used for cancers of the
prostate, cervix and uterus.
90 beads injected via the hepatic artery
• Total dose is different for different tumours and given
either as a curative or as a palliative treatment;
Fractionation, applying a total dose over several
•
sessions, thus allowing adjacent tissue to recover
and also to treat tumour cells that were in a relatively resistant phase of the cell cycle at one session
but are actively dividing at a subsequent session;
• Stereotactic targeting using cross- sectional imaging to define the tumour, which is then subjected
to a total dose of irradiation applied as beams
from different directions, which come to a focus
on the tumour, minimizing the exposure of healthy
tissue. There are several advanced types of radiation delivery using such principles.
Cancer screening
Screening is the process of testing asymptomatic individuals for a specific condition. It is commonly performed for tumours but may be used in other contexts
such as abdominal aortic aneurysm and hypertension. Effective screening for a given condition using a
particular test has several prerequisites:
The condition, if untreated, is sufficiently serious
•
to warrant its prevention.
The natural history of the condition should be
•
understood.
•
The condition has a recognizable early stage.
• Effective treatment is available.
Treatment at an early stage could improve the
•
prognosis and is of more benefit than treatment
started later in the disease.
• The screening test is simple, reliable and acceptable to the patient.
• The screening test should have minimal falsepositive and false- negative outcomes (i.e. it should
be both sensitive and specific). Incorrect diagnosis can have serious consequences.
In reality, costing the testing to those groups at highest risk of a condition. This may involve large- scale population
screening or screening of families where a genetic
predisposition exists.
effective screening requires restrict-
External radiotherapy
There are many different ways external radiotherapy
may be administered, but the principles are similar:
Population screening
Examples of population screening include breast
cancer screening by mammography, which is
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restricted to older women (over 50 years) and cervical
cancer screening for women over 25 years. In cervical
cancer, for example, a distinct progression exists from
dysplasia to invasive cancer. This progression may
take 10 years. Hence, screening the population every
3–5 years by cervical smear cytology is cost- effective.
However, the advent of immunization of females with
a vaccine against human papilloma virus may reduce
the need for such frequent population screening for
that cancer.
Screening forhigh- risk individuals
A number of cancer syndromes exist in which there is
an inherited predisposition (e.g. familial adenomatous polyposis [FAP]) or a familial risk (e.g. breast and
ovarian cancer).
Inherited cancer
syndromes
Like FAP, most inherited cancers are autosomal dominantly inherited. In at- risk families, early identification may be possible through either genetic mapping
of the cancer or early recognition of a component of
the syndrome. In FAP, early colonoscopy may identify
adenomas (polyps) while they are still dysplastic and
before they become malignant, at which stage prophylactic colectomy is indicated. In addition, identification of the APC gene (located on chromosome
5q21) will also signify carriage.
Familial clustering
Many of the familial cancers are now being associated
with mutations of specific genes. Incomplete expression of the gene may account for the sporadic incidence of the tumour. For breast cancer, many genes
associated with increased susceptibility have been
identified, the most important of which are BRCA1
(chromosome 17q21) and BRCA2 (chromosome
13q12). Mutations of either gene confer an 80% risk of
breast cancer by the age of 70 years, together with an
increased risk of ovarian cancer. Screening tests
based on the detection of these genes differ from the
other screening tests mentioned above, as they identify a tendency to malignancy and not premalignant
change or early curable malignancy. There is no consensus at present as to the best management of such
patients.
Shock
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Vijay Sujendran
Learning objective
✓ To understand what shock is, what causes it and how it is best managed
8
according to the cause.
Shock is characterized by inadequate perfusion with
consequent inadequate oxygen delivery to the vital
organs, principally the heart and brain, leading to cellular hypoxia and death.
Aetiology
Tissue perfusion requires adequate blood pressure,
which is dependent upon the systemic vascular resistance and cardiac output. The cardiac output is a function of the heart rate and stroke volume. These may
be expressed in mathematical terms:
CO = HR × SV
BP = CO × SVR
Mean Arterial Pressure = SV × HR × SVR
where CO is cardiac output, SV is stroke volume, HR is
heart rate, BP is mean arterial blood pressure and SVR
is systemic vascular resistance. Stroke volume is
determined by preload, contractility and afterload.
Normal regulation
oftissue perfusion
The autonomic nervous system is able to alter heart
rate and peripheral vascular resistance in response
to changes in blood pressure detected by the
carotid sinus and aortic arch baroreceptors.
Changes in systemic vascular resistance may alter
venous return by changing the amount of fluid circulating in the cutaneous and splanchnic vascular
beds. Venous return determines the stroke volume;
increasing venous return causes an increase in
stroke volume, the heart acting as a permissive
pump (Starling’s law):
degree of stretch of the heart muscle at the end of
diastole (Figure8.1).
Volume regulation is achieved by the kidney, in
particular by the regulation of sodium loss by the
renin–angiotensin–aldosterone system and antidiuretic hormone (ADH) produced by the posterior pituitary, which controls water loss in the renal tubules
and collecting ducts. In addition, a fall in circulating
volume prompts the sensation of thirst, stimulating
increased fluid intake.
1
the output depends on the
Abnormal regulation
oftissue perfusion
Inadequate tissue perfusion (shock) may result from
factors related to the pump (the heart) and/or the systemic circulation. The causes of shock may be classified accordingly, as follows:
Ellis and Calne’s Lecture Notes in General Surgery, Fourteenth Edition.
Edited by Christopher Watson and Justin Davies.
© 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd.
Companion website: www.wiley.com/go/Watson/GeneralSurgery14
1
Ernest Henry Starling (1866–1927), Professor of Physiology,
University College, London, UK. Also described capillary ow
dynamics and discovered secretin (with Bayliss).
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Decreasing afterload
Increased contractility
Increasing afterload
Decreased contractility
Stroke volume
Left ventricular end diastolic volume (or pressure)
Figure8.1 Starling law.
1 Cardiogenic shock. A primary failure of cardiac
output in which the heart is unable to maintain
adequate stroke volume in spite of satisfactory
filling. Compensation involves an increase in
heart rate and systemic vascular resistance, manifested clinically by a tachycardia, sweating (due
to sympathetic nervous system outflow), pallor
and coldness (due to cutaneous vasoconstriction). Causes of cardiogenic shock include the
following:
a
massive myocardial infarction;
b acute ventriculoseptal defect following myo-
cardial infarction affecting the septum;
mitral or aortic valve rupture;
c
d
arrhythmia;
e cardiomyopathy and viral myocarditis.
2 Circulatory obstruction. The heart continues to
pump, but there is an obstruction to outflow or
impairment of filling. Cardiogenic and obstructive
causes of shock are characterized by a raised
venous pressure; the other causes are characterized by a low venous pressure. Causes include:
a outflow obstruction, e.g. pulmonary embolism;
b obstruction to venous return, e.g. tension
pneumothorax, acute cardiac tamponade.
3 Hypovolaemia. Reduction in circulating volume
results in a reduction in stroke volume and cardiac
output. Blood pressure is initially maintained as in
cardiogenic shock, with increased sympathetic
activity raising the peripheral vascular resistance
leading to the clinical picture of a cold, clammy
patient with a tachycardia. As volume losses increase,
the blood pressure falls. In severe cases, the patient is
confused or semi-
a
haemorrhage, revealed or internal (e.g.
r
uptured aneurysm; bleeding into the bowel or
around a closed fracture);
burns, with massive loss of plasma and
b
electrolytes;
severe diarrhoea and/or vomiting, with fluid
c
and electrolyte loss, particularly in colitis or
pyloric stenosis;
d
bowel obstruction, in which large amounts of
fluid are sequestered into the gut, in addition
to the losses due to vomiting;
e
peritonitis, with large fluid losses into the
abdomen as a consequence of infection or
chemical irritation;
gastrointestinal fistulas, with fluid and electro-
f
lyte loss;
g
urinary losses, for example, the osmotic diure-
sis of diabetic ketoacidosis, or polyuria in
resolving acute tubular necrosis (Chapter41).
Reduction in systemic vascular resistance (‘distrib-
4
utive shock’). Reduction in systemic vascular
resistance increases the size of the systemic vascular bed, producing a relative hypovolaemia,
reduced diastolic filling, reduced stroke volume
and thus a fall in blood pressure. Unlike the previous two causes, vasodilation occurs as part of the
pathogenesis, so the patient appears warm (‘hot
shock’), not cold and peripherally shut down. The
heart compensates with an increase in output.
The principal causes are:
a
anaphylaxis;
b sepsis;
c spinal shock.
5 Confounding factors. Pre- existing medical
c onditions and medications may confuse the clinical picture. Consider a patient with hypertension
and taking a β- blocker such as bisoprolol or ateno-
lol. For that patient, a systolic blood pressure of
110mmHg may be very low, and β- blockade prevents a compensatory tachycardia in response.
conscious. Causes include:
Special causes ofshock
Adrenocortical failure
Loss of the hormones produced by the cortex of
the adrenal gland may follow bilateral adrenal
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