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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 inuence 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.

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 anddiagnosis

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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Table7.1 The 10most common cancer killers inthe UK in2018

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 (Table7.1).

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.

);

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.

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.

Table7.2 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:

Extent of spread. Microscopic appearance.

2 3

Anatomical situation. General condition of the patient.

Extent ofspread (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 theresected specimen with consequent worsening of the outlook for the patient.

The TNM classication

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 Table37.2. 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 (Table11.2) and Dukes’ staging of rectal carcinoma (Figure28.4).

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 ofthe 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.

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

and pharynx).

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

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

breast and prostate.

Radiofrequency ablation is a treatment for primary

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

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

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).

Nerve blocks, with phenol or alcohol for relief of

pain.

Psychological support. This is often impossible but

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.

•

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 CD20monoclonal antibody rituximab, which targets the CD20 epitope on B cells and is used for the treatment of B cell lymphoma.

Cell cycle chemotherapy classication

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

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:

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

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

VEGF, e.g. bevacizumab.

VEGF receptor blockade: monoclonals in

development.

VEGF receptor signal transduction: small mol-

ecule tyrosine kinase inhibition by sorafenib and sunitinib.

VEGF signal translation: mTOR inhibitors, e.g.

everolimus and temsirolimus.

Proliferation signal inhibition

a Blockade of epidermal growth factor receptor

(EGFR), e.g. cetuximab and panitumumab.

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-

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

yttriuminto the arteries feeding liver metastases.

Brachytherapy where the irradiation is from an

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 forhigh- 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

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 oftissue 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 (Figure8.1).

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.

the output depends on the

Abnormal regulation oftissue 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:

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)

Figure8.1 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:

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-

haemorrhage, revealed or internal (e.g.

uptured aneurysm; bleeding into the bowel or

around a closed fracture);

burns, with massive loss of plasma and

electrolytes;

severe diarrhoea and/or vomiting, with fluid

and electrolyte loss, particularly in colitis or pyloric stenosis;

bowel obstruction, in which large amounts of

fluid are sequestered into the gut, in addition to the losses due to vomiting;

peritonitis, with large fluid losses into the

abdomen as a consequence of infection or chemical irritation;

gastrointestinal fistulas, with fluid and electro-

lyte loss;

urinary losses, for example, the osmotic diure-

sis of diabetic ketoacidosis, or polyuria in resolving acute tubular necrosis (Chapter41).

Reduction in systemic vascular resistance (‘distrib-

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:

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 110mmHg may be very low, and β- blockade prevents a compensatory tachycardia in response.

conscious. Causes include:

Special causes ofshock

Adrenocortical failure

Loss of the hormones produced by the cortex of the adrenal gland may follow bilateral adrenal

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