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CHAPTER 20 Haemopoietic and Lymphoreticular System
351
• the paracortex: the T-cell-dependent region of the
lymph node
• the medulla: contains the medullary cords and
sinuses; also contains lymphocytes, which are much
less densely packed than in the cortex, together with
macrophages, plasma cells and a small number of
granulocytes.
Cortex
• Consists of primary lymphoid follicles, which are
unstimulated follicles, spherical in shape, containing
densely packed lymphocytes.
• Secondary follicles are present aer lymphocytes have
been stimulated antigenically.
• Secondary follicles have an outer ring of small
B-lymphocytes surrounding the germinal centre which
contains largely dividing lymphoblasts, macrophages
and dendritic cells.
• Antigen is trapped upon the surface of the dendritic
cells and presented to ‘virgin’ B-lymphocytes in the
presence of T-helper cells.
• ese B-cells subsequently undergo a series of morphological and functional changes.
• e function of germinal centres is to generate immunoglobulin-secreting plasma cells in response to antigenic challenge.
Paracortex
• T-cell-dependent region of the lymph node.
• When a T-cell response occurs there is marked proliferation of cells in this area.
• Paracortex contains large number of T-lymphocytes
with the predominance of helper/inducer cells.
• Cluster of dierentiation (CD4) is expressed by helper/
inducer T-cells.
Medulla
• Lymph enters the marginal sinus of the node and drains
to the hilum through the sinuses, which converge into
the medullary region.
• Sinuses are lined by macrophages that phagocytose foreign or abnormal particles from lymph passing through
the node, i.e. ltering function.
• Between the sinuses in the medulla lie the medullary
cords, which contain numerous plasma cells and are
one of the main sites of antibody production within the
lymph node.
e immunological function of lymph nodes is discussed
in greater detail in Chapter 19.
LYMPHATIC SYSTEM
• A network of blind-ending lymphatic capillaries line the
interstitial space near blood capillaries.
• Spaces between endothelial cells in lymphatic capillaries
are larger than those in blood capillaries, making them
readily permeable to protein and lymph uid.
• Lymph collects in thin-walled lymph vessels, which
eventually drain on the le side into the thoracic duct
and subsequently into the subclavian vein.
• Lymph from the right upper part of the body drains into
the right lymphatic duct.
• Lymph is composed of uid and lymphocytes.
• Plasma protein that leaks out of capillaries and uid that
is not reabsorbed into capillaries are returned to the circulatory system via lymphatics.
• Lymphatics also act as pathway of absorption of fat from
the gut.
• Lymph ow is aided by the rhythmical contractions of
smooth muscle in the wall of lymphatic vessels, retrograde ow being prevented by valves.
Obstruction to Lymphatics (Lymphoedema)
Lymphoedema is the accumulation of tissue uid due to
lymphatic obstruction or defective lymphatic drainage. If
the lymphatics are obstructed, protein and excess uid in
the interstitial uid cannot return to the vascular system
and accumulate behind the obstruction, producing local
oedema.
Lymphoedema may be:
• primary
• se con dar y.
Primary Lymphoedema
• Due to aplasia or hypoplasia of lymphatics.
• ere are three types:
• congenital lymphoedema or Milroy’s disease: pres-
ents shortly aer birth
• lymphoedema praecox: presents at puberty
• lymphoedema tarda: presents around age 30.
Secondary Lymphoedema
• May be secondary to result of damage to lymphatic
channels by:
• infection
• surgery
• radiotherapy
• malignant inltration
• trauma.
• Blockage of inguinal lymphatics by larial parasites frequently causes oedema of the legs and, in the male, the
scrotum also (elephantiasis).
• Blockage of lymphatic drainage from the small intestine
usually occurs because of tumour involvement, causing
malabsorption of fats and fat-soluble substances.
• Blockage of lymphatic drainage at the level of the thoracic duct causes chylous eusions in the pleura and
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SECTION III Pathology
peritoneal cavities – uid opalescent at paracentesis or
thoracocentesis because of presence of tiny fat globules
(chyle).
Lymphadenopathy
Lymphadenopathy is the enlargement of lymph nodes.
Causes are shown in Box 20.7.
SPLEEN
Gross anatomy of the spleen is covered in Chapter 2.
BOX 20.7 Causes of Lymphadenopathy
Primary infection
Viral Infectious
mononucleosis
HIV
CMV
Rubella
Measles
Bacterial TB
Syphilis
Brucellosis
Cat scratch disease
Septicaemia
Protozoal Toxoplasmosis
Parasitic Filariasis
Secondary infection E.g. tonsillitis with
cervical lymphadenitis,
abscess with regional
lymphadenitis
Primary malignancy Acute lymphoblastic
leukaemia
Chronic lymphatic
leukaemia
Hodgkin’s disease
Non-Hodgkin’s
lymphoma
Myeloproliferative
disorders
Secondary malignancy Metastases from local
and distant malignancy
Others Sarcoidosis
SLE
Rheumatoid arthritis
Internal Structure (Fig. 20.3)
When a fresh spleen is cut across, two areas can be identied on the cut surface:
• islands of pale areas, 1–2 mm in diameter, which are
white and are known as white pulp
• deep red background, which is known as red pulp.
White Pulp
• Consists of central arteries ensheathed by lymphocytes
and lymphoid nodules.
• T-lymphocytes are located in the immediate vicinity of
the central artery.
• Nodules contain mostly B-lymphocytes.
• Activated lymphocytes migrate to periphery of nodule,
the marginal zone between red and white pulp, and differentiate into plasma cells.
• Plasma cells circulate in the red pulp and enter sinusoids.
Red Pulp
• Forms most of the spleen.
• Contains sinusoids which trap defective or eete red
cells, which are destroyed by adjacent macrophages.
Functions of the Spleen
e two main functions are:
• production of antibodies
• ltration of blood and disposal of defective blood cells.
e two functions are architecturally distinct, lymphoid
function occurring in the white pulp and phagocytic activity in the red pulp.
Filtering Function
• Removal of old or abnormal red cells.
• Removal of abnormal white cells.
• Removal of normal and abnormal platelets and cellular
debris.
Immunological Function
• Opsonization: while opsonized bacteria can be removed
from the circulation by the entire reticulo-endothelial
system, the spleen is well suited to removing poorly
opsonized or encapsulated pathogens.
• Antibody synthesis: occurs chiey within the white pulp.
• Protection from infection: splenectomy leaves patients
more prone to certain types of infection (see below).
Disorders of the Spleen
Hypersplenism
Hypersplenism is splenomegaly associated with the
following:
• any combination of anaemia, leucopenia or thrombocytopenia
White pulp
Ensheathed artery
Nodule
Central artery
Red pulp
CHAPTER 20 Haemopoietic and Lymphoreticular System
Closed circulation
Venule
353
Open circulation
Fig. 20.3 The structure of the spleen showing the circulation.
• compensatory bone marrow hyperplasia
• e spleen may be so massive in size that it is palpable
• improvement aer splenectomy.
ere is an exaggerated destruction or sequestration of circulating blood elements, which can aect red cells, white
cells and platelets. e condition may be either primary or
sec ond ary.
Primary hypersplenism
• Splenomegaly may lead to hypersplenism, i.e. pancyto-
• Essentially a diagnosis of exclusion, where all causes of
secondary hypersplenism have been excluded.
• Rare condition of unknown aetiology, mainly aecting
women.
• May be massive splenomegaly and accompanying pancytopenia, especially leucopenia.
• ere may be recurring fevers and infection.
e causes of splenomegaly are shown in Box 20.8.
Effects of Splenectomy
Haematological Effects
• Reduction in the capacity of the spleen to remove
• Splenectomy results in good haematological response,
although some patients remain leucopenic.
Splenomegaly
• Red cell count does not change but red cells with cyto-
• Granulocytosis occurs immediately aer splenectomy
• e spleen must be enlarged to about three times its
normal size to become clinically palpable.
Sinusoids
in the right iliac fossa. Massive splenomegaly is likely to
be due to:
• chronic myeloid leukaemia
• myelobrosis
• lymphoma.
penia, as cells become trapped and destroyed in an overactive spleen.
immature or abnormal red cells from the circulation.
plasmic inclusion, e.g. Howell–Jolly bodies, may appear.
but is replaced in a few weeks by lymphocytosis and
monocytosis.
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SECTION III Pathology
BOX 20.8 Causes of Splenomegaly
Infective
Bacterial Typhoid
Typhus
TB
Septicaemia
Abscess
Viral Glandular fever
Spirochaetal Syphilis
Leptospirosis
Protozoal Malaria
Parasitic Hydatid cyst
Inflammatory Rheumatoid arthritis
Sarcoidosis
Lupus
Amyloid
Neoplastic Leukaemia
Lymphoma
Polycythaemia vera
Myelofibrosis
Primary tumours
Metastases
Haemolytic disease Hereditary spherocytosis
Acquired haemolytic
anaemia
Thrombocytopenic
purpura
Storage diseases Gaucher’s disease
Deficiency diseases Pernicious anaemia
Severe iron-deficiency
anaemia
Splenic vein
hypertension
Non-parasitic cysts
Cirrhosis
Splenic vein thrombosis
Portal vein thrombosis
• e platelet count is usually increased and may stay at
levels of 400 000–500 000 × 109/L for over a year.
• A thrombocytosis in excess of 1000 × 109/L may occur –
not an indication for anticoagulation, but antiplatelet
agents such as aspirin may help prevent thrombosis.
Post-Splenectomy Sepsis
• Following splenectomy, individuals are susceptible to
fulminant bacteraemia, which is potentially life-threatening but is largely preventable.
• Risk is greatest in young children, especially in the rst
2 years aer surgery.
• Risk is also greater when splenectomy is undertaken for
disorders of the reticuloendothelial system rather than
for trauma.
• Lethal sepsis is more common in children and is indeed
rare in adults.
• e most common infection is pneumococcal infection (mortality up to 60%), followed by H. influenzae
type b (less common but signicant in children) and N.
meningitides.
• Other infections include E. coli, malaria, babesiosis and
Capnocytophaga canimorsus (associated with dog bites).
• A distinct clinical syndrome starts with mild non-specic symptoms followed by high pyrexia and septicaemic shock, which may ultimately be fatal.
• Risk of fatal sepsis is less aer splenectomy for trauma,
possibly due to splenosis, i.e. multiple small implants
of splenic tissue which result from dissemination and
auto-transplantation following trauma.
• Patients undergoing splenectomy should have the following vaccinations:
• polyvalent pneumococcal vaccine (PPV). Children
under the age of 2 have a reduced ability to mount an
antibody response to polysaccharides and are at particular risk of vaccine failure. e newer conjugate
7-valent vaccine produces a better response in this
group
• vaccination against H. influenzae type b (Hib)
• vaccination against meningococci A and C. A com-
bination of MenC vaccine and MenACWY conjugate
vaccine is used according to protocol for dierent
age groups. MenACWY conjugate vaccine is particularly recommended in the under-2s
• inuenza vaccination is recommended annually.
• All vaccinations should be given at least 2 weeks before a
planned splenectomy. Following emergency splenectomy,
functional antibody responses are better with delayed
(14-day) vaccination. Re-immunization of asplenic
patients is currently recommended every 5 years.
• Antibiotic prophylaxis with penicillin (or erythromycin for penicillin-sensitive patients) should be given
in the rst 2 years post-splenectomy, especially in children under 2 years. Some authorities consider that they
should be given until age 18 years. Others recommend
life-long prophylactic antibiotics. Antibiotic prophylaxis may need to be altered depending on knowledge
CHAPTER 20 Haemopoietic and Lymphoreticular System
355
of local antibiotic resistance patterns. Patients developing infection, despite prophylactic measures, must be
admitted to hospital and given systemic antibiotics.
• Asplenic patients should be strongly advised of the
increased risk of severe falciparum malaria, should take
all anti-malarial precautions/prophylaxis, and ideally
should avoid holidays in malaria-endemic areas.
THYMUS
Disorders of the Thymus
• Agenesis results in immunodeciency syndromes.
• Histological abnormalities of the thymus, such as lymphoid hyperplasia or tumours, may be seen in association with:
• myasthenia gravis
• systemic lupus erythematosus
• dermatomyositis
• aplastic anaemia.
Thymic Tumours
• ese include:
• thymoma
• Hodgkin’s disease
• non-Hodgkin’s lymphoma
• teratoma
• thymolipoma
• thymic carcinoma.
• ymoma is rare.
• Many thymomas are asymptomatic and detected on
chest X-ray performed for other reasons.
• Some cases are detected when myasthenia gravis develops.
• Patients may present with signs of local disease such
as cough, dyspnoea, stridor or superior vena caval
obstruction.
• Majority of thymomas are benign and well encapsulated.
• Malignant tumours are locally invasive, spreading by
direct invasion of adjacent structures.
BLOOD GROUPS
ABO System (Table 20.2)
• Consists of three allelic genes: A, B and O.
• A and B are responsible for converting a basic substance
H, present in every red cell, into A or B substances, thus
converting the cells to group A or group B.
• gene has no eect on H substance.
• us, there are six genotypes and four phenotypes.
• An individual inherits one of three ABO antigen groups
(agglutinogen) from each parent: A, B or neither.
• Individuals inherit antibodies (agglutinins), which react
against red cells of groups other than their own, i.e. antiA, anti-B. ere is no anti-O.
• Blood group O is the universal donor because there are
no A or B antigens on the red cell membrane.
• Blood group AB is the universal recipient because there
is no anti-A or anti-B in the serum.
• Individuals with blood group A have A antigens on the
red cells and B antibodies in the plasma.
• Individuals who are blood group B have B antigens
on the surface of the red cells and A antibodies in the
plasma.
• Individuals who are blood group AB have both A and B
antigens on the red cells and no A or B antibodies in the
plasma.
• Individuals who are blood group O have neither A nor B
antigens on the red cells but have both A and B antibodies in the plasma.
Principles of Grouping and Cross-Matching
• Grouping:
• individuals have antibodies against those red cell
antigens they lack
• when red cells carrying one or both antigens (A, B)
are exposed to corresponding antibodies, they agglutinate or clump together
• blood is mixed with reagents including dierent
antibodies, i.e. anti-A and anti-B
• agglutination indicates that the blood has reacted
with a certain antibody and therefore is not compatible with blood containing that kind of antibody
• if agglutination does not take place it indicates that
the blood does not have the antigens binding to that
specic antibody in the reagent
TABLE 20.2 The ABO Blood Group System
Natural Agglutinins
Genotype Phenotype Agglutinogen on Cell
OO O Nil (or H substance) Anti-A, Anti-B 46
AA, AO A A Anti-B 42
BB, BO B B Anti-A 9
AB AB A, B None 3
in Plasma
% Phenotypic
Frequency (UK)
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SECTION III Pathology
• grouping is checked by determining whether anti-A
or anti-B is present in the recipient serum by adding
known group A and B cells.
• Cross-matching:
• antibodies to the A, B antigens are naturally occurring, whereas antibodies to other red cell antigens
(e.g. Rhesus, Kell, Duy) appear only aer sensitization by transfusion or pregnancy
• group-compatible red cells from a donor pack of
blood are mixed with recipient serum and examined
for agglutination, i.e. that there is no antibody present in the recipient's serum that will react with any
antigen on the donor's cells
• cross-matching will also rule out any errors that may
have occurred in the determination of the donor and
recipient blood groups
• compatibility of transfusions between various groups
is shown in Table 20.3.
Rhesus Group
• ere are a number of Rh antigens, of which group D
(RhD) is the most important agglutinogen.
• 15% of the population have no RhD antigens and are
therefore Rh negative.
• ere is no preformed Rh agglutinin (i.e. anti-D).
• An Rh-negative individual can make anti-D only aer
sensitization with Rh positive.
• Rh typing is carried out using an agglutinating IgM
anti-D.
• An Rh-negative individual has 50% chance of developing anti-D aer the transfusion of a single unit
of Rh-positive blood. It is important therefore that
Rh-negative individuals receive Rh-negative blood. A
universal donor therefore should be O Rh negative.
• e major importance of the Rh system is to avoid the
danger of RhD incompatibility between mother and
fetus.
Rhesus Incompatibility
• An Rh-negative mother and Rh-positive father may
produce an Rh-positive fetus.
• If fetal red cells enter the maternal circulation, anti-D
will be produced (IgG).
• If these IgG antibodies cross the placenta in future pregnancies they will destroy the fetal red cells, resulting in
haemolytic disease of the newborn.
• Sensitization can be prevented by administering a single
dose of anti-Rh antibodies in the form of Rh immunoglobulin during the post-partum period aer the birth
of an Rh-positive baby. is will destroy the fetal red
cells, preventing maternal sensitization.
BLOOD PRODUCTS (Fig. 20.4)
Over 90% of donated blood is separated into its various constituents so that individual components can be
administered.
Whole Blood
• Less readily available because of demand for blood
products.
• Most blood for transfusion is essentially red cells alone.
• Whole blood is product of choice for massive
transfusion.
• In practice, concentrated red cells with colloid or crystalloid are given following considerable haemorrhage.
• Whole blood may be stored for up to 42 days.
• Granulocytes and platelets lose their function in a few
days.
• Clotting Factors V and VIII are rapidly lost.
• Increasing content of lactate, phosphate and potassium
in stored blood is usually clinically insignicant, except
in massive transfusion.
Red Cell Concentrates
• Red cell concentrates or packed cells consist of whole
blood from which plasma has been removed.
• Treatment of choice for anaemia without hypovolaemia.
• Shelf life 42 days at 4°C.
• Storage changes include:
• increased lactate
• increased potassium
• increased phosphate
TABLE 20.3 Compatible Transfusions
Blood Group Antigens Antibodies Can Donate to Can Receive From
O None A, B AB, A, B, O O
A A B A, AB A, O
B B A B, AB B, O
AB A, B None AB AB, A, B, O
CHAPTER 20 Haemopoietic and Lymphoreticular System
357
Whole blood
Cells
Red cells
Platelets
Granulocytes
Fig. 20.4 Blood products.
Plasma
Fresh frozen plasma
Cryoprecipitate
Fractionation
Factor VIII concentrate
Albumin
Immunoglobulin
• decrease in pH
• haemolysis
• microaggregation of dead cells
• loss of granulocyte and platelet function
• loss of Factors V and VIII.
Indications for Blood Transfusion
• Signicant anaemia, e.g. Hb <7 g/dL.
• Signicant haemorrhage leading to hypovolaemia.
Platelet Concentrates
• Platelets suspended in plasma.
• Shelf-life 3 days at room temperature.
• Should be ABO compatible.
Indications for Platelet Transfusion
• Haemorrhage in the presence of thrombocytopenia.
• rombocytopenia prior to invasive procedures.
• Consumptive coagulopathy, e.g. DIC.
• Counts of 50 000 × 109/L are adequate for haemostasis.
Administration
• Four hours or less before procedure.
• Infuse rapidly via short-giving set with no lter.
• Usual adult dose is 6 units, which should raise the count
by 40 000 × 109/L.
• Counts should be checked 10 min to 1 h post-transfusion.
• Failure of the count to rise may be due to platelet antibodies, post-transfusion purpura or DIC.
Granulocytes
• Very short shelf-life (<24 h) at room temperature.
• Eect of infusion short-lived; expensive; induces pyrexial response; role remains controversial.
• Granulocyte-colony stimulating factor (G-CSF) is now
used to stimulate bone marrow response.
Fresh Frozen Plasma (FFP)
• Separated from fresh blood and frozen at −30°C.
• Contains all clotting factors.
• Shelf-life 1 year at −30°C.
• Use within 1 h of thawing.
Indications for FFP Transfusion
• Used to replace clotting factors following major haemorrhage (due to poor clotting ability of stored blood).
• Patients short of clotting factors, e.g. liver disease or
rapid reversal of warfarin.
• DIC in conjunction with platelets and cryoprecipitate.
• Prophylaxis or treatment of haemorrhage in patients
with specic clotting defects for which the specic factor is unavailable.
Administration
• Group-compatible FFP should be used.
Cryoprecipitate
• Concentrate prepared by freeze-thawing plasma from a
single donor.
• Rich in Factor VIII, brinogen and von Willebrand’s
fa ctor.
Indications for Cryoprecipitate Transfusion
• Haemophilia.
• Von Willebrand’s disease.
• Fibrinogen deciency, e.g. DIC.
Factor VIII Concentrate
• Used for treatment of haemophilia A.
Complications of Blood Transfusion
Haemolytic Transfusion Reactions
Immediate
• ABO incompatibility.
• Symptoms and signs:
• pyrexia
• dyspnoea
• chest pain
• severe loin pain
• collapse
• hypotension
• haemoglobinuria
• oliguria (oen proceeding to acute renal failure)
• jaundice
• DIC with spontaneous bruising and haemorrhage.
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SECTION III Pathology
Delayed
• Low-titre antibody too weak to detect in cross-match
and unable to cause lysis at the time of transfusion.
• Occurs 5–10 days post-transfusion.
• Symptoms and signs:
• pyrexia
• anaemia
• jaundice
• haemoglobinuria.
Reaction to white blood cells
• Febrile reaction.
• Relatively common in patients who have had previous
transfusions or pregnancy.
• Fever and ushing soon aer starting transfusion.
• Due to recipient leucocyte antibodies.
• If patient known to have previous similar reaction,
washed red cells should be given.
Infection
Infection is unlikely with the present testing in the UK but
may be a problem where testing is not carried out. Causes
include:
• HIV
• hepatitis B
• hepatitis C
• CMV
• malaria
• syphilis
• prion disease, e.g. Creutzfeldt–Jakob disease.
Complications of Massive Blood Transfusion
• Fluid overload.
• Cardiac arrhythmias due to cold blood.
• Citrate toxicity with resulting hypocalcaemia.
• Hypothermia.
• Hyperkalaemia.
• Metabolic acidosis because of acidity of stored blood.
• Haemorrhage due to coagulopathy unless FFP and
platelets are administered simultaneously.
• DIC.
• ARDS (acute respiratory distress syndrome)/TRALI
(transfusion-related acute lung injury).
Autologous Blood Transfusion
Methods of reducing blood bank transfusion involve
‘recycling’ of patient's own blood (autotransfusion).
Autotransfusion may be carried out in several ways:
• Predonation:
• blood is taken from the patient at weekly intervals
prior to elective surgery (up to 4 units over 4 weeks).
• Normovolaemic haemodilution:
• collect blood immediately prior to surgery and
replace with colloid
• up to 2 L can be removed safely from adults without
cardiac disease
• blood is fresh; contains viable platelets and clotting
factors.
• Intraoperative blood salvage techniques:
• blood spilled at operation is collected by suction,
processed and reinfused (using a ‘cell saver’)
• blood is anticoagulated and returned to the patient
via a ne lter
• useful when massive bleeding occurs in an uncon-
taminated operative eld, e.g. ruptured aortic aneurysm, liver trauma
• unsuitable where contamination occurs, e.g. in
abdominal surgery where the bowel is breached.
OSCE SCENARIOS
OSCE Scenario 20.1
A 73-year-old female is seen in pre-assessment clinic as
she is due to have a hip replacement in 4 weeks’ time. Her
bloods show a haemoglobin of 6.7 g/dL and an MCV of
69 fL with a normal clotting screen.
1. What type of anaemia is shown in the test results?
2. What are the common causes of this type of anaemia?
Which is the most likely in this case?
You discuss the case with the operating surgeon, who asks
you to take a full history and arrange any investigations
required.
3. Ask the patient relevant questions about her health sta-
tus, and explain what the next investigations you would
suggest will involve. You should also introduce the possibility of her hip operation needing to be delayed.
OSCE Scenario 20.2
You are fast-bleeped to a surgical ward by the nursing sta
as a 68-year-old male patient has become pyrexial, short of
breath and hypotensive. e sta nurse informs you that the
patient is normally t and well, on no medications and had
an uncomplicated hip replacement yesterday. is morning
CHAPTER 20 Haemopoietic and Lymphoreticular System
359
he was prescribed 2 units of blood as his haemoglobin was
6.9 g/dL and his transfusion was commenced about 5 min
before the onset of these symptoms. e patient cannot
answer your questions due to his dyspnoea.
1. What is your dierential diagnosis?
e nurse in charge shows you that the rst name and date
of birth on the detail label on the partially transfused bag of
blood do not match those on the patient’s wristband.
2. Outline your immediate actions.
OSCE Scenario 20.3
A 19-year-old female patient is admitted with a femoral fracture aer a road trac accident. When preparing
her for theatre she tells you that she is a Jehovah’s Witness
and does not want blood under any circumstances, even
if it would mean her death, and informs you she has an
Advanced Decision recorded in her medical notes and wallet stating the same. You assess her as having full capacity,
conrmed by a senior colleague.
1. If this patient required a life-saving transfusion during
her operation, should you administer it?
2. What if she was unconscious?
3. What if she was three years old?
4. What methods can be employed to reduce the need for
transfusion?
OSCE Scenario 20.4
A 38-year-old male has been involved in a high-speed
motorbike accident. He has multiple injuries and has been
in theatre for some time, having received 12 units of blood.
He has returned to the ITU following surgery.
1. One of the nurses on ITU calls you an hour later and
says that every time the blood pressure cu goes up
the hand of the patient spasms. What do you think this
might be due to and what is the cause?
2. While you are examining the patient you notice the ECG
looks odd and the T waves are very high and peaked.
What is the cause of this and what would be the urgent
treatment?
3. Unfortunately, despite managing the above problems,
aer 3–4 h the patient starts to ooze from his nose, operative wounds and various dierent cannula sites. What
could be the potential causes of this and how could you
prevent it?
OSCE Scenario 20.5
A 78-year-old male is seen in clinic for potential total hip
replacement; he tells you he is on warfarin for a prosthetic
heart valve – it is metallic.
1. Describe how you will manage this patient’s warfarin
prior to surgery.
2. On the evening before the operation the INR has come
back as 1.9; you tell your consultant who says it must
be below 1.5 and asks if you will kindly sort this out.
Describe what you can do to lower the INR and why it
will work given the method of action of warfarin.
3. Imagine the patient has presented with an INR of 6 and
has small bowel obstruction and needs urgent surgery,
describe what options you have to reverse the action of
warfarin.
Answers in Appendix pages 478–481
Please check your eBook at https://studentconsult.inkling.com/ for more self-assessment questions. See inside cover for
registration details.
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Basic Microbiology
SOURCES OF SURGICAL INFECTION
Hospital-acquired infections (nosocomial infection) occur
in about 10% of hospitalized patients. Of these, 75% occur
in surgical patients. Most postoperative infection arises
from the patient’s own ora.
e commonest sites of infection are:
• urinary tract
• respiratory tract
• wound
• skin and so tissue.
Predisposition to hospital-acquired infections include:
• age: the extremes of life
• susceptible patient, e.g. immunocompromised, diabe-
tes, prosthetic implants
• modes of treatment, e.g. intravenous lines, indwelling
catheters.
e origin of bacterial infection may be divided into two
main sources:
• endogenous: patient’s own ora
• exogenous: from other people or objects in the
environment.
Endogenous Infection
Endogenous infection occurs when organisms are carried
by the patient as:
• part of normal ora
• part of ‘replacement’ ora, i.e. organisms that colonize
various sites when the patient is treated with antimicro-
bial drugs.
Normal Body Flora
• Skin: coagulase-negative staphylococci, diphtheroids.
• Nostrils: Staphylococcus aureus.
• Oral cavity: streptococci, anaerobes.
• Upper respiratory tract: viridans streptococci, diphthe-
roids, anaerobes, commensal neisseria.
• Lower gastrointestinal (GI) tract: coliforms, faecal
enterococci, anaerobes (Bacteroides and clostridia).
• Anterior urethra: skin ora (as above), faecal ora (as
above).
Commensal Organisms
• Potential pathogens.
• Infection may result if balance is disturbed by breach
of body defences or if an organism gains access to a site
where it is not a commensal, e.g. Escherichia coli (normal in the colon) gaining access to the urinary tract and
causing a urinary tract infection (UTI).
• Normal ora may be altered by broad-spectrum antibiotics, allowing overgrowth of resistant bacteria, which
may result in serious infection.
• ‘Replacement’ organisms (conditional pathogens)
resulting from antibiotic therapy may cause infection,
e.g. Klebsiella may colonize the upper respiratory tract
aer a course of antibiotics and give rise to a chest
infection, especially in intubated, ventilated patients.
Prevention of Endogenous Infection
is involves:
• disinfection of skin
• bowel preparation
• appropriate antibiotic prophylaxis.
Exogenous Infection
is is derived from either people or objects in the
environment.
• People:
• medical sta
• nursing sta
• other patients with infection, subclinical infection,
or asymptomatic carriers.
• Inanimate objects (fomites):
• surgical instruments
• anaesthetic equipment
• ventilators
• humidiers
• parenteral uids (especially if drugs are added under
non-sterile conditions).
• Other sources:
• oors
• blankets
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