Oxford Handbook of Clinical Medicine (9 edn)
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Surgery: Contents
Perioperative care:
Consent 570
Sutures 572
Surgical drains 573
Anaesthesia 574
Control of pain 576
dvts 580
Swollen legs 580
Stoma care 584
Thyroid disease 593
Lumps in head, neck & skin:
Lumps 596
Skin diagnoses 598
Breast surgery:
Breast carcinoma 604
gi surgery:
Abdominal masses 606
Acute abdomen 608
Paralytic ileus 613
Sigmoid volvulus 613
Gastric surgery 624
Angiodysplasia 630
Rectal bleeding 631
Around the anus 632
Anal cancer 633
Hepatobiliary surgery:
Gallstones 636
Urology:
Renal stones 640
Peri-aortitis 642
Prostatitis 647
Bladder tumours 648
Vascular surgery:
Varicose veins 660
Skin ulcers 662
When Wertheim attempted his radical hysterectomy for cervical cancer, the first dozen women died. Undeterred, he continued. Thousands of women owe their lives to his skill—and to the sacrifice of those 12 dead women (see p595 for more).
We thank our Specialist Readers for this chapter: Mr Mohamed Elkalaawy (General and gi surgery); Professor Thomas Lennard (Breast and endocrine surgery); Mr David Chadwick (Urology); Mr George Peaches (Vascular surgery); Mr Graham Cox (Head and neck surgery); Mr Mark Malak (Urogynaecology). We also thank our Junior Reader, Eleanor Zimmermann.
Surgery: Overview
See also in other chapters:
Abdominal areas.
Right upper quadrant (ruq) or hypochondrium
Epigastrium
Left upper quadrant (luq) or hypochondrium
Right flank (merges posteriorly with right loin, p57)
Periumbilical or central area
Left flank (merges posteriorly with left loin, p57)
Right iliac fossa (rif)
Suprapubic area
Left iliac fossa (lif)
Incisions.
-ectomy | Cutting something out. |
-gram | A radiological image. |
-pexy | Anchoring of a structure to keep it in position. |
-plasty | Surgical refashioning in order to regain good function/cosmesis. |
-scopy | Procedure with instrumentation for looking into the body. |
-stomy | An artificial union between a conduit and the outside or another conduit. |
-tomy | Cutting something open to the outside world. |
-tripsy | Fragmentation of an object. |
-ectomy | Cutting something out. |
-gram | A radiological image. |
-pexy | Anchoring of a structure to keep it in position. |
-plasty | Surgical refashioning in order to regain good function/cosmesis. |
-scopy | Procedure with instrumentation for looking into the body. |
-stomy | An artificial union between a conduit and the outside or another conduit. |
-tomy | Cutting something open to the outside world. |
-tripsy | Fragmentation of an object. |
angio- | Tube or vessel | lith- | Stone |
appendic- | Appendix | mast- | Breast |
chole- | Relating to gall/bile | meso- | Mesentery |
colp- | Vagina | nephr- | Kidney |
cyst- | Bladder | orchid- | Testicle |
-doch- | Ducts | oophor- | Ovary |
enter- | Small bowel | phren- | Diaphragm |
eschar- | Dead tissue, eg from burn | pyloro- | Pyloric sphincter |
gastr- | Stomach | pyel- | Renal pelvis |
hepat- | Liver | proct- | Anal canal |
hyster- | Uterus | salping- | Fallopian tube |
lapar- | Abdomen | splen- | Spleen |
angio- | Tube or vessel | lith- | Stone |
appendic- | Appendix | mast- | Breast |
chole- | Relating to gall/bile | meso- | Mesentery |
colp- | Vagina | nephr- | Kidney |
cyst- | Bladder | orchid- | Testicle |
-doch- | Ducts | oophor- | Ovary |
enter- | Small bowel | phren- | Diaphragm |
eschar- | Dead tissue, eg from burn | pyloro- | Pyloric sphincter |
gastr- | Stomach | pyel- | Renal pelvis |
hepat- | Liver | proct- | Anal canal |
hyster- | Uterus | salping- | Fallopian tube |
lapar- | Abdomen | splen- | Spleen |
abscess | A cavity containing pus. Remember: if there is pus about, let it out. |
cyst | Fluid-filled cavity lined by epi/endothelium. |
fistula | An abnormal connection between two epithelial surfaces. Fistulae often close spontaneously, but will not in the presence of malignant tissue, distal obstruction, foreign bodies, chronic inflammation, and the formation of a muco-cutaneous junction (eg stoma). |
hernia | The protrusion of a viscus/part of a viscus through a defect of the wall of its containing cavity into an abnormal position. |
ileus | Used in this book as a term for adynamic bowel. |
colic | Intermittent pain from over-contraction/obstruction of a hollow viscus. |
sinus | A blind-ending tract, typically lined by epithelial or granulation tissue, which opens to an epithelial surface. |
stent | An artificial tube placed in a biological tube to keep it open. |
stoma | (p584) An artificial union between conduits or a conduit and the outside. |
ulcer | (p662) Interruption in the continuity of an epi/endothelial surface. |
volvulus | (p613) Twisting of a structure around itself. Common gi sites include the sigmoid colon and caecum, and more rarely the stomach. |
abscess | A cavity containing pus. Remember: if there is pus about, let it out. |
cyst | Fluid-filled cavity lined by epi/endothelium. |
fistula | An abnormal connection between two epithelial surfaces. Fistulae often close spontaneously, but will not in the presence of malignant tissue, distal obstruction, foreign bodies, chronic inflammation, and the formation of a muco-cutaneous junction (eg stoma). |
hernia | The protrusion of a viscus/part of a viscus through a defect of the wall of its containing cavity into an abnormal position. |
ileus | Used in this book as a term for adynamic bowel. |
colic | Intermittent pain from over-contraction/obstruction of a hollow viscus. |
sinus | A blind-ending tract, typically lined by epithelial or granulation tissue, which opens to an epithelial surface. |
stent | An artificial tube placed in a biological tube to keep it open. |
stoma | (p584) An artificial union between conduits or a conduit and the outside. |
ulcer | (p662) Interruption in the continuity of an epi/endothelial surface. |
volvulus | (p613) Twisting of a structure around itself. Common gi sites include the sigmoid colon and caecum, and more rarely the stomach. |
epi- | Upon | pan- | Whole | peri- | Around |
end- | Inside | para- | Alongside | sub- | Beneath |
mega- | Enlarged | per- | Going through | trans- | Across |
epi- | Upon | pan- | Whole | peri- | Around |
end- | Inside | para- | Alongside | sub- | Beneath |
mega- | Enlarged | per- | Going through | trans- | Across |
Pre-operative care
Aims
To provide diagnostic and prognostic information. To ensure the patient understands the nature, aims, and expected outcome of surgery. To allay anxiety and pain:
Ensure that the right patient gets the right surgery. Have the symptoms and signs changed? If so, inform the surgeon.
Get informed consent (p570).
Check proposed anaesthesia/analgesia with anaesthetist.
Pre-op checks
The World Health Organization ‘Surgical Safety Checklist’ should be completed for every patient undergoing a surgical procedure. Is dvt/pe prophylaxis needed (p580)? Special tests, eg sickle cell, see box 1. If for ‘unilateral’ surgery, mark the correct arm/leg/kidney.Family history
Drugs
Antibiotics: Tetracycline and neomycin may ↑neuromuscular blockade.
Anticoagulants: Tell the surgeon. Avoid epidural, spinal, and regional blocks. Aspirin should probably be continued unless there is a major risk of bleeding. Discuss stopping clopidogrel therapy with the cardiologists/neurologists.
Anticonvulsants: Give as usual pre-op. Post-op, give drugs iv (or by ngt) until able to take orally. Valproate: give usual dose iv. Phenytoin: give iv slowly (<50mg/min, on cardiac monitor). im phenytoin absorption is unreliable.
β-blockers: Continue up to and including the day of surgery as this precludes a labile cardiovascular response.
Contraceptive pill: See bnf. Stop 4wks before major/leg surgery; ensure alternative contraception is used. Restart 2wks after surgery, provided patient is mobile.
Digoxin: Continue up to and including morning of surgery. Check for toxicity (ecg; plasma level); do plasma K+ and Ca2+ (suxamethonium can ↑K+ and lead to ventricular arrhythmias in the fully digitalized).
Diuretics: Beware hypokalaemia, dehydration. Do u&e (and bicarbonate).
Eye-drops: β-blockers get systemically absorbed.
hrt: As with contraceptive pill there may be an increased risk of dvt/pe.
Levodopa: Possible arrhythmias when patient under ga.
Lithium: Get expert help; it may potentiate neuromuscular blockade and cause arrhythmias. See ohcs p354.
maois: Get expert help as interactions may cause hypotensive/hypertensive crises.
Thyroid medication: see p593.
Tricyclics: These enhance adrenaline (epinephrine) and arrhythmias.
Preparation
Is any bowel or skin preparation needed, or prophylactic antibiotics (p572)?
Start dvt prophylaxis as indicated, eg graduated compression stockings (not if there is peripheral arterial disease); low molecular weight heparin (lmwh, p344): eg enoxaparin 20mg/d sc; start 2h pre-op, increased to 40mg/d in major-risk surgery; or heparin 5000u sc 2h pre-op, then every 8–12h sc for 7d or until ambulant.
Write up the pre-meds (p574); book any pre-, intra-, or post-operative x-rays or frozen sections. Book post-operative physiotherapy.
Careful planning prevents peri-operative death.1 A good thought exercise is to imagine yourself at the next surgical Mortality Meeting and ask “If I were looking back at the pre-op period, knowing that this patient had died, would I still consider that surgery was indicated?” The uk National Confidential Enquiry into Peri-operative Deaths (ncepod) found that ‘too many’ operations are performed on high-risk patients.It is the anaesthetist’s duty to assess suitability for anaesthesia. The ward doctor assists with a good history and examination, and can also reassure, inform, and get informed written consent (p570; ideally this should be from the surgeon).
Be alert to chronic lung disease, bp↑, arrhythmias, and murmurs.
Be guided by the history and examination and local/nice protocols.
u&e, fbc, and finger-prick blood glucose in most patients. If Hb <100g/L tell anaesthetist. Investigate/treat as appropriate. u&e are particularly important if the patient is starved, diabetic, on diuretics, a burns patient, has hepatic or renal disease, has an ileus, or is parenterally fed.
Crossmatch: Blood type is identified and units are allocated to the patient. Group and save (g&s): Blood type is identified and held, pending crossmatch (if required). Contact your lab to discuss requirements—this decreases wastage and allows increased efficiency of blood stocks.
Specific blood tests: lft in jaundice, malignancy, or alcohol abuse. Amylase in acute abdominal pain. Blood glucose if diabetic (p590). Drug levels as appropriate (eg digoxin, lithium). Clotting studies in liver or renal disease, dic (p346), massive blood loss, or if on valproate, warfarin, or heparin. hiv, hbsag in high-risk patients, after counselling. Sickle test in those from Africa, West Indies, or Mediterranean—and if origins are in malarial areas (including most of India). Thyroid function tests in those with thyroid disease.
cxr if known cardiorespiratory disease, pathology or symptoms, possible lung metastases, or >65yrs old. Remember to check the film prior to surgery.
ecg if >55yrs old or poor exercise tolerance, or history of myocardial ischaemia, hypertension, rheumatic fever, or other heart disease.
Echocardiogram may be performed if there is a suspicion of poor lv function.
Pulmonary function tests in known pulmonary disease/obesity.
Lateral cervical spine x-ray (flexion and extension views) if history of rheumatoid arthritis/ankylosing spondylitis/Down’s syndrome, to warn of difficult intubations.
mrsa screen: Screen and decolonize nasal carriers according to local policy (eg nasal mupirocin ointment). Colonization is not a contraindication to surgery. Place patients last on the list to minimize transmission to others and cover with appropriate antibiotic prophylaxis, eg vancomycin or teicoplanin.
Blood tests (inc. G & S or crossmatch)
iv cannula
ecg + cxr
Drug chart:
regular medications
analgesia/anti-emetic
antibiotics
lmwh/heparin
Compression stockings
Consent
Marked site/side
Anaesthetist informed
Theatres informed
Infection risk? (eg mrsa/hiv/hbv/hcv)
Class i | Normally healthy patient |
Class ii | Mild systemic disease |
Class iii | Severe systemic disease that limits activity but is not incapacitating |
Class iv | Incapacitating systemic disease which poses a constant threat to life |
Class v | Moribund: not expected to survive 24h even with operation |
Class i | Normally healthy patient |
Class ii | Mild systemic disease |
Class iii | Severe systemic disease that limits activity but is not incapacitating |
Class iv | Incapacitating systemic disease which poses a constant threat to life |
Class v | Moribund: not expected to survive 24h even with operation |
You will see a space for an asa number on most anaesthetic charts. It is a health index at the time of surgery. The suffix e is used in emergencies, eg asa 2e.
Consent
In which of the following situations would you seek ‘informed written consent’ from a patient?
Feeling for a pulse.
Taking blood.
Inserting a central line.
Removing a section of small bowel during a laparotomy for division of adhesions.
Orchidectomy after a failed operation for testicular torsion.
For consent to be valid
It can be given any time before the intervention/treatment is initiated. Earlier is better as this will give the patient time to think about the risks, benefits and alternatives—he may even bring forward questions on issues that you had not considered relevant. Think of consent as an ongoing process throughout the patient’s time with you, not just the moment of signing the form.
The proposed treatment or test must be clearly understood by the patient, taking into account the benefits, risks (including complication rates if known), additional procedures, alternative courses of action and their consequences.
It must be given voluntarily. This can be difficult to evaluate—eg when live organ donation is being considered—see box for other difficult situations.
The doctor who is providing treatment or undertaking the test needs to ensure that the patient has given valid consent. The act of seeking consent is ultimately the responsibility of the doctor looking after the patient, though the task may be delegated to another health professional, as long as they are suitably trained and qualified. Sometimes you may have to be certified to get consent.
The patient must have the capacity (can understand, retain, and weigh the necessary information) to give consent. Assessment of capacity must be time- and decision-specific.
When taking consent
Think about whether you are the right person to be obtaining consent.
Use words the patient understands and avoid jargon and abbreviations.
Ensure that he believes your facts and can retain ‘pros’ and ‘cons’ long enough to inform his decision. Fact sheets/diagrams for individual operations help.
Make sure his choice is free from pressure from others, and explain that after he has signed the form he is free to choose not to have the proposed treatment (ie withdraw consent) at any time. Some patients may view the consent form as a contract from which they cannot renege.
If the patient is illiterate, a witnessed mark does endorse valid consent. Similarly, if the patient is willing but physically unable to sign the consent form, then an entry into the medical notes stating so is valid.
Remember to discuss further procedures that may become necessary during the proposed treatment. This avoids waking up to a nasty surprise (eg a missing testicle as in scenario 5 above).
If you suspect the patient is not capable of giving consent then a formal assessment needs to be documented in the medical notes.
Consent is complex, but remember that it exists for the benefit of the patient and the doctor, giving you an opportunity to revisit expectations and involve the patient in his own care.
There are some areas of treatment or investigation for which it may be advisable to seek specialist advice if it is not part of your regular practice:
Photography of a patient.
Innovative or novel treatment.
Living organ donation.
Storage, use, or removal of human tissue (for any length of time), as regulated under the Human Tissue Act 2004.
The storage, loss, or use of gametes, as regulated under the Human Fertilisation and Embryology Act 1990.
The use of patient records or tissue in research or teaching.
In the presence of an advanced directive or living will expressly refusing a particular treatment, investigation or action.
Your team’s senior/consultant
Your employing organization
Legal defence organization
National medical association
Local research ethics committee
The right to refuse treatmentTheirs not to make reply,
Theirs not to reason why,
Theirs but to do and die.
Alfred, Lord Tennyson from The Charge of the Light Brigade, 1854
The rights of a patient are something of an antithesis to this military macabre of Tennyson, and it is our responsibility to respect the legal and ethical rights of those we treat. We do this not only for the sake of the individual, but also for the sake of an enduring trust between the patient and doctor, remembering that is the patient’s right to refuse treatment (if a fully competent adult) even when this may result in death of the patient, or even the death of an unborn child, whatever the stage of pregnancy. The only exception is in circumstances outlined by the Mental Health Act 2007 (amends Mental Health Act 1983 and Mental Capacity Act 2005).
Assumption of capacity (unless it is established a person lacks capacity).
A person is not to be treated as unable to make a decision unless all practicable steps to help him to do so have been taken without success.
A person is not to be treated as unable to make a decision merely because he makes an unwise decision.
An act done, or decision made for or on behalf of a person who lacks capacity must be done, or made, in his best interests.
Before the act is done or the decision is made, regard must be paid as to whether the purpose for which it is needed can be effectively achieved in a way that is less restrictive of the person’s rights and freedom of action.
Prophylactic antibiotics in surgery
Wound infections are not necessarily trivial since sepsis may lead to haemorrhage, wound dehiscence, and initiate a fatal chain of events, so take measures to minimize the risk of wound infection:Time administration correctly (eg iv prophylaxis should be given 30min prior to surgery to maximize skin concentration; metronidazole pr is given 2h before).
Use antibiotics which will kill anaerobes and coliforms.
Practise strictly sterile surgical technique. (Ask for a hand with scrubbing up if you are not sure—theatre staff will be more than pleased to help!)
| Category | Description | Infection risk |
|---|---|---|
Clean | Incising uninfected skin without opening a viscus | <2% |
Clean-contaminated | Intra-operative breach of a viscus (but not colon) | 8–10% |
Contaminated | Breach of a viscus + spillage or opening of colon | 12–20% |
Dirty | The site is already contaminated with pus or faeces, or from exogenous contagion, eg trauma | 25% |
| Category | Description | Infection risk |
|---|---|---|
Clean | Incising uninfected skin without opening a viscus | <2% |
Clean-contaminated | Intra-operative breach of a viscus (but not colon) | 8–10% |
Contaminated | Breach of a viscus + spillage or opening of colon | 12–20% |
Dirty | The site is already contaminated with pus or faeces, or from exogenous contagion, eg trauma | 25% |
Table after mrcs Core Modules: Essential Revision Notes, S. Andrews, Pastest
Antibiotic regimens
Appendicectomy; colorectal resections and open biliary surgery: A single dose of iv cefuroxime 1.5g + metronidazole 500mg or gentamicin 1.5mg/kg + metronidazole 500mg or co-amoxiclav 1.2g alone.
Oesophageal or gastric surgery: 1 dose of iv gentamicin or cefuroxime or co-amoxiclav (doses above).
Vascular surgery: 1 dose of iv cefuroxime or flucloxacillin 1–2g + gentamicin. Add metronidazole if risk of anaerobes (eg amputations, gangrene or diabetes).
mrsa: For high-risk patients add teicoplanin or vancomycin to the above.
Bowel preparation in colorectal surgery
If in doubt, check with the surgeon to see if preparation is required.
Sutures
Sutures (stitches) are central to the art of surgery. In their broadest sense they are absorbable or non-absorbable, synthetic or natural, and their structure may be divided into monofilament, twisted, or braided. See table (box). Monofilament sutures are quite slippery but minimize infection and produce less reaction. Braided sutures have plaited strands and provide secure knots, but they may allow infection to occur between their strands. Twisted sutures have 2 twisted strands and similar qualities to braided sutures. 3-0 or 4-0 (smaller) are the best sizes for skin closure.
Timing of suture removal depends on site and the general health of the patient. Face and neck sutures may be removed after 5d (earlier in children), scalp and back of neck after 5d, abdominal incisions and proximal limbs (including clips) after ∼10d, distal extremities after 14d. In patients with poor wound healing, eg steroids, malignancy, infection, cachexia (p29), the elderly, or smokers, sutures may need ∼14d.
(OHClinSurg p80)
The decision when to insert and remove drains may seem to be one of the great surgical enigmas—but there are basically 3 types to get a grip of:
Most are inserted to drain the area of surgery and are often put under suction or −ve pressure (Redivac® uses a ‘high vacuum’). These are removed when they stop draining. They protect against collection, haematoma and seroma formation (in breast surgery this can cause overlying skin necrosis).
The second type of drain is used to protect sites where leakage may occur in the post-operative period, such as bowel anastomoses. These form a tract and are removed after about 1 week.
The third type (eg Bellovac®) collects red blood cells from the site of the operation, which can then be autotransfused within 6h, protecting from the hazards of allotransfusion—it is used commonly in orthopaedics.
Check the individual surgeon’s wishes before altering a drain.(OHClinSurg p84)
The perfect suture material is monofilament, strong, easy to handle, holds knots well, has predictable absorption and causes minimal tissue reaction. Unfortunately no single suture fits the bill for every occasion, and so suture selection (including size) depends on the job in hand:
| Name | Material | Construction | Use |
|---|---|---|---|
Monocryl® | Poliglecaprone | Monofilament | Subcuticular skin closure |
pds® | Polydioxanone | Monofilament | Closing abdominal wall |
Vicryl® | Polyglactin | Braided multifilament | Tying pedicles; bowel anastomosis; subcutaneous closure |
Dexon® | Polyglycolic acid | Braided multifilament | Very similar to vicryl® |
| Name | Material | Construction | Use |
|---|---|---|---|
Monocryl® | Poliglecaprone | Monofilament | Subcuticular skin closure |
pds® | Polydioxanone | Monofilament | Closing abdominal wall |
Vicryl® | Polyglactin | Braided multifilament | Tying pedicles; bowel anastomosis; subcutaneous closure |
Dexon® | Polyglycolic acid | Braided multifilament | Very similar to vicryl® |
| Name | Material | Construction | Use |
|---|---|---|---|
Ethilon® | Polyamide | Monofilament | Closing skin wounds |
Prolene® | Polypropylene | Monofilament | Arterial anastomosis |
Mersilk®N | Silk | Braided multifilament | Securing drains |
Metal | Eg steel | Clips or monofilament | Skin wound/sternotomy closure |
| Name | Material | Construction | Use |
|---|---|---|---|
Ethilon® | Polyamide | Monofilament | Closing skin wounds |
Prolene® | Polypropylene | Monofilament | Arterial anastomosis |
Mersilk®N | Silk | Braided multifilament | Securing drains |
Metal | Eg steel | Clips or monofilament | Skin wound/sternotomy closure |
N = natural; other natural materials (eg cotton and catgut) are rarely used these days.
Anaesthesia
Before anaesthesia, explain to the patient what will happen and where they will wake up, otherwise the recovery room or itu will be frightening. Explain that they may feel ill on waking. The premedication aims to allay anxiety and to make the anaesthesia itself easier to conduct (see box 1). Typical regimens might include:
Anxiolytics: Benzodiazepines, eg lorazepam 2mg po; temazepam 10–20mg po. In children, use oral premeds as first choice eg midazolam 0.5mg/kg (tastes bitter so often put in paracetamol suspension).
Analgesics: See p576. Pre-emptive analgesia is not often used and effects are hard to determine. The aim is to dampen pain signals before they arrive. In children or anxious adults, local anaesthetic cream may be used on a few sites before inserting an ivi (the anaesthetist may prefer to site the cannula themselves!)
Antiemetics: Post-operative nausea and vomiting is experienced by ∼25% of all patients. 5ht3 antagonists (eg ondansetron 4mg iv/im) are the most effective agents; others, eg metoclopramide 10mg/8h iv/im/po, are also used—see p241.
Antacids: Ranitidine 50mg iv or omeprazole 40mg po/iv in patients at particular risk of aspiration.
Antisialogues: Glycopyrronium (200–400µg in adults, 4–8µg/kg in children; given iv/im 30–60min before induction) is sometimes used to decrease secretions that may cause respiratory obstruction in smaller airways.
Antibiotics: See p572.
Give oral premedication 2h before surgery (1h if im route used).
Side-effects of anaesthetic agents
Hyoscine, atropine: Anticholinergic ∴ tachycardia, urinary retention, glaucoma, sedation (especially in the elderly).
Opioids: Respiratory depression, cough reflex↓, nausea and vomiting, constipation.
Thiopental: (induction agent) laryngospasm.
Propofol: (induction agent) respiratory depression, cardiac depression, pain on injection.
Volatile agents, eg isoflurane: Nausea and vomiting, cardiac depression, respiratory depression, vasodilatation, hepatotoxicity (see bnf).
The complications of anaesthesia are due to loss of:
Pain sensation: Urinary retention, diathermy burns, pressure necrosis, local nerve injuries (eg radial nerve palsy from arm hanging over the table edge).
Muscle power: Corneal abrasion (∴ tape the eyes closed), no respiration, no cough (leads to pneumonia and atelectasis—partial lung collapse causing shunting ± impaired gas exchange: it starts minutes after induction, and may be related to the use of 100% O2, supine position, surgery, age and to loss of power).
Local/regional anaesthesia
If unfit/unwilling to undergo general anaesthesia, local nerve blocks (eg brachial plexus) or spinal blocks (contraindication: anticoagulation, local infection) using long-acting local anaesthetics such as bupivacaine may be indicated. See table for doses and toxicity effects.
| % concn | Lidocaine concn (mg/mL) | Approx. allowable volume (mL/kg) | Approx. allowable volume for 70kg adult (mL) |
|---|---|---|---|
0.25% | 2.5 | 1.12 | ≤80 |
0.5% | 5 | 0.56 | ≤40 |
1% | 10 | 0.28 | ≤20 |
2% | 20 | 0.14 | ≤10 |
| % concn | Lidocaine concn (mg/mL) | Approx. allowable volume (mL/kg) | Approx. allowable volume for 70kg adult (mL) |
|---|---|---|---|
0.25% | 2.5 | 1.12 | ≤80 |
0.5% | 5 | 0.56 | ≤40 |
1% | 10 | 0.28 | ≤20 |
2% | 20 | 0.14 | ≤10 |
Drugs complicating anaesthesia
Inform anaesthetist. See p568 for lists of specific drugs, and actions to take.
Malignant hyperpyrexia
This is a rare complication, precipitated by any volatile agent, eg halothane, or suxamethonium. It exhibits autosomal dominant inheritance. There is a rapid rise in temperature (>1°C every 30min); masseter spasm may be an early sign. Complications include hypoxaemia, hypercarbia, hyperkalaemia, metabolic acidosis, and arrhythmias. Get expert help immediately. Prompt treatment with dantrolene1 (skeletal muscle relaxant), active cooling and itu care can reduce mortality significantly.
The general principles of anaesthesia centre on the triad of hypnosis, analgesia, and muscle relaxation.
The conduct of anaesthesia typically involves:
Induction: Either intravenous (eg propofol 1.5–2.5mg/kg iv at a rate of 20–40mg every 10s; thiopental is an alternative) or, if airway obstruction or difficult iv access, gaseous (eg sevoflurane or nitrous oxide, mixed in O2).
Airway control: Either using a facemask, an oropharyngeal (Guedel) airway or by intubation. The latter usually requires muscle relaxation with a depolarizing/non-depolarizing neuromuscular blocker (ohcs p622).
Maintenance of anaesthesia: Either a volatile agent added to N2O/O2 mixture, or high-dose opiates with mechanical ventilation, or iv infusion anaesthesia (eg propofol 4–12mg/kg/h ivi).
Recovery: Change inspired gases to 100% oxygen only, then discontinue any anaesthetic infusions and reverse muscle paralysis. Extubate once spontaneously breathing, place patient in recovery position and give oxygen by facemask.
For further details, see the Anaesthesia chapter in ohcs (p612).
After a few minutes’ conversation with an anaesthetist at work, it becomes apparent that they are masters of the drug dose by weight! It is important to remember the maximum doses for local anaesthetics, not least because we use them so frequently, but because the effects of overdose can be lethal.
Local anaesthetic toxicity starts with peri-oral tingling and paraesthesiae, progressing to drowsiness, seizures, coma and cardiorespiratory arrest. If suspected (the patient feels ‘funny’ and develops early signs) then stop administration immediately and commence abc resuscitation as required.
Handy to remember (though it can be worked out with a pen, paper and si units) is that a 1% concentration is equivalent to 10mg/mL. Local anaesthetics are also basic, and so do not work well in acidic environments, eg abscesses.
The control of pain
Humans are the most exquisite devices ever made for experiencing pain: the richer our inner lives, the greater the varieties of pain there are for us to feel, and the more resources we have for dealing with pain. If we can connect with patients’ inner lives we may make a real difference. Never forget how painful pain is, nor how fear magnifies pain. Try not to let these sensations, so often interposed between your patient and his recovery, be invisible to you as he bravely puts up with them.
Guidelines for success
Identify and treat the underlying pathology wherever possible.
Give regular doses rather than on an ‘as-required’ basis.
Choose the best route: po, pr, im, epidural, sc, inhalation, or iv.
Explanation and reassurance contribute greatly to analgesia.
Allow the patient to be in charge. This promotes wellbeing, and does not lead to overuse. Patient-controlled continuous iv morphine delivery systems are useful.
Liaise with the Acute Pain Service, if possible.
Non-narcotic (simple) analgesia
Paracetamol 0.5–1.0g/4h po (up to 4g daily; 15mg/kg/4h iv over 15min in children <50kg; up to 60mg/kg/d). Caution in liver impairment. nsaids, eg ibuprofen 400mg/8h po (see bnfc for dosing in children) or diclofenac 50mg/8h po, or 100mg pr, or 75mg im stat; these are good for musculoskeletal pain and renal or biliary colic. ci: peptic ulcer, clotting disorders, anticoagulants. Cautions: asthma, renal or hepatic impairment, heart failure, ihd, pregnancy and the elderly. Aspirin is contraindicated in children due to the risk of Reye’s syndrome (ohcs p652).
Opioid drugs for severe pain
Morphine (eg 10–15mg/2–4h iv/im) or diamorphine (5–10mg/2–4h po, sc, or slow iv, but you may need much more) are best. nb: these are ‘controlled’ drugs. For palliative care, see p538.
Side-effects of opioids:
These include nausea (so give with an anti-emetic, p241), respiratory depression, constipation, cough suppression, urinary retention, bp↓, and sedation (do not use in hepatic failure or head injury). Dependency is rarely a problem. Naloxone (eg 100–200µg iv, followed by 100µg increments, eg every 2min until responsive) may be needed to reverse the effects of excess opioids (p854).
How effective are standard analgesics?
Pain is subjective, but its measurement by patients is surprisingly consistent and reproducible. The table below gives ‘number needed to treat’ (nnt, p669), ie the number of patients who need to receive the drug for one to achieve at least 50% pain relief over 4–6h (the range is 95% confidence intervals).
Codeine60mg | 11–48 | Paracetamol1000mg | 3–4 |
Tramadol50mg | 6–13 | Paracetamol1000mg/codeine60mg | 2–3 |
Aspirin650mg/codeine60mg | 4–7 | Diclofenac50mg or ibuprofen400mg | 2–3 |
Codeine60mg | 11–48 | Paracetamol1000mg | 3–4 |
Tramadol50mg | 6–13 | Paracetamol1000mg/codeine60mg | 2–3 |
Aspirin650mg/codeine60mg | 4–7 | Diclofenac50mg or ibuprofen400mg | 2–3 |
Epidural analgesia
Opioids and anaesthetics are given into the epidural space by infusion or as boluses. Ask the advice of the Pain Service. ses are thought to be less, as the drug is more localized: watch for respiratory depression and local anaesthetic-induced autonomic blockade (bp↓).
Adjuvant treatments
Eg radiotherapy for bone cancer pain; anticonvulsants, antidepressants, gabapentin or steroids for neuropathic pain, antispasmodics, eg hyoscine butylbromide1 (Buscopan® 10–20mg/8h po/im/iv) for intestinal, renal tract colic. If brief pain relief is needed (eg for changing dressings or exploring wounds), try inhaled nitrous oxide (with 50% O2—as Entonox®) with an ‘on-demand’ valve. Transcutaneous electrical nerve stimulation (tens), local heat, local or regional anaesthesia, and neurosurgical procedures (eg excision of neuroma) may be tried but can prove disappointing. Treat conditions that exacerbate pain (eg constipation, depression, anxiety).
Why is controlling post-operative pain so important?Psychological reasons: Pain control is a humanitarian undertaking.
Social reasons: Pain relief makes surgery less feared.
Biological reasons: There is evidence for the following sequence: pain → autonomic activation → increased adrenergic activity → arteriolar vasoconstriction → reduced wound perfusion → decreased tissue oxygenation → delayed wound healing → serious or mortal consequences.
General post-operative complications
Pyrexia
Mild pyrexia in the 1st 48h is often from atelectasis (needs prompt physio, not antibiotics), tissue damage/necrosis or even from blood transfusions, but still have a low threshold for infection screen. See minibox for where to look for infection—also check the legs for dvt (causes ↑°t). Send blood for fbc, u&e, crp, and cultures (±lft). Dipstick the urine. Consider msu, cxr, and abdominal ultrasound/ct depending on clinical findings.
Confusion
may manifest as agitation, disorientation, and attempts to leave hospital, especially at night. Gently reassure the patient in well-lit surroundings. See p488 for a full work-up. Common causes are:
Hypoxia (pneumonia, atelectasis, lvf, pe)
Drugs (opiates, sedatives, and many others)
Urinary retention
mi or stroke
Infection (see above)
Alcohol withdrawal (p282)
Liver/renal failure
Occasionally, sedation is necessary to examine the patient; consider lorazepam 1mg po/im (antidote: flumazenil) or haloperidol 0.5–2mg im. Reassure relatives that post-op confusion is common (seen in up to 40%) and reversible.
Dyspnoea or hypoxia
Any previous lung disease? Sit patient up and give O2, monitor peripheral O2 sats by pulse oximetry (p156). Examine for evidence of:
Tests
fbc; abg; cxr; ecg. Manage according to findings.
bp↓
If severe, tilt bed head-down and give O2. Check pulse and bp yourself; compare it with pre-op values. Post-op ↓bp is often from hypovolaemia resulting from inadequate fluid input, so check fluid chart and replace losses. Monitor urine output (may need catheterization). A cvp line can help monitor fluid resuscitation (normal is 0–5cm H2O relative to sternal angle). Hypovolaemia may also be caused by haemorrhage so review wounds and abdomen. If unstable, return to theatre for haemostasis. Beware cardiogenic and neurogenic causes and look for evidence of mi or pe. Consider sepsis and anaphylaxis.
Management:
p804.
bp↑
may be from pain, urinary retention, idiopathic hypertension (eg missed medication) or inotropic drugs. Oral cardiac medications (including antihypertensives) should be continued throughout the perioperative period even if nbm. Treat the cause, consider increasing the regular medication, or if not absorbing orally try 50mg labetalol iv over 1min (see p134).
Urine output↓ (oliguria)
Aim for output of >30mL/h in adults (or >0.5mL/kg/h). Anuria often means a blocked or malsited catheter (see p777) rather than aki and never, we hope, an impending lawsuit from both ureters tied. Flush or replace catheter. Oliguria is usually due to too little replacement of lost fluid. Treat by increasing fluid input. Acute renal failure may follow shock, drugs, transfusion, pancreatitis or trauma (see p292 for pre-renal/intrinsic/post-renal causes and management of aki).
Review fluid chart and examine for signs of volume depletion.
Urinary retention is also common, so examine for a palpable bladder.
Establish normovolaemia (a cvp line may help here); you may need 1L/h ivi for 2–3h. A ‘fluid challenge’ of 250–500mL over 30min may also help.
Catheterize bladder (for accurate monitoring)—see p776; check u&e.
If intrinsic renal failure is suspected, stop any nephrotoxic drugs (eg nsaids, ace-i) and refer to a nephrologist early.
Nausea/vomiting
Any mechanical obstruction, ileus, or emetic drugs (opiates, digoxin, anaesthetics)? Consider axr, ngt, and an anti-emetic (not metoclopramide because of its prokinetic property). See p241 for choice of anti-emetics.
↓Na+
Check for signs of:
Peritonism
Chest infection
uti
Wound infection
Cannula site erythema
Meningism
Endocarditis
Continuous bleeding, starting during surgery. Replace blood loss. If severe, return to theatre for adequate haemostasis. Treat shock vigorously (p804).
Haemostasis appears secure until bp rises and bleeding starts. Replace blood and re-explore wound.
(caused by infection) occurs 1–2 weeks post-op.
When asked to give your thoughts on the complications of an operation—maybe with an examiner or a patient—a good starting point is to divide them up accordingly (and for each of the following stratify as immediate, early and late):
From the anaesthetic: (p574) eg respiratory depression from induction agents.
From the specific procedure: eg saphenous nerve damage in stripping of the long varicose vein.
Tailor the discussion towards the individual who, eg if an arteriopath, may have a significant risk of cardiac ischaemia during hypotensive episodes whilst under the anaesthetic. For some other post-op complications, see:
Pain (p576)
Wound dehiscence (p582)
Complications in post-gastric surgery (p624)
Other complications of specific operations (p582).
A normal duplex ultrasound (sagittal view) of the superficial femoral vein with a normal Doppler trace. Compression ultra-sound (fig 2) is the best image in suspected dvt.
Ultrasound showing a transverse view of the femoral artery and vein. Here, the lumen of the femoral vein (deeper and medial to the artery) is occluded by thrombus, giving a hyperechoic signal compared to the arterial lumen.
Transverse ultrasound of the superficial femoral vein and artery with (right) and without (left) compression. Collapse of the vein (deeper to the artery) on compression means absence of thrombus.
Ultrasound showing evidence of an acute thrombus within a dilated superficial femoral vein. This will not always show an intraluminal echo (compare with fig 4) and so confirm its presence by lack of compression of the vein with the ultrasound probe.
Deep vein thrombosis (dvt)
See figs, p579
Risk factors
Age↑, pregnancy, synthetic oestrogen, trauma, surgery (especially pelvic/orthopaedic), past dvt, cancer, obesity, immobility, thrombophilia (p368).
Signs
Calf warmth/tenderness/swelling/erythema
Mild fever
Pitting oedema.
ΔΔ:
Cellulitis; ruptured Baker’s cyst. Both may coexist with a dvt.
Tests
A colostomy sits flush with the skin and is typically sited in the left iliac fossa.
Prevention
Stop the Pill 4wks pre-op.
Mobilize early.
Low molecular weight heparin (lmwh, eg enoxaparin 20mg/24h sc, ↑ to 40mg for high-risk patients, p369, starting 12h pre-op).
Treatment
Swollen legs
Bilateral oedema
implies systemic disease with ↑venous pressure (eg right heart failure) or ↓intravascular oncotic pressure (any cause of ↓albumin, so test the urine for protein). It is dependent (distributed by gravity), which is why legs are affected early, but severe oedema extends above the legs. In the bed-bound, fluid moves to the new dependent area, causing a sacral pad. The exception is the local increase in venous pressure occurring in ivc obstruction: the swelling neither extends above the legs nor redistributes.
Causes:
Right heart failure (p128);
Albumin ↓ (p700, eg renal or liver failure);
Venous insufficiency: acute, eg prolonged sitting, or chronic, with haemosiderin-pigmented, itchy, eczematous skin ± ulcers;
Vasodilators, eg nifedipine, amlodipine.
Pregnancy—if bp↑ + proteinuria, diagnose pre-eclampsia (ohcs p48): find an obstetrician urgently. In all the above, both legs need not be affected to the same extent.
Unilateral oedema:
Pain ± redness implies dvt or inflammation, eg cellulitis or insect bites (any blisters?). Bone or muscle may be to blame, eg tumours; necrotizing fasciitis (p662); trauma (check for sensation, pulses and severe pain esp. on passive movement: a compartment syndrome with ischaemic necrosis needs prompt fasciotomy). Impaired mobility suggests trauma, arthritis, or a Baker’s cyst (p708). Non-pitting oedema is oedema you cannot indent: see p29.
In patients with symptoms in both legs, the more symptomatic leg is used.
| Clinical features | Score |
|---|---|
Active cancer (treatment within last 6 months or palliative) | 1 point |
Paralysis, paresis, or recent plaster immobilization of leg | 1 point |
Recently bedridden for >3d or majory surgery in last 12wks | 1 point |
Local tenderness along distribution of deep venous system | 1 point |
Entire leg swollen | 1 point |
Calf swelling >3cm compared with asymptomatic leg (measured 10cm below tibial tuberosity) | 1 point |
Pitting oedema (greater in the symptomatic leg) | 1 point |
Collateral superficial veins (non-varicose) | 1 point |
Previously documented dvt | 1 point |
Alternative diagnosis at least as likely as dvt | –2 points |
| Clinical features | Score |
|---|---|
Active cancer (treatment within last 6 months or palliative) | 1 point |
Paralysis, paresis, or recent plaster immobilization of leg | 1 point |
Recently bedridden for >3d or majory surgery in last 12wks | 1 point |
Local tenderness along distribution of deep venous system | 1 point |
Entire leg swollen | 1 point |
Calf swelling >3cm compared with asymptomatic leg (measured 10cm below tibial tuberosity) | 1 point |
Pitting oedema (greater in the symptomatic leg) | 1 point |
Collateral superficial veins (non-varicose) | 1 point |
Previously documented dvt | 1 point |
Alternative diagnosis at least as likely as dvt | –2 points |
Perform d-dimer. If negative, dvt excluded. If positive, proceed to uss (if uss negative, dvt excluded; if positive, treat as dvt).
Do d-dimer and uss. If both negative, dvt excluded. If uss positive, treat as dvt. If d-dimer positive and uss negative, repeat uss in 1 week.
Reproduced from cmaj 2006, Scarvelis D, Wells PS: Diagnosis and treatment of deep-vein thrombosis, Oct 24;175(9):1087–92. Vol 350, used with permission.
Is it both legs?
Is she pregnant?
Is she mobile?
Any trauma?
Any pitting (p29)?
Past diseases/on drugs?
Any pain?
Any skin changes?
Any oedema elsewhere?
Look for proteinuria (+hypoalbuminaemia (≈nephrotic syndrome)). Is there ccf (echocardiogram)?
In 1954, Homans reported an association between air travel and venous thromboembolism. Factors such as dehydration, immobilization, decreased oxygen tension, and prolonged pressure on the popliteal veins resulting from long periods in aircraft seats have all been suggested to be contributory factors. While the evidence linking air travel to an increased risk of dvt is still largely circumstantial, the following facts may help answer questions from your patients, family, and friends:
The risk of developing a dvt from a long-distance flight has been estimated at 1 in 10,000 to 1 in 40,000 for the general population.
Measures to minimize risk of dvt include leg exercises, increased water intake, and refraining from alcohol or caffeine during the flight.
Specific post-operative complications
Laparotomy
Biliary surgery
After exploration of the common bile duct (cbd), a t-tube is usually left in the bile duct draining freely to the exterior. A t-tube cholangiogram is done at 8–10d, and if there are no retained stones the tube may be pulled out. Retained stones may be removed by ercp (p756), further surgery, or instillation of stone-dissolving agents (via t-tube). If there is distal obstruction in the cbd, fistula formation may occur with a chronic leakage of bile. Other complications of biliary surgery are cbd stricture; cholangitis; bleeding into the biliary tree (haemobilia) which may lead to biliary colic, jaundice, and haematemesis; pancreatitis; bile leak causing biliary peritonitis. If jaundiced, it is important to maintain a good urine output, monitor coagulation and consider antibiotics. There is a danger of hepatorenal syndrome (p259).
Thyroid surgery
relieve by immediate removal of stitches or clips using the cutter/remover that should remain at the beside; may require urgent surgery.Mastectomy
Arterial surgery
Bleeding; thrombosis; embolism; graft infection; mi; av fistula formation.
Complications of aortic surgery:
Gut ischaemia; renal failure; respiratory distress; aorto-enteric fistula; trauma to ureters or anterior spinal artery (leading to paraplegia); ischaemic events from distal trash from dislodged thrombus.
Colonic surgery
Small bowel surgery
Tracheostomy
Stenosis; mediastinitis; surgical emphysema.
Splenectomy
(p367) Acute gastric dilatation (a serious consequence of not using a ngt, or to check that the one in place is working); thrombocytosis; sepsis. Lifetime sepsis risk is partly preventable with pre-op vaccines—ie Haemophilus type b, meningococcal, and pneumococcal (p391 & p160) and prophylactic penicillin.
Genitourinary surgery
Septicaemia (from instrumentation in the presence of infected urine)—consider a stat dose of gentamicin; urinoma—rupture of a ureter or renal pelvis leading to a mass of extravasated urine.
Gastrectomy
See p624.
Prostatectomy
p645.
Haemorrhoidectomy
p634.
When re-operating on the abdomen, the struggle against adhesions tests the farthest and darkest boundaries of patience of the abdominal surgeon and the assistant. The skill and persistence required to gently and atraumatically tease apart these fibrous bands that restrict access and vision makes any progression, no matter how slight, cause for subdued celebration. Perseverance is the name of this game.
Stoma care
A stoma (Greek=mouth) is an artificial union between a conduit and the outside world—eg a colostomy, in which faeces are made to pass through an opening in the abdominal wall when a loop of colon is brought out onto the skin. nb A stoma can also be made between 2 internal conduits (eg a choledochojejunostomy).
Colostomies
Loop colostomy: A loop of colon is exteriorized and partially divided, forming 2 stomas that are joined together (the proximal end passes stool, the distal end passes mucus, see fig 1). A rod under the loop prevents retraction and may be removed after 7d. A loop colostomy is often temporary and performed to protect a distal anastamosis, eg after anterior resection.
End colostomy: The bowel is divided and the proximal end brought out as a stoma; the distal end may be:
resected, eg abdominoperineal (ap) resection (inspect the perineum for absent anus when examining a stoma);
closed and left in the abdomen (Hartmann’s procedure);
exteriorized, forming a ‘mucous fistula’.
Paul–Mikulicz colostomy: A double-barrelled colostomy in which the colon is divided completely (eg to excise a section of bowel). Each end is exteriorized as two separate stomas.
A loop colostomy with double-barrelled stoma and supporting ostomy rod.
Output:
Colostomies ideally pass 1–2 formed motions/day into an adherent plastic pouch. Some may be managed with irrigation, thus avoiding a pouch.
Incidence:
Ileostomies
protrude from the skin and emit frequent fluid motions which contain active enzymes (so the skin needs protecting), see fig 2. End ileostomy usually follows total proctocolectomy, typically for uc; loop ileostomies can also be formed.
An ileostomy sits proud, has prominent mucosal folds, and is often right-sided.
Defunctioning stomas
The alternatives to colostomy
Low/ultralow anterior resection:
All or part of the rectum is excised and the proximal colon anastamosed to the top of the anal canal (the lower the level of anastamosis, the higher the risk of complication).
Ileoanal pouch formation:
Total anorectal reconstruction:
An electrically stimulated sphincter is created using gracilis muscle, or an artificial mechanical sphincter implanted after, eg ap excision of the rectum.
Transanal endoscopic microsurgery:
Early direct self-referral prevents problems. Without input from the stoma nurse, a patient may reject his colostomy, never attend to it, or even become suicidal.Urostomies
Liaise early with the stoma nurse, starting pre-operatively.
Haemorrhage at stoma site
Stoma ischaemia—colour progresses from dusky grey to black
High output (can lead to K+↓)—consider loperamide ± codeine to thicken output
Obstruction secondary to adhesions (see p583)
Stoma retraction
Obstruction (failure at operation to close lateral space around stoma)
Dermatitis around stoma site (worse with ileostomy)
Stoma prolapse
Stomal intussusception
Stenosis
Fistulae
Psychological problems
When choosing the site for a stoma, avoid:
Bony prominences (eg anterior superior iliac spine, costal margins)
The umbilicus
Old wounds/scars—there may be adhesions beneath
Skin folds and creases
The waistline
The site should be assessed pre-operatively by the stoma nurse, with the patient both lying and standing
Colostomies are most often placed in the left iliac fossa (fig 3) whereas a stoma in the right iliac fossa is more likely to be an ileostomy/ileal conduit.
Nutritional support in hospital
Over 25% of hospital inpatients may be malnourished. Hospitals can become so focused on curing disease that they ignore the foundations of good health—malnourished patients recover more slowly and experience more complications.1
Why are so many hospital patients malnourished?
Increased nutritional requirements (eg sepsis, burns, surgery)
Increased nutritional losses (eg malabsorption, output from stoma)
Decreased intake (eg dysphagia, nausea, sedation, coma)
Effect of treatment (eg nausea, diarrhoea)
Enforced starvation (eg prolonged periods nil by mouth)
Missing meals through being whisked off, eg for investigations
Difficulty with feeding (eg lost dentures; no one available to assist)
Unappetizing food
Identifying the malnourished patient
History: Recent weight↓ (>20%, accounting for fluid balance); recent reduced intake; diet change (eg recent change in consistency of food); nausea, vomiting, pain, diarrhoea which might have led to reduced intake.
Examination: State of hydration (p680): dehydration can go hand-in-hand with malnutrition, and overhydration can mask malnutrition. Evidence of malnutrition: skin hanging off muscles (eg over biceps); no fat between fold of skin; hair rough and wiry; pressure sores; sores at corner of mouth. Calculate body mass index (p236); bmi <20kg/m2 suggests malnourishment. Anthropomorphic indices, eg mid arm circumference, skin fold measures and grip strength are also used.
Investigations: Generally unhelpful. Low albumin suggestive, but is affected by many things other than nutrition. Albumin ↑ can be helpful in monitoring recovery.
Prevention of malnutrition
Assess nutrition state and weight on admission, and, eg weekly thereafter. Identify those at risk (see above). Ensure that meals are uninterrupted, when possible. Provide appetizing food to the patient when they want to eat it. If the patient requires nutritional support, seek help from a dietician.
Enteral nutrition
Tube feeding:
Guidelines for success
Use fine-bore (9 Fr) nasogastric feeding tube when possible.
Check position of nasogastric tube (pH testing) or nasoduodenal tube (x-ray) before starting feeding.
Build up feeds gradually to avoid diarrhoea and distension.
Weigh weekly, check blood glucose and plasma electrolytes (including phosphate, zinc, and magnesium, if previously malnourished).
Treat underlying conditions vigorously, eg sepsis may impede +ve nitrogen balance.
Close liaison with a dietician is essential.
If in doubt about what is acceptable oral intake prior to induction for general anaesthesia (eg for gi surgery), it is best to liaise with the anaesthetist concerned. However, guidelines have been published by many colleges and societies to outline what is safe in the perioperative period:
Parenteral (intravenous) nutrition
Even if there is gi disease, studies show that enteral nutrition is safer, cheaper, and at least as efficacious as parenteral nutrition in the perioperative period.1Administration
Neck veins
Right arm picc (peripherally inserted central catheter) still with a wire in the lumen. This is a radiograph at the time of insertion to determine if placement is correct. The tip lies in the svc—ie good positioning for long-term antibiotic therapy. The tip of a Hickman line, for cytotoxic administration, is better in the right atrium, to avoid possible irritation of the svc and consequent thrombosis or stenosis.
Requirements
There are many different regimens for parenteral feeding. Most provide 2000kCal and 10–14g nitrogen in 2–3L; this usually meets a patient’s daily requirements (see table, p587). ∼50% of calories are provided by fat and ∼50% by carbohydrate. Regimens comprise vitamins, minerals, trace elements, and electrolytes; these will normally be included by the pharmacist.
| Substance | Requirement (/kg/d) | Notes |
|---|---|---|
Energy | 20–40kCal | Normal adult requirements will be 2000–2500kCal/d; even catabolic patients rarely require >2500kCal/d. Very high calorie diets (eg >4000kCal/d) can lead to a fatty liver. |
84–168kJ | Multiply kCal by a factor of 4.2. | |
Nitrogen | 0.2–0.4g | 6.25g of enteral protein gives 1g of nitrogen. Considering nitrogen balance is important because although catabolism is inevitable, replenishment is vital. |
Protein | 0.5g | Contains 5kCal/g. |
Fat | 3g | Contains 10kCal/g. |
Carbohydrate | 2g | Contains 4kCal/g. |
Water | 30–35mL | +500mL/d for each °C of pyrexia. |
Na/K/Cl | 1.0mmol each | Electrolytes need to be considered, even if not on ivi. |
| Substance | Requirement (/kg/d) | Notes |
|---|---|---|
Energy | 20–40kCal | Normal adult requirements will be 2000–2500kCal/d; even catabolic patients rarely require >2500kCal/d. Very high calorie diets (eg >4000kCal/d) can lead to a fatty liver. |
84–168kJ | Multiply kCal by a factor of 4.2. | |
Nitrogen | 0.2–0.4g | 6.25g of enteral protein gives 1g of nitrogen. Considering nitrogen balance is important because although catabolism is inevitable, replenishment is vital. |
Protein | 0.5g | Contains 5kCal/g. |
Fat | 3g | Contains 10kCal/g. |
Carbohydrate | 2g | Contains 4kCal/g. |
Water | 30–35mL | +500mL/d for each °C of pyrexia. |
Na/K/Cl | 1.0mmol each | Electrolytes need to be considered, even if not on ivi. |
Complications
Thrombosis: Central vein thrombosis may occur, resulting in pulmonary embolus or superior vena caval obstruction (p526). Heparin in the nutrient solution may be useful for prophylaxis in high-risk patients, though there is little clear-cut evidence in adult studies.
Mechanical: Pneumothorax; embolism of iv line tip.
Guidelines for success
Liaise closely with line insertion team, nutrition team and pharmacist.
Meticulous sterility. Do not use central venous lines for uses other than nutrition. Remove the line if you suspect infection. Culture its tip.
Review fluid balance at least twice daily, and requirements for energy and electrolytes daily.
Check weight, fluid balance, and urine glucose daily throughout period of parenteral nutrition. Check plasma glucose, creatinine and electrolytes (including calcium and phosphate), and fbc daily until stable and then 3 times a week. Check lft and lipid clearance three times a week until stable and then weekly. Check zinc and magnesium weekly throughout.
Do not rush. Achieve the maintenance regimen in small steps.
Treat underlying conditions vigorously—eg sepsis may impede +ve nitrogen balance.
This is a life-threatening metabolic complication of refeeding via any route after a prolonged period of starvation. As the body turns to fat and protein metabolism in the starved state, there is a drop in the level of circulating insulin (because of the paucity of dietary carbohydrates). The catabolic state also depletes intracellular stores of phosphate, although serum levels may remain normal (0.85–1.45mmol/L). When refeeding begins, the level of insulin rises in response to the carbohydrate load, and one of the consequences is to increase cellular uptake of phosphate.A hypophosphataemic state (<0.50mmol/L) normally develops within 4d and is mostly responsible for the features of ‘refeeding syndrome’, which include: rhabdomyolysis; red and white cell dysfunction; respiratory insufficiency; arrhythmias; cardiogenic shock; seizures; sudden death.
requires at-risk patients to be identified, assessed and monitored closely during refeeding (glucose, lipids, sodium, potassium, phosphate, calcium, magnesium, and zinc). Close involvement of a nutritionist is required.
Malignancy
Anorexia nervosa
Alcoholism
gi surgery
Starvation
When trying to judge the position of a central venous line tip on cxr (see figs 2 and 3) it helps to know the anatomical landmarks of the venous system. The subclavian veins join the internal jugular veins behind the sternoclavicular joints to form the brachiocephalic veins. These come together behind the right 1st sternocostal joint to form the superior vena cava (svc), which runs from this point to the right 3rd sternocostal joint. The right atrium starts here.
cxr showing placement of a dual lumen haemodialysis catheter. It is tunnelled through the subcutaneous tissues, enters the left internal jugular vein, and travels through the left brachiocephalic vein and svc to enter the right atrium. The tip lies best in the svc or right atrium, any further and it might damage the tricuspid valve.
Both images were acquired in the angiography room, where radio-opaque material appears black (it is easier to see contrast media against a white background).
Diabetic patients undergoing surgery58
Insulin-treated diabetes mellitus
Try to place the patient first on the list in order to minimize the fasting period.
Give all usual insulin the night before surgery.
Long-acting (basal) insulin is usually continued at normal times (eg Glargine; Detemir), even when patients are on a variable rate intravenous insulin infusion (vriii)—previously known as a ‘sliding scale’ (see box 1).
If on am list, ensure no subcutaneous rapid-acting (bolus) or mixed insulin is given on the morning of surgery. If pm list, give the normal morning bolus insulin, or half the mixed insulin dose.
If eating and drinking post-operatively, resume the usual insulin with evening meal. If am list (or early pm) and eating a late lunch, give half the morning insulin dose with this meal. If not eating until evening, a vriii may be needed if the capillary glucose readings are high.
Omit all rapid-acting and mixed insulin whilst the patient is on a vriii.
It not eating or drinking post-op, start a vriii 2 hours prior to surgery. Aim for serum glucose levels of 6–10mmol/L and check finger-prick glucose every 2 hours. When ready to eat, give normal dose of rapid acting or mixed insulin with the 1st meal and stop the vriii 30–60min later.
iv fluid is required whilst the patient is on a vriii: see box 1.
A glucose–potassium–insulin (gki) infusion can be used as an alternative to a vriii (see box 2), although it is no longer used as standard in the uk.
Tablet-treated diabetes mellitus
If diabetes is poorly controlled (eg fasting glucose >10mmol/L), treat as for patients on insulin (above).
Give usual medications the night before surgery, except long-acting sulfonylureas (eg glibenclamide) which can cause prolonged hypoglycaemia when fasting and may need to be substituted 2–3 days pre-operatively. Discuss with the diabetes team.
If eating and drinking post-operatively: On am list, omit morning medication and take any missed drugs with lunch, after surgery. If pm list, take normal medications with breakfast, omit midday doses and take any missed drugs with a late lunch. The dose of these may need reducing, depending on dietary intake.
If not eating or drinking post-op, start a vriii 2 hours prior to surgery. Once eating and drinking, oral hypoglycaemics can be restarted.
Some patients may need a phase of subcutaneous insulin following major surgery—refer to the diabetes team if serum glucose levels are persistently raised.
Diet-controlled diabetes
There are usually no issues and patients should be treated as if not diabetic (and do not need to be first on the list). Check capillary blood glucose perioperatively. Avoid 5% glucose ivi as this increases blood glucose levels.
Perioperative morbidity and mortality
| Capillary blood glucose (mmol/L) | iv soluble insulin (rate of infusion) |
|---|---|
<4.0 | 0.5 units/h (0.0 if long-acting insulin continued) |
4.1–7.0 | 1 unit/h |
7.1–9.0 | 2 units/h |
9.1–11.0 | 3 units/h |
11.1–14.0 | 4 units/h |
14.1–17.0 | 5 units/h |
17.1–20 | 6 units/h |
>20 | 6 units/h; request urgent diabetic review |
| Capillary blood glucose (mmol/L) | iv soluble insulin (rate of infusion) |
|---|---|
<4.0 | 0.5 units/h (0.0 if long-acting insulin continued) |
4.1–7.0 | 1 unit/h |
7.1–9.0 | 2 units/h |
9.1–11.0 | 3 units/h |
11.1–14.0 | 4 units/h |
14.1–17.0 | 5 units/h |
17.1–20 | 6 units/h |
>20 | 6 units/h; request urgent diabetic review |
Fluids should be prescribed to run with the vriii (through the same cannula via a non-return valve). Ideally use 0.45% sodium chloride with 5% glucose and either 0.15% potassium chloride (kcl) (=20mmol/L) or 0.3% kcl (=40mmol/L). This provides a constant supply of substrate, but it is not widely available.
Alternatively, use 10% glucose + kcl. This has a lower risk of hypoglycaemia and hyponatraemia than 5% glucose. If capillary glucose >15mmol/L when starting the vriii use 0.9% saline until <15mmol/L, then use 10% glucose.
Fluid should infuse at 83–125mL/h (ie 1L over 8–12 hours). Omit potassium if there is renal impairment or hyperkalaemia and slow the rate of infusion in heart failure.
| Blood glucose (mmol/L) | Insulin dose (units/bag) | Serum K+ (mmol/L) | KCl to be added (mmol/bag ) |
|---|---|---|---|
<4 | None | <3 | 20 |
4–6 | 5 | 3–5 | 10 |
6–10 | 10 | >5 | None |
10–20 | 15 | ||
>20 | 20 |
| Blood glucose (mmol/L) | Insulin dose (units/bag) | Serum K+ (mmol/L) | KCl to be added (mmol/bag ) |
|---|---|---|---|
<4 | None | <3 | 20 |
4–6 | 5 | 3–5 | 10 |
6–10 | 10 | >5 | None |
10–20 | 15 | ||
>20 | 20 |
Check blood glucose every 2h. If levels too high or low, start a new 500mL bag of glucose with the correct insulin dose (aim for 7–10mmol/L).
gki infusions are not suitable in poorly controlled diabetes or patients who are very unwell (where close serum glucose monitoring is required).
If the patient is fluid restricted use 250mL of 20% glucose with the same insulin dose as above. If the patient is hyponatraemic then a concomitant infusion of 0.9% saline should be considered.
Check u&e daily.
nb: regimens vary and sometimes more insulin will be required. See bnf section 6.1.
Jaundiced patients undergoing surgery
Operating in patients with obstructive jaundice is best avoided, especially with the availability of ercp. There is increased risk of perioperative infection, bleeding and renal failure. Prevention of these is key:
Coagulopathy
Sepsis
Susceptibility to infection is due (in part) to
Increased bacterial translocation
Bacterial colonization of the biliary tree and
Renal failure
Surgery in those on steroids
Minor procedures under local anaesthetic: No supplementation required.
Moderate procedures: (Eg joint replacement) Give 50mg hydrocortisone before induction and 25mg every 8h for 24h. Resume normal dose thereafter.
Major surgery: Give 100mg hydrocortisone before induction and 50mg every 8h for 24h. After 24h, halve this dose each day until the level of maintenance.
Patients with primary adrenal insufficiency will need extra cover—discuss with an endocrinologist. The major risk with adrenal insufficiency is hypotension, so if this is encountered without an obvious cause, consider a stat dose of hydrocortisone. 
See p846 for treatment of Addisonian crisis and bnf section 6.3 for steroid dose equivalents.
Surgery in those on anticoagulants
Inform the surgeon and anaesthetist. Minor surgery can be undertaken without stopping warfarin (if inr <3.5 it may be safe to proceed). In major surgery, drugs may be stopped for 2–5d pre-op. Risks and benefits are individual to each patient, so exact rules are impossible. Discuss these issues when arranging consent. Vitamin k ± ffp or Beriplex® may be needed for emergency reversal of inr. One elective option is conversion to heparin (stop 6h prior to surgery, and monitor aptt perioperatively): unfractionated heparin’s short t½ allows swift reversal with protamine (p344). When re-warfarinizing, continue heparin until the inr is therapeutic, as warfarin is prothrombotic in the early stages.Surgery can play a significant role in the management of thyroid disease. Operations include partial lobectomy or lobectomy (for isolated nodules); and thyroidectomy (for thyroid cancers, multinodular goitre or Graves’ disease). See also p602.
Pre-operative management:
The cause of hyperthyroidsim or swelling should be fully investigated prior to any surgery.
Check serum Ca2+ (and pth if abnormal).
Arrange laryngoscopy to visualize vocal cords (risk of recurrent laryngeal nerve injury).
Treat hyperthyroidism pre-operatively with antithyroid drugs until the patient is euthyroid (p210), eg carbimazole up to 20mg/12h po or propylthiouracil 200mg/12h po. Potassium iodide also has a role.
Propranolol up to 80mg/8h po can be used to control tachycardia or tremor associated with hyperthyroidism (continue for 5d post-op).
Complications of thyroid surgery: See p582.
Thyrotoxic storm is a rare but potentially fatal consequence of thyroid surgery (mortality 50%). See p845.
Minimally invasive surgery
The terms ‘keyhole surgery’ or ‘minimal access surgery’ may be preferred, because these procedures can be as invasive as any laparotomy, having just the same set of side-effects—plus some new ones. It is the size of the incision and the use of laparoscopes that marks out this branch of surgery. Laparoscopy was developed within gynaecology and is now in widespread use for diagnostic purposes and surgical procedures such as appendicectomy, fundoplication, splenectomy, adrenalectomy, hernia repair, colectomy, prostatectomy and nephrectomy. Minimally invasive surgery is also used for thyroidectomy and parathyroidectomy.
Problems with minimal access surgery:
For the surgeon
The 2-dimensional visual representation and different surgical approach alters the normal appearance of familiar anatomy. Palpation is impossible and it may be harder to locate colonic lesions prior to resection. As a result, pre-operative imaging may need to be more extensive. A fundamental problem is that of skill: not just that a new skill has to be learned and taught but that old skills may become attenuated. New surgeons may not achieve optimal skill in either open or laparoscopic surgery if they try to do both.
For patients and gps
Post-operative complications: What may be easily managed on a well-run surgical ward (eg haemorrhage) may be a challenge for a gp and terrify the patient, who may be all alone after early discharge.
Loss of tell-tale scars: Afterwards there may only be a few abdominal wounds, so future carers have to guess at what has been done. The answer here is to communicate carefully with the patient, so that they know what has been done—see box 2.
For hospitals
Just because minimal access surgery is often cost-effective, it does not follow that hospitals can afford the procedures. Instruments are continuously being refined, and quickly become obsolete—so that many are now produced in disposable single-use form. Because of budgeting boundaries, hospitals cannot use the cash saved, by early return to work or by freeing-up bed space, to pay for capital equipment and extra theatre time that may be required.
See also: OHClinSurg p46.
Perioperative care has evolved from the inpatient setting, with better results for the patient.1 Many operations are performed as day-cases. Theoretically any procedure is suitable, provided the time under general anaesthetic does not exceed ∼1h. The use of regional anaesthesia helps to avoid the se of nausea and disorientation that may accompany a general anaesthetic, thus facilitating discharge.
To avoid putting the patient at unnecessary risk, it is important to identify those who are not suitable for day-case surgery:
Poor communication (if co-operation required during anaesthetic procedure), severe claustrophobia.
Lucid, not vomiting, and cough reflex established.
Easy breathing; easy urination.
Ambulant without fainting.
Pain relief + post-op drugs dispensed and given. Does the patient understand doses?
Follow-up arranged (if required).
Rhythm, pulse & bp checked: is trend satisfactory? Check no postural drop.
Operation site checked and explained to patient.
GP letter sent with patient or carer—the gp must know what has happened.
Exposing patients to our learning curves? The jury is still out…All surgeons get better over time (for a while), as they perform new techniques with increasing ease and confidence. When Wertheim did his first hysterectomies, his first dozen patients died—but then one survived. He assumed it was a good operation, and pressed ahead. He was a brave man, and thousands of women owe their lives to him. But had he tried to do this today, he would have been stopped. The uk’s General Medical Council (gmc) and other august bodies tell us that we must protect the public by reporting doctors whose patients have low survival rates. The reason for this is partly ethical, and partly to preserve self-regulation.
We have the toughest codes of practice and disciplinary procedures of any group of workers. It is assumed that doctors are loyal to each other out of self-interest, and that this loyalty is bad. This has never been tested formally, and is not evidence-based. We can imagine two clinical worlds: one of constant ‘reportings’ and recriminatory audits, and another of trust and team-work. Both are imperfect, but we should not assume that the first world would be better for our patients.
When patients are sick with fear, they do not, perhaps, want to know everything. We may tell to protect ourselves. We may not tell to protect ourselves. Perhaps what we should do is, in our hearts, appeal to those 12 dead women-of-Wertheim—a jury as infallible as sacrificial—and try to hear their reply. And to those who complain that in doing so we are playing God, it is possible to reply with some humility that, whatever it is, it does not seem like play.
“It is amazing what little harm doctors do when one considers all the opportunities they have” M. Twain.
Lumps
Examine the regional lymph nodes as well as the lump. If the lump is a node, examine its area of drainage. Always examine the circulation & nerve supply distal to any lump.
History
How long has it been there? Does it hurt? Any other symptoms, eg itch? Any other lumps? Is it getting bigger? Ever been abroad? Otherwise well?
Physical exam
Remember the 6 S’s: site, size, shape, smoothness (consistency), surface (contour/edge/colour), and surroundings.
Other questions:
Does it transilluminate (see below)? Is it fixed/tethered to skin or underlying structures (see box)? Is it fluctuant/compressible? Temperature? Tender? Pulsatile (us duplex may help)?
Transilluminable lumps
After eliminating as much external light as possible, place a bright, thin ‘pen’ torch on the lump, from behind (or at least to the side), so the light is shining through the lump towards your eye. If the lump glows red it is said to transilluminate—a fluid-filled lump such as a hydrocele is a good example.
Lipomas
Sebaceous cysts
Refer to either epidermal (fig 1) or pilar cysts (they are not of sebaceous origin and contain keratin, not sebum). They appear as firm, round, mobile subcutaenous nodules of varying size. Look for the characteristic central punctum. Infection is quite common, and foul pus exits through the punctum. They are common on the scalp, face, neck and trunk.
Epidermal cyst.
Treatment:
Excision of cyst and contents.
Lymph nodes
Causes of enlargement:
Infection:
Glandular fever; brucellosis; tb; hiv; toxoplasmosis; actinomycosis; syphilis.
Infiltration:
Malignancy (carcinoma, lymphoma); sarcoidosis.
Cutaneous abscesses
Staphylococci are the most common organisms. Haemolytic streptococci only common in hand infections. Proteus is a common cause of non-staphylococcal axillary abscesses. Below the waist faecal organisms are common (aerobes & anaerobes).
Treatment:
Incise and drain. Boils (furuncles) are abscesses involving a hair follicle and associated glands. A carbuncle is an area of subcutaneous necrosis which discharges itself on to the surface through multiple sinuses. Think of hidradenitis suppurativa if recurrent inguinal or axillary abscesses.
Rheumatoid nodules
Rheumatoid nodule.
Ganglia
Ganglion.
Fibromas
These may occur anywhere in the body, but most commonly under the skin. These whitish, benign tumours contain collagen, fibroblasts, and fibrocytes.
Dermoid cysts
Contain dermal structures and are found at the junction of embryonic cutaneous boundaries, eg in the midline or lateral to the eye.
Malignant tumours of connective tissue
Fibrosarcomas, liposarcomas, leiomyosarcomas (smooth muscle), and rhabdomyosarcomas (striated muscle). These are staged using modified tnm system including tumour grade. Needle-core (Trucut®) biopsies of large tumours precede excision. Any lesion suspected of being a sarcoma should not be simply enucleated. Refer to a specialist.
Neurofibromas
See p518.
Keloids
Caused by irregular hypertrophy of vascularized collagen forming raised edges at sites of previous scars that extend outside the scar (fig 4). Common in dark skin. Treatment can be difficult. Intralesional steroid injections are a mainstay.
Keloid scar.
| Intradermal | Subcutaneous |
|---|---|
• Sebaceous cyst • Abscess • Dermoid cyst • Granuloma | • Lipoma • Ganglion • Neuroma • Lymph node |
| Intradermal | Subcutaneous |
|---|---|
• Sebaceous cyst • Abscess • Dermoid cyst • Granuloma | • Lipoma • Ganglion • Neuroma • Lymph node |
If a lump is intradermal, you cannot draw the skin over it, while if the lump is subcutaneous you should be able to manipulate it independently from the skin.
Skin diagnoses not to be missed
Malignant tumours
if in doubt, refer. Refer if there are ≥3 points on the Glasgow scale, or with 1 point if suspicious. See fig 1.Squamous cell cancer Usually presents as an ulcerated lesion, with hard, raised edges, in sun-exposed sites. May begin in solar keratoses (below), or be found on the lips of smokers or in long-standing ulcers (=Marjolin’s ulcer). Metastasis to lymph nodes is rare, local destruction may be extensive. ℞: Excision + radiotherapy to treat recurrence/affected nodes. See fig 2. nb: the condition may be confused with a keratoacanthoma—a fast-growing, benign, self-limiting papule plugged with keratin.
Basal cell carcinoma (aka rodent ulcer) Nodular: Typically a pearly nodule with rolled telangiectatic edge, on the face or a sun-exposed site. May have a central ulcer. See fig 3. Metastases are very rare. It slowly causes local destruction if left untreated. Superficial: Lesions appear as red scaly plaques with a raised smooth edge, often on the trunk or shoulders. Cause: (most frequently) uv exposure. ℞: Excision; cryotherapy; for superficial bccs topical flurouracil or imiquimod (see below).
Melanoma.
Squamous cell cancer.
Basal cell carcinoma (bcc).
| Major (2 pts each) | Minor (1 pt each) | Less helpful signs |
|---|---|---|
• Change in size | • Inflammation, crusting, or bleeding | • Asymmetry |
• Change in shape | • Sensory change | • Irregular colour |
• Change in colour | • Diameter >7mm (unless growth is in the vertical plane: beware) | • Elevation • Irregular border |
| Major (2 pts each) | Minor (1 pt each) | Less helpful signs |
|---|---|---|
• Change in size | • Inflammation, crusting, or bleeding | • Asymmetry |
• Change in shape | • Sensory change | • Irregular colour |
• Change in colour | • Diameter >7mm (unless growth is in the vertical plane: beware) | • Elevation • Irregular border |
Pre-malignant tumours
Solar (actinic) keratoses appear on sun-exposed skin as crumbly, yellow-white crusts. Malignant change to squamous cell carcinoma may occur after several years. Treatment: Cryotherapy; 5% fluorouracil cream or 5% imiquimod—these work by causing: erythema → vesiculation → erosion → ulceration → necrosis → healing epithelialization, leaving healthy skin unharmed. Warn patients of the expected inflammatory reaction. See bnf for dosing regimens. Alternatively try diclofenac gel (3%; Solaraze®, use thinly twice-daily for ≤90d).
Bowen’s disease Slow-growing red/brown scaly plaque, eg on lower legs. Histology: Full-thickness dysplasia (carcinoma in situ). It infrequently progresses to squamous cell cancer. Penile Bowen’s disease is called Queyrat’s erythroplasia. Treatment: Cryotherapy, topical fluorouracil (see above) or photodynamic therapy.
Others
Secondary carcinoma Most common metastases to skin are from breast, kidney, or lung. Usually a firm nodule, most often on the scalp. See also acanthosis nigricans (p564)
Mycosis fungoides Cutaneous t-cell lymphoma usually confined to skin. Causes itchy, red plaques (Sézary syndrome-variant also associated with erythroderma)
Leucoplakia This appears as white patches (which may fissure) on oral or genital mucosa (where it may itch). Frank carcinomatous change may occur
Leprosy Suspect in any anaesthetic hypopigmented lesion (p428)
Asymmetry
Border—irregular
Colour—non-uniform
Diameter >7mm
Elevation
Lumps in the neck
Don’t biopsy lumps until tumours within the head and neck have been excluded by an ent surgeon. Culture all biopsied lymph nodes for tb.
Diagnosis
First, ask how long the lump has been present. If <3wks, self-limiting infection is the likely cause and extensive investigation is unwise. Next ask yourself where the lump is. Is it intradermal—eg sebaceous cyst with a central punctum (p596)? Is it a lipoma (p596)? If the lump is not intradermal, and is not of recent onset, you are about to start a diagnostic hunt over complicated terrain. 85% of neck swellings are lymph nodes (examine areas which they serve). Consider tb, viruses such as hiv or ebv (infectious mononucleosis), any chronic infection or, if >20yrs, consider lymphoma (hepatosplenomegaly?) or metastases (eg from gi or bronchial or head and neck neoplasia1), 8% are goitres (p602), and other diagnoses account for 7%.
Tests
Ultrasound shows lump consistency: cystic, solid, complex, vascular. ct defines masses in relation to their anatomical neighbours. Do virology and Mantoux test. cxr may show malignancy or, in sarcoid, reveal bilateral hilar lymphadenopathy. Consider fine-needle aspiration (fna).
Midline lumps:
If patient is <20yrs old, likely diagnosis is dermoid cyst (p596).
If it moves up on tongue protrusion and is below the hyoid, likely to be a thyroglossal cyst, a fluid-filled sac resulting from incomplete closure of the thyroid’s migration path. ℞: surgery; they are the commonest congenital cervical cystic lump.
If >20yrs old, it is probably a thyroid isthmus mass.
If it is bony hard, the diagnosis may be a chondroma (benign cartilaginous tumour).
Submandibular triangle:
(Bordered by the mental process, mandible, and the line between the two angles of the mandible.)
If <20yrs, self-limiting lymphadenopathy is likely. If >20yrs, exclude malignant lymphadenopathy (eg firm and non-tender). Is tb likely?
If it is not a node, think of submandibular salivary stone, sialadenitis, or tumour (see box for Salivary gland pathology).
Anterior triangle:
(Between midline, anterior border of sternocleidomastoid, and the line between the two angles of the mandible.)
Branchial cysts emerge under the anterior border of sternocleidomastoid where the upper third meets the middle third (age <20yrs). Due to non-disappearance of the cervical sinus (where 2nd branchial arch grows down over 3rd and 4th). Lined by squamous epithelium, their fluid contains cholesterol crystals. Treat by excision. There may be communication with the pharynx in the form of a fistula
If lump in the supero-posterior area of the anterior triangle, is it a parotid tumour (more likely if >40yrs)?
Laryngoceles are an uncommon cause of anterior triangle lumps. They are painless and may be made worse by blowing. These cysts are classified as external, internal, or mixed, and may be associated with laryngeal cancer. If pulsatile may be:
Carotid artery aneurysm,
Tortuous carotid artery, or
Carotid body tumours (chemodectoma). These are very rare, move from side to side but not up and down, and splay out the carotid bifurcation. They are usually firm and occasionally soft and pulsatile. They do not usually cause bruits. They may be bilateral, familial, and malignant (5%). Suspect in any mass just anterior to the upper third of sternomastoid. Diagnose by duplex uss (splaying at the carotid bifurcation) or digital computer angiography. ℞: Extirpation by vascular surgeon.
Posterior triangle:
(Behind sternocleidomastoid, in front of trapezius, above clavicle.)
Cervical ribs may intrude into this area. These are enlarged costal elements from c7 vertebra. The majority are asymptomatic but can cause Raynaud’s syndrome by compressing subclavian artery and neurological symptoms (eg wasting of 1st dorsal interosseous) from pressure on lower trunk of the brachial plexus.
Pharyngeal pouches can protrude into the posterior triangle on swallowing (usually left-sided).
Cystic hygromas (usually infants) arise from jugular lymph sac. These macrocystic lymphatic malformations transilluminate brightly. Treat by surgery or hypertonic saline sclerosant injection. Recurrence can be troublesome.
Pancoast’s tumour (see p722).
Subclavian artery aneurysm will be pulsatile.
Important structures in the head and neck.
There are 3 pairs of major salivary glands: parotid, submandibular, and sublingual (there are many minor glands).
Lumps; swelling related to food; pain.
Note external swelling; look for secretions; bimanual palpation for stones. Examine viith nerve and regional lymph nodes.
This may be ascertained by fna.
Think of mumps and hiv. Recurrent unilateral pain and swelling is likely to be from a stone. 80% are submandibular. The classical story is of pain and swelling on eating—with a red, tender, swollen, but uninfected gland. The stone may be seen on plain x-ray or by sialography (fig 2). Distal stones are removed via the mouth but deeper stones may require excision of the gland. Chronic bilateral symptoms may coexist with dry eyes and mouth and autoimmune disease, eg hypothyroidism, Mikulicz’s or Sjögren’s syndrome (p720 & p724)—also bulimia. Fixed swelling may be from a tumour/all (fig 5, p349), sarcoid, amyloid, Wegener’s
syndrome, or be idiopathic.
Normal sialogram of the submandibular gland. Wharton’s (submandibular) duct opens into the mouth near the frenulum of the tongue.
‘80% are in the parotid, 80% of these are pleomorphic adenomas, 80% of these are in the superficial lobe.’ Deflection of the ear outwards is a classic sign. Remove any salivary gland swelling for assessment if present for >1 month. viith nerve palsy means malignancy.
| Benign or malignant | Malignant | Malignant |
|---|---|---|
Cystadenolymphoma | Mucoepidermoid | Squamous or adeno ca |
Pleomorphic adenoma | Acinic cell | Adenoid cystic ca |
| Benign or malignant | Malignant | Malignant |
|---|---|---|
Cystadenolymphoma | Mucoepidermoid | Squamous or adeno ca |
Pleomorphic adenoma | Acinic cell | Adenoid cystic ca |
Pleomorphic adenomas often present in middle age and grow slowly. Remove by superficial parotidectomy. Adenolymphomas (Warthin’s tumour): usually older men; soft; treat by enucleation. Carcinomas: rapid growth; hard fixed mass; pain; facial palsy. Treatment: surgery + radiotherapy.
Lumps in the thyroid
If the thyroid is enlarged (=goitre), ask yourself:
Diffuse goitre:
Causes:
Endemic (iodine deficiency); congenital; secondary to goitrogens (substances that ↓ iodine uptake); acute thyroiditis (de Quervain’s); physiological (pregnancy/puberty); autoimmune (Graves’ disease; Hashimoto’s thyroiditis).
Nodular goitre:
Multinodular goitre (mng): The most common goitre in the uk. 50% who present with a single nodule actually have mng. Patients are usually euthyroid, but may become hyperthyroid (‘toxic’). mng may be retro- or substernal. Hypothyroidism and malignancy within mng are rare. Plummer’s disease is hyperthyroidism with a single toxic nodule (uncommon).
Fibrotic goitre: Eg Reidel’s thyroiditis.
Solitary thyroid nodule: See minibox; ∼10% are malignant.
Investigations
Do t3, t4 and tsh
Thyroid autoantibodies (p208, eg if Hashimoto’s/Graves suspected)
cxr with thoracic inlet view (tracheal goitres and metastases?)
uss (solid, cystic, complex or part of a group of lumps)
Radionuclide scans may show malignant lesions as hypofunctioning or ‘cold’, whereas a hyperfunctioning ‘hot’ lesion suggests adenoma
What should you do if high-resolution ultrasound shows impalpable nodules?
Such thyroid nodules can usually be observed provided they are:
<1cm across (which accounts for most; ultrasound can detect lumps <2mm; such ‘incidentalomas’ occur in 46% of routine autopsies) and are asymptomatic.
There is no past history of thyroid cancer or radiation.
No family history of medullary cancer (if present, do uss-guided fna).
Thyroid cancer87
Papillary: (60%). Often in younger patients. Spread: lymph nodes & lung (jugulodigastric node metastasis is the so-called lateral aberrant thyroid). ℞: total thyroidectomy to remove non-obvious tumour ± node excision ± radioiodine (131I) to ablate residual cells. Give thyroxine to suppress tsh. Prognosis: better if young & ♀.
Follicular: (≤25%). Occur in middle-age & spreads early via blood (bone, lungs). Well-differentiated. ℞: total thyroidectomy + t4 suppression + radioiodine ablation.
Medullary: (5%). Sporadic (80%) or part of men syndrome (p215). May produce calcitonin which can be used as a tumour marker. They do not concentrate iodine. Perform a phaeochromocytoma screen pre-op. ℞: thyroidectomy + node clearance. External beam radiotherapy should be considered to prevent regional recurrence.
Lymphoma: (5%). ♀:♂≈3:1. May present with stridor or dysphagia. Do full staging pre-treatment (chemoradiotherapy). Assess histology for mucosa-associated lymphoid tissue (malt) origin (associated with a good prognosis).
Anaplastic: Rare. ♀:♂≈3:1. Elderly, poor response to any treatment. In the absence of unresectable disease, excision + radiotherapy may be tried.
Thyroid surgery
Indications:
Pressure symptoms, relapse hyperthyroidism after >1 failed course of drug treatment, carcinoma, cosmetic reasons, symptomatic patients planning pregnancy. Render euthyroid pre-op with antithyroid drugs (but stop 10 days prior to surgery as these increase vascularity). Check vocal cords by indirect laryngoscopy pre- and post-op.
Complications:
See also p582.
Early:
Recurrent laryngeal nerve palsy; haemorrhage if compresses airway, instantly remove sutures for evacuation of clot; hypoparathyroidism (check plasma Ca2+ daily; there is commonly a transient drop in serum concentration); thyroid storm (symptoms of severe hyperthyroidism—see p844).
Late:
Hypothyroidism; recurrent hyperthyroidism.
Cyst
Adenoma
Malignancy
Discrete nodule in multinodular goitre
The anatomy of the region of the thyroid gland. The important structures that must be considered when operating on the thyroid gland include:
Recurrent laryngeal nerve
Superior laryngeal nerve
Parathyroid glands
Trachea
Common carotid artery
Internal jugular vein (not depicted—see fig 3).
Transverse ultrasound of the left lobe of the thyroid showing a small low-reflectivity cyst within higher-reflectivity thyroid tissue. Note the proximity to the gland of the common carotid artery and internal jugular vein (the latter compressed slightly by pressure from the probe), both seen beneath the body of sternocleidomastoid muscle.
Breast carcinoma
(OHOncol Ch15)
Epidemiology
Affects 1 in 9 ♀; ∼40,000 new cases per year in uk (incidence increasing). Rare in men (∼1% of all breast cancers).
Risk factors
Risk is related to family history, age and uninterrupted oestrogen exposure, hence: nulliparity; 1st pregnancy >30yrs old, early menarche; late menopause; hrt; obesity; brca genes (p524); not breastfeeding; past breast cancer (metachronous rate ≈2%, synchronous rate ≈1%).
Pathology
Non-invasive ductal carcinoma-in-situ (dcis) is premalignant and seen as microcalcification on mammography (unifocal or widespread). Non-invasive lobular cis is rarer and tends to be multifocal. Invasive ductal carcinoma is most common (∼70%) whereas invasive lobular carcinoma accounts for 10–15% of breast cancers. Medullary cancers (∼5%) tend to affect younger patients while colloid/mucoid (∼2%) tend to affect the elderly. Others: papillary, tubular, adenoid-cystic and Paget’s (p722). 60–70% of breast cancers are oestrogen receptor +ve, conveying better prognosis. ∼30% over-express her2 (growth factor receptor gene) associated with aggressive disease and poorer prognosis.
Investigations
Triple assessment and investigation of a breast lump.
Staging:
Stage 1: Confined to breast, mobile Stage 2: Growth confined to breast, mobile, lymph nodes in ipsilateral axilla Stage 3: Tumour fixed to muscle (but not chest wall), ipsilateral lymph nodes matted and may be fixed, skin involvement larger than tumour Stage 4: Complete fixation of tumour to chest wall, distant metastases. Also tnm staging: (p527) t1<2cm, t2 2–5cm, t3 >5cm, t4 Fixity to chest wall or peau d’orange; n1 Mobile ipsilateral nodes; n2 Fixed nodes; m1 Distant metastases.
Treating stage 1–2 cancer
Surgery: Removal of tumour by wide local excision (wle) or mastectomy ± breast reconstruction + axillary node sampling/surgical clearance or sentinel node biopsy (box).
Chemotherapy: Adjuvant chemotherapy improves survival & reduces recurrence in most groups of women (consider in all except excellent prognosis patients), eg epirubicin + ‘cmf’ (cyclophosphamide + methotrexate + 5-fu). Neoadjuvant chemotherapy has shown no difference in survival but may facilitate breast-conserving surgery.
Support: Breastcare nurses
Reconstruction options: eg tissue expanders/implants, latissimus dorsi flap, tram (transverse rectus abdominis myocutaneous) flap.
Treating distant disease
(Stage 3–4) Long-term survival is possible and median survival is >2yrs. Staging investigations should include cxr, bone scan, liver uss, ct/mri or pet-ct (p752) + lfts and Ca2+. Radiotherapy (p530) to painful bony lesions (bisphosphonates, p696, may ↓pain and fracture risk). Tamoxifen is often used in er+ve; if relapse after initial success, consider chemotherapy. Trastuzumab should be given for her2 +ve tumours, in combination with chemothreapy. cns surgery for solitary (or easily accessible) metastases may be possible; if not—radiotherapy. Get specialist help for arm lymphoedema (try decongestive methods first).nice
Preventing deaths
Promote awareness
Screening: 2-view mammography every 3yrs for women aged 47–73 in uk has ↓ breast cancer deaths by 30% in women >50yrs.
Patent blue dye and/or radiocolloid injected into periareolar area or tumour.
A gamma probe/visual inspection is used to identify the sentinel node.
The sentinel node is biopsied and sent for histology ± immunohistochemistry.
Trials suggest sentinel node identified in 90% of patients. False-negative rates are 9–14% (drop to <5% as surgeons become more experienced).
Tumour size, grade, lymph node status, er/pr status, presence of vascular invasion all help assess prognosis. Nottingham Prognostic Index (npi) is widely used to predict survival and risk of relapse, and to help select appropriate adjuvant systemic therapy:3 npi = 0.2 x tumour size (cm) + histological grade + nodal status.
If treated with surgery alone, 10yr survival rates are: npi <2.4: 95%; npi 2.4–3.4: 85%; npi 3.4–4.4: 70%; npi 4.4–5.4: 50%; npi >5.4: 20%.
Usually presents <30yrs but can occur up to menopause. Benign overgrowth of collagenous mesenchyme of one breast lobule. Firm, smooth, mobile lump. Painless. May be multiple. ⅓ regress, ⅓ stay the same, ⅓ get bigger.
Observation and reassurance, but if in doubt refer for uss (usually conclusive) ± fna. Surgical excision if large.
Common >35yrs, esp. perimenopausal. Benign, fluid-filled rounded lump. Not fixed to surrounding tissue. Occasionally painful.
Diagnosis confirmed on aspiration (perform only if trained).
Infection of mammary duct often associated with lactation (usually S. aureus). Abscess presents as painful hot swelling of breast segment.
Antibiotics. Open incision or percutaneous drainage if abscess.
Typically around menopause. Ducts become blocked and secretions stagnate. Present with nipple discharge (green/brown/bloody) ± nipple retraction ± lump. Refer for confirmation of diagnosis. Usually no ℞ needed.
Fibrosis and calcification after injury to breast tissue. Scarring results in a firm lump. Refer for triple assessment. No ℞ once diagnosis confirmed.
Abdominal masses
As with any mass (see p596), determine size, site, shape, and surface. Find out if it is pulsatile and if it is mobile. Examine supraclavicular and inguinal nodes. Is the lump ballotable (like bobbing an apple up and down in water)?
| Right iliac fossa masses: | ||
|---|---|---|
• Appendix mass/abscess • Caecal carcinoma • Crohn’s disease • Pelvic mass (see below) | • Transplanted kidney • Kidney malformation • Tumour in an undescended testis | |
| Right iliac fossa masses: | ||
|---|---|---|
• Appendix mass/abscess • Caecal carcinoma • Crohn’s disease • Pelvic mass (see below) | • Transplanted kidney • Kidney malformation • Tumour in an undescended testis | |
Abdominal distension
| Causes of ascites: | Ascites with portal hypertension: |
|---|---|
• Malignancy★ • Infections★—esp tb • ★Albumin (eg nephrosis) • ccf; pericarditis • Pancreatitis★ • Myxoedema |
| Causes of ascites: | Ascites with portal hypertension: |
|---|---|
• Malignancy★ • Infections★—esp tb • ★Albumin (eg nephrosis) • ccf; pericarditis • Pancreatitis★ • Myxoedema |
Tests:
Left upper quadrant mass
Is it spleen, stomach, kidney, colon, pancreas, or a rare cause (eg neurofibroma)? Pancreatic cysts may be true (congenital; cystadenomas; retention cysts of chronic pancreatitis; cystic fibrosis) or pseudocysts (fluid in lesser sac from acute pancreatitis).
Splenomegaly
Causes are often said to be infective, haematological, neoplastic, etc, but grouping by associated feature is more useful clinically:
| Splenomegaly with fever | With lymphadenopathy | With purpura |
|---|---|---|
• Infectionhs (malaria, sbe/ie hepatitis,hs ebv,hs tb, cmv, hiv) • Sarcoid; malignancyhs | • Glandular feverhs • Leukaemias; lymphoma • Sjögren’s syndrome | • Septicaemia; typhus • dic; amyloidhs • Meningococcaemia |
| Splenomegaly with fever | With lymphadenopathy | With purpura |
|---|---|---|
• Infectionhs (malaria, sbe/ie hepatitis,hs ebv,hs tb, cmv, hiv) • Sarcoid; malignancyhs | • Glandular feverhs • Leukaemias; lymphoma • Sjögren’s syndrome | • Septicaemia; typhus • dic; amyloidhs • Meningococcaemia |
| With arthritis | With ascites | With a murmur |
|---|---|---|
• Carcinoma • Portal hypertensionhs |
| With anaemia | With weight↓ + cns signs | Massive splenomegaly |
|---|---|---|
• Cancer; lymphoma • tb; arsenic poisoning • Paraproteinaemiahs | • Malaria (hyper-reactivity after chronic exposure) • Myelofibrosis; cmlhs • Gaucher’s syndromehs • Leishmaniasis |
| With anaemia | With weight↓ + cns signs | Massive splenomegaly |
|---|---|---|
• Cancer; lymphoma • tb; arsenic poisoning • Paraproteinaemiahs | • Malaria (hyper-reactivity after chronic exposure) • Myelofibrosis; cmlhs • Gaucher’s syndromehs • Leishmaniasis |
hs=causes of hepatosplenomegaly.
Smooth hepatomegaly
Hepatitis, ccf, sarcoidosis, early alcoholic cirrhosis (a small liver is typical later); tricuspid incompetence (→ pulsatile liver).
Craggy hepatomegaly
Secondaries or 1° hepatoma. (Nodular cirrhosis typically causes a small, shrunken liver, not an enlarged craggy one.)
Pelvic masses
Is it truly pelvic?—Yes, if by palpation you cannot get ‘below it’.
Investigating lumps
There is much to be said for performing an early ct to save time and money compared with leaving the test to be the last in a long chain. If unavailable, ultrasound is the first test (transvaginal approach may be useful).
Others:
ivu; liver and spleen radioisotope scans; Mantoux test (p398). Routine tests: fbc (with film); esr; u&e; lft; proteins; Ca2+; cxr; axr; biopsy—a tissue diagnosis may be made using a fine needle guided by ultrasound or ct control. mri also has a role.
Fibroids
Fetus
Bladder
Ovarian cysts or malignancies
The first successful laparotomy…The acute abdomen
Someone who becomes acutely ill and in whom symptoms and signs are chiefly related to the abdomen has an acute abdomen. Prompt laparotomy is sometimes essential: repeated examination is the key to making the decision.
Clinical syndromes that usually require laparotomy
Rupture of an organ (Spleen, aorta, ectopic pregnancy) Shock is a leading sign—see table for assessment of blood loss. Abdominal swelling may be seen. Any history of trauma: blunt trauma → spleen; penetrating trauma → liver. Delayed rupture of the spleen may occur weeks after trauma. Peritonism may be mild.
Peritonitis (Perforation of peptic ulcer/duodenal ulcer, diverticulum, appendix, bowel, or gallbladder) Signs: prostration, shock, lying still, +ve cough test (p62), tenderness (± rebound/percussion pain, p62), board-like abdominal rigidity, guarding, and no bowel sounds. Erect cxr may show gas under the diaphragm (fig 2). nb: acute pancreatitis (p638) causes these signs, but does not require a laparotomy so don’t be caught out and always check serum amylase.
| Pneumonia (p160) | Sickle-cell crisis (p335) |
Gastroenteritis or uti | Thyroid storm (p844) | Phaeochromocytoma (p846) |
Diabetes mellitus/dka (p198) | Zoster (p400) | Malaria (p394) |
Bornholm disease (p376) | Tuberculosis (p398) | Typhoid fever (p426) |
Pneumococcal peritonitis | Porphyria (p706) | Cholera (p426) |
Henoch–Schönlein (p716) | Narcotic addiction | Yersinia enterocolitica (p422) |
Tabes dorsalis (p431) | pan (p558) | Lead colic |
| Pneumonia (p160) | Sickle-cell crisis (p335) |
Gastroenteritis or uti | Thyroid storm (p844) | Phaeochromocytoma (p846) |
Diabetes mellitus/dka (p198) | Zoster (p400) | Malaria (p394) |
Bornholm disease (p376) | Tuberculosis (p398) | Typhoid fever (p426) |
Pneumococcal peritonitis | Porphyria (p706) | Cholera (p426) |
Henoch–Schönlein (p716) | Narcotic addiction | Yersinia enterocolitica (p422) |
Tabes dorsalis (p431) | pan (p558) | Lead colic |
Erect cxr showing air beneath the right hemidiaphragm, indicating presence of a pneumoperitoneum. Causes:
Perforation of the bowel (visible only in 75%)
Gas-forming infection, eg C. perfringens
Iatrogenic, eg open or laparoscopic surgery (gas under the diaphragm can be still detected on cxr up to 10 days post-op)
Per vaginam (prolonged intercourse)
Interposition of bowel between liver and diaphragm
Syndromes that may not require a laparotomy
Local peritonitis:
Eg diverticulitis, cholecystitis, salpingitis, and appendicitis (the latter will need surgery). If abscess formation is suspected (swelling, swinging fever, and wcc↑) do ultrasound or ct. Drainage can be percutaneous (ultrasound or ct-guided), or by laparotomy. Local peritoneal inflammation can cause localized ileus with a ‘sentinel loop’ of intraluminal gas visible on plain axr (p743).
Colic is a regularly waxing and waning pain, caused by muscular spasm in a hollow viscus, eg gut, ureter, salpinx, uterus, bile duct, or gallbladder (in the latter, pain is often dull and constant). Colic, unlike peritonitis, causes restlessness and the patient may well be pacing around when you go to see him!
Obstruction of the bowel
See p612.
Tests
u&e; fbc; amylase; lft; crp; abg (is there mesenteric ischaemia?); urinalysis. Erect cxr (fig 2), axr may show Rigler’s sign (p742). Laparoscopy may avert open surgery. ct can be helpful provided it is readily available and causes no delay (p746–747); uss may identify perforation or free fluid immediately, but appropriate performer training is important.
Pre-op
The medical acute abdomen
Irritable bowel syndrome (p276) is the chief cause, so always ask about episodes of pain associated with loose stools, relieved by defecation, bloating, and urgency (but not blood—this may be uc). Other causes:
Hidden diagnoses
Mesenteric ischaemia (p622), acute pancreatitis (p638) and a leaking aaa (p656) are the Unterseebooten of the acute abdomen—unsuspected, undetectable unless carefully looked for, and underestimatedly deadly. They may have non-specific symptoms and signs that are surprisingly mild, so always think of them when assessing the acute abdomen and hopefully you will ‘spot’ them! Finally: always exclude pregnancy (± ectopic?) in females.
Causes of abdominal pain.
The most likely cause of shock in a surgical patient is hypovolaemia (but don’t forget the other causes—p804). The chief physiological parameters for assessing shock assess target organ perfusion rather than the direct measurement of bp and pulse, which may be ‘normal’ in one individual and yet totally abnormal for another. The most perfused organs in a normal state are the kidney, brain, and skin, so check urine output, gcs and capillary refill (cr). The best quick test is: “do you feel dizzy if you sit up?”
Of course, bp, pulse, and respirations are still vital signs, but the message here is: treat suspected shock rather than wait for bp to fall. When there is any blood loss (eg a trauma situation), assess the status of the following:
| Parameter | Class I | Class II | Class III | Class IV |
|---|---|---|---|---|
Blood loss | <750mL | 750–1500mL | 1500–2000mL | >2000mL |
<15% | 15–30% | 30–40% | >40% | |
Pulse | <100bpm | >100bpm | >120bpm | >140bpm |
bp | ↔ | ↔ | ↓ | ↓ |
Pulse pressure | ↔ or ↑ | ↓ | ↓ | ↓ |
Respirations | 14–20/min | 20–30/min | 30–40/min | >35/min |
Urine output | >30mL/h | 20–30mL/h | 5–15mL/h | Negligible |
Mental state | Slightly anxious | Anxious | Confused → | →Lethargic |
Fluid to give | Crystalloid | Crystalloid | Crystalloid + blood |
| Parameter | Class I | Class II | Class III | Class IV |
|---|---|---|---|---|
Blood loss | <750mL | 750–1500mL | 1500–2000mL | >2000mL |
<15% | 15–30% | 30–40% | >40% | |
Pulse | <100bpm | >100bpm | >120bpm | >140bpm |
bp | ↔ | ↔ | ↓ | ↓ |
Pulse pressure | ↔ or ↑ | ↓ | ↓ | ↓ |
Respirations | 14–20/min | 20–30/min | 30–40/min | >35/min |
Urine output | >30mL/h | 20–30mL/h | 5–15mL/h | Negligible |
Mental state | Slightly anxious | Anxious | Confused → | →Lethargic |
Fluid to give | Crystalloid | Crystalloid | Crystalloid + blood |
Assumes a body mass of 70kg and a circulating blood volume of 5L.
Reproduced with permission from American Col. of Surgeons’ Committee on Trauma, Advanced Trauma Life Support® for Doctors (atls®) Student Manual 7e, Chicago: Am Coll Surg, 2004.
Acute appendicitis
Incidence
Most common surgical emergency (lifetime incidence = 6%). Can occur at any age, though highest incidence is between 10–20yrs. It is rare before age 2 because the appendix is cone shaped with a larger lumen.
Pathogenesis
Gut organisms invade the appendix wall after lumen obstruction by lymphoid hyperplasia, faecolith, or filarial worms. This leads to oedema, ischaemic necrosis and perforation. There may be impaired ability to prevent invasion, brought about by improved hygiene & less exposure to pathogens (the ‘hygiene hypothesis’).
Symptoms
Classically periumbilical pain that moves to the rif (see minibox). Anorexia is an important feature; vomiting is rarely prominent—pain normally precedes vomiting in the surgical abdomen. Constipation is usual. Diarrhoea may occur.
Special tests
Rovsing’s sign (pain > in rif than lif when the lif is pressed). Psoas sign (pain on extending hip if retrocaecal appendix). Cope sign (pain on flexion and internal rotation of right hip if appendix in close relation to obturator internus).
Investigations
Variations in the clinical picture
The child with vague abdominal pain who will not eat their favourite food.
The shocked, confused octogenarian who is not in pain.
Appendicitis occurs in ∼1/1000 pregnancies. It is not commoner, but mortality is higher, especially from 20wks’ gestation. Perforation is commoner, and increases fetal mortality. Pain is often less well localized (may be ruq), & signs of peritonism less obvious.
Hints
If a child is anxious, use their hand to press their tummy—see also p629 for tips.
Check for recent viral illnesses and lymphadenopathy—mesenteric adenitis?
Don’t start palpating in the rif (makes it difficult to elicit pain elsewhere).
Treatment
Prompt appendicectomy.
Antibiotics:
Metronidazole 500mg/8h + cefuroxime 1.5g/8h, 1 to 3 doses iv starting 1h pre-op, reduces wound infections. Give a longer course if perforated.
Laparoscopy:
Complications
Appendix mass may result when an inflamed appendix becomes covered with omentum. us/ct may help with diagnosis. Some advocate early surgery. Alternatively, initial conservative management—nbm and antibiotics. If the mass resolves, some perform an interval (ie delayed) appendicectomy. Exclude a colonic tumour (laparotomy or colonoscopy), which can present as early as the 4th decade.
Appendix abscess May result if an appendix mass fails to resolve but enlarges and the patient gets more unwell. Treatment usually involves drainage (surgical or percutaneous under us/ct-guidance). Antibiotics alone may bring resolution.
Tachycardia
Fever 37.5–38.5°C
Furred tongue
Lying still
Coughing hurts (p62)
Foetor ± flushing
Shallow breaths
Ectopic (do a pregnancy test!)
uti (test urine!)
Mesenteric adenitis
Cystitis
Cholecystitis
Diverticulitis
Salpingitis/pid
Dysmenorrhoea
Crohn’s disease
Perforated ulcer
Food poisoning
Meckel’s diverticulum
Internal organs and the visceral peritoneum have no somatic innervation, so the brain attributes the visceral (splanchnic) signals to a physical location whose dermatome corresponds to the same entry level in the spinal cord. Importantly, there is no laterality to the visceral unmyelinated c-fibre pain signals, which enter the cord bilaterally and at multiple levels. Division of the gut according to embryological origin is the important determinant here:
| Gut | Division points | Somatic referral | Arterial supply |
|---|---|---|---|
Fore | Proximal to 2nd part of duodenum | Epigastrium | Coeliac axis |
Mid | Above to ⅔ along transverse colon | Periumbilical | Superior mesenteric |
Hind | Distal to above | Suprapubic | Inferior mesenteric |
| Gut | Division points | Somatic referral | Arterial supply |
|---|---|---|---|
Fore | Proximal to 2nd part of duodenum | Epigastrium | Coeliac axis |
Mid | Above to ⅔ along transverse colon | Periumbilical | Superior mesenteric |
Hind | Distal to above | Suprapubic | Inferior mesenteric |
Early inflammation irritates the structure and walls of the appendix, so a colicky pain is referred to the mid-abdomen—classically periumbilical. As the inflammation progresses and irritates the parietal peritoneum (especially on examination!) the somatic, lateralized pain settles at McBurney’s point, ⅔ of the way along from the umbilicus to the right anterior superior iliac spine.
These principles also help us understand patterns of referred pain. In pneumonia, the t9 dermatome is shared by the lung and the abdomen. Also, irritation of the underside of the diaphragm (sensory innervation is from above through the phrenic nerve, c3–5) by an inflamed gallbladder or a subphrenic abscess refers pain to the right shoulder: dermatomes c3–5.
The open appendectomy.
Traditional approach is Gridiron incision over McBurney’s point, at 90° to line from umbilicus to the anterior superior iliac spine. Lanz incision is more horizontal in Langer’s lines (skin creases) and gives a better scar.
Divide subcutaneous fat and superficial/Scarpa’s fascia. Fibres of external oblique, internal oblique and transversus abdominus divided with muscle splitting incision.
Incise pre-peritoneal fat and peritoneum to reveal caecum. Deliver caecum through incision. Appendix located at convergence of taenia coli.
Mesoappendix (blood vessels and mesentery) and appendix divided, ligated and excised (stump may be inverted).
In case of a normal-looking appendix, excise (may be histologically if not macroscopically inflamed); look for Meckel’s diverticulum.
Wash, close in layers, dress wound.
Obstruction of the bowel
Features of obstruction
Vomiting, nausea and anorexia. Fermentation of the intestinal contents in established obstruction causes ‘faeculent’ vomiting (‘faecal’ vomiting is found when there is a colonic fistula with the proximal gut). Colic occurs early (may be absent in long-standing complete obstruction). Constipation need not be absolute (ie no faeces or flatus passed) if obstruction is high, though in distal obstruction nothing will be passed. Abdominal distension is more marked as the obstruction progresses. There are active, ‘tinkling’ bowel sounds.
The key decisions:
Is it obstruction of the small or large bowel? In small bowel obstruction, vomiting occurs earlier, distension is less, and pain is higher in the abdomen. The axr plays a key role in diagnosis—see p742. In small bowel obstruction, axr shows central gas shadows with valvulae conniventes that completely cross the lumen and no gas in the large bowel. In large bowel obstruction, pain is more constant; axr shows peripheral gas shadows proximal to the blockage (eg in caecum) but not in the rectum, unless you have done a pr examination which is always essential! Large bowel haustra do not cross all the lumen’s width. If the ileocaecal valve is competent (ie doesn’t allow reflux) pain may be felt over a distended caecum (see below).
Is the obstructed bowel simple/closed loop/strangulated? Simple: One obstructing point and no vascular compromise. Closed loop: Obstruction at two points (eg sigmoid volvulus, distension with competent ileocaecal valve) forming a loop of grossly distended bowel at risk of perforation (tenderness and perforation usually at caecum where the bowel is thinnest and widest; >12cm requires urgent decompression). Strangulated: Blood supply is compromised and the patient is more ill than you would expect. There is sharper, more constant and localized pain. Peritonism is the cardinal sign. There may be fever + wcc↑ with other signs of mesenteric ischaemia (p622).
Management
General principles: Cause, site, speed of onset, and completeness of obstruction determine definitive therapy: strangulation and large bowel obstruction require surgery; ileus and incomplete small bowel obstruction can be managed conservatively, at least initially.
Immediate action: ‘Drip and suck’—ngt and iv fluids to rehydrate and correct electrolyte imbalance (p680). Being nbm does not give adequate rest for the bowel because it can produce up to 9L of fluid/d. Also: analgesia, blood tests (inc. amylase, fbc, u&e), axr, erect cxr, catheterize to monitor fluid status.
Surgery: Strangulation needs emergency surgery, as does ‘closed loop obstruction’. Stents may be used for obstructing large bowel malignancies either in palliation or as a bridge to surgery in acute obstruction (p618). Small bowel obstruction secondary to adhesions should rarely lead to surgery—see box, p583.
Unenhanced axial ct of the abdomen showing multiple loops of dilated, fluid-filled small bowel in a patient with small bowel obstruction.
Axial ct of the abdomen post-oral contrast showing dilated loops of fluid and air-filled large bowel (contrast medium is in the small bowel). The cause or level of obstruction is not clear.
Vomiting
Colicky pain
Constipation
Distension
is adynamic bowel due to the absence of normal peristaltic contractions. Contributing factors include abdominal surgery, pancreatitis (or any localized peritonitis), spinal injury, hypokalaemia, hyponatraemia, uraemia, peritoneal sepsis and drugs (eg tricyclic antidepressants).
Sigmoid volvulus occurs when the bowel twists on its mesentery, which can produce severe, rapid, strangulated obstruction. There is a characteristic axr with an ‘inverted u’ loop of bowel that looks a bit like a coffee bean. It tends to occur in the elderly, constipated and comorbid patient, and is often managed by sigmoidoscopy and insertion of a flatus tube. Sigmoid colectomy is sometimes required. If not treated successfully, it can progress to perforation and fatal peritonitis.
Gastric volvulus is rare. Rotation is typically 180° left to right, about a line joining the relatively fixed pylorus and oesophagus. This creates a closed loop obstruction that can result in incarceration and strangulation. The classical triad of gastrooesophageal obstruction may occur: vomiting (then retching), pain, and failed attempts to pass an ng tube. Regurgitation of saliva also occurs. Dysphagia and noisy gastric peristalsis (relieved by lying down) may occur in chronic volvulus.
Paraoesophageal hernia; congenital bands; bowel malformations; pyloric stenosis.
Gastric/oesophageal surgery.
Look for gastric dilatation and a double fluid level on erect films.
Hernias
Definition
The protrusion of a viscus or part of a viscus through a defect of the walls of its containing cavity into an abnormal position.
Terminology:
Hernias involving bowel are said to be irreducible if they cannot be pushed back into the right place. This does not mean that they are either necessarily obstructed or strangulated. Incarceration implies that the contents of the hernial sac are stuck inside by adhesions. Gastrointestinal hernias are obstructed if bowel contents cannot pass through them—the classical features of intestinal obstruction soon appear (p612). They are strangulated if ischaemia occurs—the patient becomes toxic and requires urgent surgery. Care must be taken when attempting reduction (see p616 for the technique) as it is possible to perform reduction en masse, pushing the strangulated bowel and hernial sac back into the abdominal cavity, but giving the initial appearance of successful reduction.
Inguinal hernia
The commonest type (far more common in men), described on p616.
Femoral hernia
Bowel enters the femoral canal, presenting as a mass in the upper medial thigh or above the inguinal ligament where it points down the leg, unlike an inguinal hernia which points to the groin. They occur more often in women especially in middle age and the elderly. They are likely to be irreducible and to strangulate due to the rigidity of the canal’s borders.
Anatomy:
The neck of the hernia is felt inferior and lateral to the pubic tubercle (inguinal hernias are superior and medial to this point). The boundaries of the femoral canal are anteriorly the inguinal ligament; medially the lacunar ligament (and pubic bone); laterally the femoral vein (and iliopsoas); and posteriorly the pectineal ligament and pectineus. The canal contains fat and Cloquet’s node.
Differential diagnosis:108
(see also p653)
Inguinal hernia
Saphena varix
An enlarged Cloquet’s node (p619)
Lipoma
Femoral aneurysm
Psoas abscess.
Treatment:
Surgical repair is recommended. (Herniotomy is ligation and excision of the sac, herniorrhaphy is repair of the hernial defect.)
Paraumbilical hernias
occur just above or below the umbilicus. Risk factors are obesity and ascites. Omentum or bowel herniates through the defect. Surgery involves repair of the rectus sheath (Mayo repair).
Epigastric hernias
pass through linea alba above the umbilicus.
Incisional hernias
Spigelian hernias
occur through the linea semilunaris at the lateral edge of the rectus sheath, below and lateral to the umbilicus.
Lumbar hernias
occur through the inferior or superior lumbar triangles in the posterior abdominal wall.
Richter’s hernias
involve bowel wall only—not the whole lumen.
Maydl’s hernias
involve a herniating ‘double loop’ of bowel. The strangulated portion may reside as a single loop inside the abdominal cavity.
Littre’s hernias
are hernial sacs containing strangulated Meckel’s diverticulum.
Obturator hernias
occur through the obturator canal. Typically there is pain along the medial side of the thigh in a thin woman.
Sciatic hernias
Sliding hernias
contain a partially extraperitoneal structure (eg caecum on the right, sigmoid colon on the left). The sac does not completely surround the contents.
Other examples of hernias:
Of the nucleus pulposus into the spinal canal (slipped disc).
Of the uncus and hippocampal gyrus through the tentorium (tentorial hernia) in space-occupying lesions.
Of brainstem and cerebellum through the foramen magnum (Arnold–Chiari, p708).
Of the stomach through the diaphragm (hiatus hernia, p245).
Of the terminal (intravesical) portion of the ureter into the bladder. This is a ureterocele and results from stenosis of the ureteral meatus.
Some examples of hernias.
(see ohcs, p130)
Exomphalos (also called omphalocele)1 is associated with other congenital abnormalities, such as anencephaly, cardiac defects, hydrocephalus and spina bifida. In this condition the abdominal contents are found outside the abdomen, covered in a three-layer membrane consisting of peritoneum, Wharton’s jelly and amnion. Surgical repair is less urgent than in gastroschisis because the bowel is protected by these membranes. The challenge of surgery is to fit the contents back into the relatively small abdominal cavity without compromising venous return and lung ventilation.
Inguinal hernias Indirect occur in ∼4% of all male infants (due to patent processus vaginalis)—prematurity is a risk factor. They are uncommon in female infants and, if found, should prompt thoughts of testicular feminization. If the patent processus vaginalis contains peritoneal fluid only, then it is a communicating hydrocele. Surgical repair is required for both. Reinforcement of the posterior wall (eg with a mesh) is not needed as the internal ring has not been chronically dilated.
True umbilical hernias (3% of live births) are a result of a persistent defect in the transversalis fascia—the umbilical ring, through which the umbilical vessels passed to reach the fetus (more common in African-Caribbeans, trisomy 21 and congenital hypothyroidism). Surgical repair is rarely needed in children (3 in 1000) as most resolve by the age of 3.
Inguinal hernias
(OHClinSurg p320)
Indirect hernias pass through the internal inguinal ring and, if large, out through the external ring. Direct hernias push their way directly forward through the posterior wall of the inguinal canal, into a defect in the abdominal wall (Hesselbach’s triangle; medial to the inferior epigastric vessels and lateral to the rectus abdominus). Predisposing conditions: males (♂:♀≈8:1), chronic cough, constipation, urinary obstruction, heavy lifting, ascites, past abdominal surgery (eg damage to the iliohypogastric nerve during appendicectomy). There are 2 landmarks to identify: The deep (internal) ring may be defined as being the mid-point of the inguinal ligament, ∼1½ cm above the femoral pulse (which crosses the mid-inguinal point). The superficial (external) ring is a split in the external oblique aponeurosis just superior and medial to the pubic tubercle (the bony prominence forming the medial attachment of the inguinal ligament). Relations of the inguinal canal are:
Floor: Inguinal ligament and lacunar ligament medially.
Roof: Fibres of transversalis, internal oblique.
Anterior: External oblique aponeurosis + internal oblique for the lateral ⅓.
Posterior: Laterally, transversalis fascia; medially, conjoint tendon.
Examination
Look for previous scars; feel the other side (more common on the right); examine the external genitalia. Then ask:
Is the lump visible? If so, ask the patient to reduce it—if he cannot, make sure that it is not a scrotal lump. Ask him to cough. Appears above and medial to the pubic tubercle.
If no lump is visible, feel for a cough impulse.
Repeat the examination with the patient standing.
Distinguishing direct from indirect hernias:
This is loved by examiners but is of little clinical use—not least because repair is the same for both (see below). The best way is to reduce the hernia and occlude the deep (internal) ring with two fingers. Ask the patient to cough or stand—if the hernia is restrained, it is indirect; if not, it is direct. The ‘gold standard’ for determining the type of inguinal hernia is at surgery: direct hernias arise medial to the inferior epigastric vessels; indirect hernias are lateral.
| Indirect hernias: | Direct hernias: | Femoral hernias: |
|---|---|---|
• Common (80%) • Can strangulate | • Less common (20%) • Reduce easily • Rarely strangulate | • More frequent in females • Frequently irreducible • Frequently strangulate |
| Indirect hernias: | Direct hernias: | Femoral hernias: |
|---|---|---|
• Common (80%) • Can strangulate | • Less common (20%) • Reduce easily • Rarely strangulate | • More frequent in females • Frequently irreducible • Frequently strangulate |
Irreducible hernias
You may be called because a long-standing hernia is now irreducible and painful. It is always worth trying to reduce these yourself to prevent strangulation and necrosis (demanding prompt laparotomy). Learn how to do this from an expert, ie one of your patients who has been reducing his hernia for years. Then you will know how to act correctly when the emergency presents. Notice that such patients use the flat of the hand, directing the hernia from below, up towards the contralateral shoulder. Sometimes, as the hernia obstructs, reduction requires perseverance, which may be rewarded by a gurgle from the retreating bowel and a kiss from the attending spouse who had thought that surgery was inevitable.
Repairs
Return to work:
We used to advise 4 weeks’ rest and convalescence over 10 weeks, but with new mesh or laparoscopic repairs, if comfortable, return to manual work (and driving) after ≤2 weeks is ok if all is well; explain this pre-operatively.
Anatomy of the inguinal canal.
The external spermatic fascia (from external oblique), cremasteric fascia (from internal oblique and transverses abdominus) and internal spermatic fascia (from transversalis fascia) covering the cord.
The spermatic cord:
Vas deferens, obliterated processus vaginalis, and lymphatics
Arteries to the vas, cremaster, and testis
The pampiniform plexus and the venous equivalent of the above
The genital branch of the genitofemoral nerve and sympathetic nerves
The ilioinguinal nerve, which enters the inguinal canal via the anterior wall and runs anteriorly to the cord.
nb: in the female the round ligament of the uterus is in place of the male structures. A hydrocele of the canal of Nuck is the female equivalent of a hydrocele of the cord.
Colorectal carcinoma
(OHOncol Ch16)
Predisposing factors
Prevention:
Presentation
depends on site:
Left-sided:
Bleeding/mucus pr; altered bowel habit or obstruction (25%); tenesmus; mass pr (60%).
Right:
Weight↓; Hb↓; abdominal pain; obstruction less likely.
Either:
Distribution of colorectal carcinomas. These are averages: black females tend to have more proximal neoplasms. White men tend to have more distal neoplasms.
Tests
fbc (microcytic anaemia); faecal occult blood (fob, see box); sigmoidoscopy; barium enema or colonoscopy (figs 2 & 3, p257), which can be done ‘virtually’ by ct (fig 1, p757); lft, ct/mri; liver uss. cea (p535) may be used to monitor disease and effectiveness of treatment. If family history of fap, refer for dna test once >15yrs old.
Spread
Surgery
aims to cure and may ↑survival times by up to 50% (eg in tme1).
Right hemicolectomy for caecal, ascending or proximal transverse colon tumours.
Left hemicolectomy for tumours in distal transverse or descending colon.
Sigmoid colectomy for sigmoid tumours.
Abdominoperineal (ap) resection for tumours low in the rectum (≲8cm from anus): permanent colostomy and removal of rectum and anus (but see p584 for total anorectal reconstruction).
Hartmann’s procedure in emergency bowel obstruction, perforation or palliation.
Radiotherapy
is mostly used in palliation for colonic cancer. It is occasionally used pre-op in rectal cancer to allow resection. Post-op radiotherapy is only used in patients with rectal tumours at high risk of local recurrence.
Chemotherapy
Prognosis
Polyps
are lumps that appear above the mucosa.
Inflammatory: Ulcerative colitis, Crohn’s, lymphoid hyperplasia.
Hamartomatous: Juvenile polyps, Peutz–Jeghers (p722).
Neoplastic: Tubular or villous adenomas: malignant potential, esp. if >2cm. Polyps should be biopsied and removed if they show malignant change. Most can be reached by flexible colonoscope; diathermy can avoid morbidity of colectomy.
| Stage | Description | Treated 5yr survival rate 127 |
|---|---|---|
A | Limited to muscularis mucosae | 93% |
B | Extension through muscularis mucosae | 77% |
C | Involvement of regional lymph nodes | 48% |
D | Distant metastases | 6.6% |
| Stage | Description | Treated 5yr survival rate 127 |
|---|---|---|
A | Limited to muscularis mucosae | 93% |
B | Extension through muscularis mucosae | 77% |
C | Involvement of regional lymph nodes | 48% |
D | Distant metastases | 6.6% |
See also tnm staging p527.
Home test kits are used to sample 3 separate bowel motions and are returned for analysis. Approximately 2% of tests are positive and these patients are offered an appointment with a specialist nurse, plus further investigation (usually colonoscopy). The positive predictive value (p674) is 5–15%. There can be problems with ‘acceptability’ of home testing and also of high false positive rates (up to 10%).
Carcinoma of the stomach
(OHOncol p338)
Incidence of adenocarcinoma at the gastro-oesophageal junction is increasing in the West, though incidence of distal and body gastric carcinoma has fallen sharply. It remains a tumour notable for its gloomy prognosis and non-specific presentation.
Incidence
23/100,000/yr in the uk, but there are unexplained wide geographical variations; it is especially common in Japan, as well as Eastern Europe, China, and South America. ♂ : ♀ ≈ 2 : 1.
Pathology
Borrmann classification:
Polypoid
Excavating
Ulcerating and raised
Diffusely infiltrative. Some are confined to mucosa and submucosa— ‘early’ gastric carcinoma.
Presentation
Symptoms:
Often non-specific. Dyspepsia (p59; for >1 month and age ≥50yrs demands investigation), weight ↓, vomiting, dysphagia, anaemia. Signs suggesting incurable disease: epigastric mass, hepatomegaly; jaundice, ascites (p606); large left supraclavicular (Virchow’s) node (=Troisier’s sign); acanthosis nigricans (p564). Most patients in the West present with locally advanced (inoperable) or metastatic disease. Spread is local, lymphatic, blood-borne, and transcoelomic, eg to ovaries (Krukenberg tumour).
Tests
Aim to biopsy all gastric ulcers as even malignant ulcers may appear to heal on drug treatment. Endoscopic ultrasound (eus) can evaluate depth of invasion; ct/mri helps staging. Staging laparoscopy is recommended for locally advanced tumours. Cytology of peritoneal washings can help identify peritoneal metastases.Treatment
5yr survival
<10% overall, but nearly 20% for patients undergoing radical surgery. The prognosis is much better for ‘early’ gastric carcinoma.
Pernicious anaemia
Blood group A
H. pylori (p242)
Atrophic gastritis
Adenomatous polyps
Lower social class
Smoking
Diet (high nitrate, high salt, pickling, low vitamin C)
Nitrosamine exposure
Carcinoma of the oesophagus
Incidence
Australia <5/100,000/yr; uk <9; Brittany >50; Iran >100.
Risk factors:
Site
20% occur in the upper part, 50% in the middle, and 30% in the lower part. They may be squamous cell (proximal) or adenocarcinomas (distal; incidence rising).
Presentation
Dysphagia; weight↓; retrosternal chest pain.
Signs from the upper third of the oesophagus:
Hoarseness; cough (may be paroxysmal if aspiration pneumonia).
ΔΔ:
See Dysphagia, p240.
Tests
Oesophagoscopy with biopsy is the investigation of choice ± eus, ct/mri for staging (fig 1), or laparoscopy if significant infra-diaphragmatic component.
Axial ct of the chest after iv contrast medium showing concentric thickening of the oesophagus (arrow); the diagnosis here is oesophageal carcinoma. Loss of the fatty plane around the oesophagus suggests local invasion. Anterior to the oesophagus is the trachea and next to it is the arch of the aorta.
Staging:
See table.
Tis | Carcinoma in situ | Nx | Nodes cannot be assessed |
T1 | Invading lamina propria/submucosa | N0 | No node spread |
T2 | Invading muscularis propria | N1 | Regional node metastases |
T3 | Invading adventitia | M0 | No distant spread |
T4 | Invasion of adjacent structures | M1 | Distant metastasis |
Tis | Carcinoma in situ | Nx | Nodes cannot be assessed |
T1 | Invading lamina propria/submucosa | N0 | No node spread |
T2 | Invading muscularis propria | N1 | Regional node metastases |
T3 | Invading adventitia | M0 | No distant spread |
T4 | Invasion of adjacent structures | M1 | Distant metastasis |
Treatment
(See also p527)
Spread of oesophageal cancer is direct, by submucosal infiltration and local spread—or to nodes, or, later, via the blood.
Iatrogenic, eg endoscopy/biopsy/dilatation (accounts for 85–90% of perforations)
Trauma, eg penetrating injury/ingestion of foreign body
Carcinoma
Boerhaave syndrome—rupture due to violent vomiting
Corrosive ingestion.
Odynophagia, tachypnoea, dyspnoea, fever, shock, surgical emphysema (a crackling sensation felt on palpating the skin over the chest or neck caused by air tracking from the lungs; ΔΔ: pneumothorax).
Iatrogenic perforations are less prone to mediastinitis and sepsis and may be managed conservatively with ng tube, ppi and antibiotics. Others require resuscitation, ppi, antibiotics, antifungals and surgery (debridement of mediastinum and placement of t-tube for drainage and formation of a controlled oesophagocutaneous fistula).
All are rare, have an overall poor prognosis and are difficult to diagnose. They account for ∼3% of all gi cancers worldwide, but there is geographical variation (↑ in north-east Thailand, Japan, Korea and Eastern Europe). Most are adenocarcinomas. Primary sclerosing cholangitis (p266) is the commonest predisposing factor in the West.
Varies according to location and may include obstructive jaundice, pruritus, abdominal pain, weight loss and anorexia.
uss, ct, and ercp. mri has a role for determining extent of invasion in bile duct cancers.
Bile duct cancer: Surgical resection is the only potentially curative treatment yet ∼80% present with inoperable disease. Palliation includes biliary stenting and chemotherapy.
Gallbladder cancer: Again, radical surgery is the only chance of cure. 25% of patients with a porcelain gallbaldder have cancer—prophylactic surgery should be considered. Palliative treatment of inoperable disease includes bilary stenting and chemotherapy.
Mesenteric ischaemia
There are 3 main types of bowel ischaemia: af with abdominal pain should always prompt thoughts of mesenteric ischaemia.
1 Acute mesenteric ischaemia142
Presentation
is a classical clinical triad: Acute severe abdominal pain; no abdominal signs; rapid hypovolaemia→shock. Pain tends to be constant, central, or around the rif. The degree of illness is often far out of proportion with clinical signs.
Tests:
Treatment:
The main life-threatening complications secondary to acute mesenteric ischaemia are
septic peritonitis and
progression of a systemic inflammatory response syndrome (sirs) into a multi-organ dysfunction syndrome (mods), mediated by bacterial translocation across the dying gut wall. Resuscitation with fluid, antibiotics (gentamicin + metronidazole, p381) and, usually, heparin are required. If arteriography is done, thrombolytics may be infused locally via the catheter. At surgery dead bowel must be removed. Revascularization may be attempted on potentially viable bowel but it is a difficult process and often needs a 2nd laparotomy.
Prognosis:
2 Chronic mesenteric ischaemia
3 Chronic colonic ischaemia
(aka ischaemic colitis) usually follows low flow in the inferior mesenteric artery (ima) territory and ranges from mild ischaemia to gangrenous colitis. Presentation: Lower left-sided abdominal pain ± bloody diarrhoea. Tests: ct may be helpful but colonoscopy and biopsy is ‘gold-standard’. Barium enema shows characteristic ‘thumb printing’ of submucosal swelling. Treatment: Usually conservative with fluid replacement and antibiotics. Most recover but strictures are common. Gangrenous ischaemic colitis (presenting with peritonitis and hypovolaemic shock) requires prompt resuscitation followed by resection of the affected bowel and stoma formation. Mortality is high.
Arterial
Thrombotic(35%)
Embolic(35%)
Non-occlusive (20%)
Venous (5%)
Other
Usually a combination of a low-flow state with atheroma.
The arterial supply to the colon.
Gastric surgery and its aftermath
Operations for benign gastric ulceration
Pyloric ulcers may be considered similarly to duodenal ulceration (p626). Away from the pylorus, elective surgery is rarely needed as ulcers respond well to medical treatment, stopping smoking, and avoidance of nsaids. In patients who are unable to tolerate medical treatment, a laparoscopic highly selective vagotomy (hsv) can be done (p626). Emergency surgery may be needed for haemorrhage or perforation. Haemorrhage is usually treated by under-running the bleeding ulcer base or excision of the ulcer. If the former is done, then a biopsy should be taken to exclude malignancy. Perforation is usually managed by excision of the hole for histology, then closure.
Operations for duodenal ulceration
See p626.
Gastric carcinoma
Surgery
Billroth i:
Partial gastrectomy with simple gastroduodenal re-anastomosis.
Billroth ii (aka polya) gastrectomy
(fig 1) Partial gastrectomy with gastrojejunal anastamosis. The duodenal stump is oversewn (leaving a blind afferent loop), and anastomosis is achieved by a longitudinal incision into the proximal jejunum.
Billroth ii.
Roux-en-Y
(fig 2) Following total or subtotal gastrectomy, the proximal duodenal stump is oversewn, the proximal jejunum is divided from the distal duodenum and connects with the oesophagus (or proximal stomach after subtotal gastrectomy) whilst the distal duodenum is connected to the distal jejunum.
The Roux-en-Y reconstruction and gastric bypass
Physical complications of gastrectomy and peptic ulcer surgery
Recurrent ulceration: Symptoms are similar to those experienced pre-operatively but complications are more common and response to medical treatment is poor. Further surgery is difficult.
Abdominal fullness: Feeling of early satiety (± discomfort and distension) improving with time. Advise to take small, frequent meals.
Afferent loop syndrome: Post-gastrectomy (eg Billroth ii), the afferent loop may fill with bile after a meal, causing upper abdominal pain and bilious vomiting. This is difficult to treat—but often improves with time.
Diarrhoea: May be disabling after vagotomy. Codeine phosphate may help.
Gastric tumour: A rare complication of any surgery which ↓acid production.
Metabolic complications
Weight loss: Often due to poor calorie intake.
Bacterial overgrowth ± malabsorption (blind loop syndrome) may occur.
Anaemia: Usually from lack of iron, hypochlorhydria and stomach resection. b12 levels are frequently low but megaloblastic anaemia is rare.
Osteomalacia: There may be pseudofractures which look like metastases.
| Partial gastrectomy | Vagotomy & pyloroplasty | Highly selective vagotomy | |
|---|---|---|---|
Recurrence | 2% | 7% | >7% |
Dumping | 20% | 14% | 6% |
Diarrhoea | 1% | 4% | <1% |
Metabolic | ++++ | ++ | 0 |
| Partial gastrectomy | Vagotomy & pyloroplasty | Highly selective vagotomy | |
|---|---|---|---|
Recurrence | 2% | 7% | >7% |
Dumping | 20% | 14% | 6% |
Diarrhoea | 1% | 4% | <1% |
Metabolic | ++++ | ++ | 0 |
(These values are approximate and depend on the skill of the surgeon.)
Theodor BillrothTheodor Billroth was a surgeon of German-Austrian origin, whose name lives on as a set of operations on the stomach. He was a pioneer of abdominal surgery and the use of aseptic techniques, performing the first Billroth I procedure in 1881 for the resection of a pyloric gastric carcinoma. Among the many of his remarkable achievements is included the first laryngectomy. He was also a talented musician (a close friend of Brahms) and a dedicated educator with something of a realist’s view of the world:
Operations for peptic ulcers
Peptic ulcers usually present as epigastric pain and dyspepsia (p242). There is no reliable method of distinguishing clinically between gastric and duodenal ulcers. Although management of both is usually medical in the first instance (eg with H. pylori eradication, p242); surgery is usually only required for complications such as haemorrhage, perforation, and pyloric stenosis, though may be considered for the few patients who are not responsive to, or tolerant of, medical therapy.
Several types of operation have been tried, but whenever surgery is considered, one must consider efficacy, side-seffects, and mortality.
Elective surgery
Highly selective vagotomy: May be useful in patients unable to tolerate medical treatment. The vagus supply is denervated only where it supplies the lower oesophagus and stomach. The nerve of Latarget to the pylorus is left intact; thus, gastric emptying is unaffected. The results of surgery are greatly dependent on the skill of the surgeon.
Vagotomy and pyloroplasty: This operation is now almost obsolete, and is only performed in exceptional circumstances.
Emergency surgery may be required for the following complications:
Haemorrhage may be controlled endoscopically by adrenaline injection, diathermy, laser coagulation, or heat probe. Surgery should be considered for severe haemorrhage or rebleeding, especially in the elderly—see p254 for indications. In theatre, the bleeding ulcer base is underrun or oversewn.
Pyloric stenosis Adult pyloric stenosis is a late complication of duodenal ulcers due to scarring (and has nothing to do with congenital hypertrophic pyloric stenosis, p629). Patients complain of vomiting large amounts of food some hours after meals. Treatment: Endoscopic balloon dilatation, followed by maximal acid suppression (p242), may be tried in the first instance (nb: 5% risk of perforation). If this is unsuccessful, a drainage procedure (eg gastro-enterostomy or pyloroplasty) ± highly selective vagotomy may be performed, often laparoscopically. The operation should be done on the next available list, after correction of the metabolic defect—a hypochloraemic, hypokalaemic metabolic alkalosis.
Fundoplication for gastro-oesophageal reflux
Laparoscopic fundoplication is the surgical procedure of choice when symtoms of gord are retractable and refractory to medical therapy and there is severe reflux (confirmed by pH-monitoring)—see p244. Symptoms may be complicated by a hiatus hernia, which is repaired during the procedure.
Surgery
The defect in the diaphragm is repaired by tightening the crura. Reflux is prevented by wrapping the gastric fundus around the lower oesophageal sphincter—see fig 1. There are various types of procedure, eg Nissen (360° wrap), Toupet (270° posterior wrap), Watson (anterior hemifundoplication).
Laparoscopic Nissen fundoplication.
Laparoscopic surgery is at least as effective at controlling reflux as open surgery but with a lower mortality and morbidity. Wound infections and respiratory complications are also more common in open surgery, though the incidence of dysphagia is similar for the two procedures—but see p594.
Complications
Surgical management of obesity
Surgical management of severe obesity
Indications
According to nice guidelines, weight-loss surgery in adults should be considered if all the following criteria are met:
bmi ≥40 or ≥35 with significant comorbidities that could improve with ↓weight.
Failure of non-surgical management to achieve and maintain clinically beneficial weight loss for 6 months.
Fitness for surgery and anaesthesia.
As part of an integrated programme that provides guidance on diet, physical activity, and psychosocial concerns, as well as lifelong medical monitoring.
The patient must be well-informed and motivated.
nb: if bmi ≥50 surgery is recommended as first-line treatment.
Comparison with medical therapy
Procedures
There are 2 main mechanisms causing weight loss:
Restriction of calorie intake by reducing stomach capacity
Malabsorption of nutrients by reducing the length of functional small bowel.
nb: This also affects the levels of circulating gut peptides (eg pyy and glp-1), which are thought to play a role in the mechanism of satiety and weight loss. The 2 most popular procedures are:
Adjustable gastric band.
Some paediatric surgical emergencies
Congenital hypertrophic pyloric stenosis
See ohcs p172. Usually presents in first 3–8wks as projectile vomiting (4 in 1000 live births). ♂:♀≈4:1. The baby is malnourished and always hungry.
Diagnosis:
palpate the olive-shaped pyloric mass in the ruq during a feed. Visible gastric peristalsis starts in the luq. The baby can be severely alkalotic and depleted of water and ions from vomiting. Needs correcting before surgery. uss may be useful in assessment. Pass ngt (p773).
Treatment:
Ramstedt’s pyloromyotomy (involves incision of muscle down to mucosa).
Intussusception
See ohcs, p172. Small bowel telescopes, as if swallowing itself by invagination.
Presentation:
Tests/Management:
Least invasive approach is uss with reduction by air enema or pneumatic reduction under radiographic control. If reduction fails, surgery is needed. Prompt treatment may avoid necrosis.
Pre-op care:
Resuscitate, crossmatch blood, pass ngt. nb: children >4yrs present differently: rectal bleeding less common, more likely to have a long history (>3wks) and some sort of contributing pathology, eg Henoch–Schönlein purpura, cystic fibrosis, Peutz–Jeghers’ syndrome or tumours, eg lymphomas—where obstructive symptoms caused by intussusception are the chief mode of presentation. Recurrence rate: ∼5%.
Midgut malrotation
See ohcs p130. During embryonic development, the midgut undergoes 270° anticlockwise rotation. If malrotated the gut is prone to undergo volvulus upon its abnormally pedicled mesentery. Usually presents in neonatal period with dark green bilious vomiting, distension, and rectal bleeding. Can be asymptomatic for years before acute presentation.
Treatment:
Resuscitation, then surgery (involves broadening the mesentery and replacing bowel in a non-rotated position).
Examining the abdomen of a child or infant can prove extremely difficult and requires patience, practice and opportunism. So:
An age-directed approach will help develop your relationship with the child.
Remember that the parents will be closely involved in what you do.
Play specialists may be able to provide distraction.
The abdomen may need to be examined with the child sitting in mum’s lap.
There is no hope of eliciting any signs whilst the child is crying and tensing his tummy—everyone will be better off if you return when the child has settled!
Examining for rebound tenderness in young children is probably of little use for us and definitely uncomfortable for them.
You should always examine the scrotum and inguinal regions in young boys to exclude the possibility of testicular torsion or a strangulated hernia.
Performing a pr examination, if required, is best left to a specialist.
Unless you have a magical way with children, don’t be surprised to get the cold shoulder once in a while!
Diverticular disease
A gi diverticulum is an outpouching of the gut wall, usually at sites of entry of perforating arteries. Diverticulosis means that diverticula are present, and diverticular disease implies they are symptomatic. Diverticulitis refers to inflammation of a diverticulum. Diverticulum can be aquired or congenital and may occur elsewhere, but the most important are acquired colonic diverticula, to which this page refers.
Pathology
Most occur in the sigmoid colon with 95% of complications at this site, but right-sided and massive single diverticula can occur. Lack of dietary fibre is thought to lead to high intraluminal pressures which force the mucosa to herniate through the muscle layers of the gut at weak points adjacent to penetrating vessels. 30% of Westerners have diverticulosis by age 60. The majority are asymptomatic.
Diagnosis
Complications of diverticulosis
There may be altered bowel habit ± left-sided colic relieved by defecation; nausea and flatulence. A high-fibre diet (wholemeal bread, fruit and vegetables) may be tried. Antispasmodics, eg mebeverine 135mg/8h po, may help. Surgical resection is occasionally resorted to. Other complications:
Diverticulitis
—with features above + pyrexia, wcc↑, crp/esr↑, a tender colon ± localized or generalized peritonism.
℞:
analgesia, nbm, iv fluids, antibiotics, ct-guided percutaneous drainage (if abscess). Beware diverticulitis in immunocompromised patients (eg on steroids) who often have few symptoms and may present late.
Perforation
Haemorrhage is usually sudden and painless. It is a common cause of big rectal bleeds. See box 2. Bleeding usually stops with bed rest. Transfusion may be needed. Embolization or colonic resection may be necessary after locating bleeding points by angiography or colonoscopy (here diathermy ± local adrenaline injections may obviate the need for surgery).
Fistulae Enterocolic, colovaginal, or colovesical (pneumaturia ± intractable utis). Treatment is surgical, eg colonic resection.
Abscesses, eg with swinging fever, leucocytosis, and localizing signs, eg boggy rectal mass (pelvic abscess—drain rectally). If no localizing signs, remember the aphorism: pus somewhere, pus nowhere = pus under the diaphragm. A subphrenic abscess is a horrible way to die, so do an urgent ultrasound. Antibiotics ± ultrasound/ct-guided drainage may be needed.
Post-infective strictures may form in the sigmoid colon.
Angiodysplasia
Angiodysplasia refers to submucosal arteriovenous malformations that typically present as fresh pr bleeding in the elderly. The underlying cause is unknown.
Pathology:
70–90% of lesions occur in right colon, though angiodysplasia can affect anywhere in the gi tract.
Diagnosis:
pr examination, colonoscopy (fig 5, p257) may exclude competing diagnoses;99mTc radionuclide-labelled red-cell imaging (p752) is useful in identifying lesions during active bleeding (if >0.1mL/min). Mesenteric angiography is very helpful in diagnosing angiodysplasia (shows early filling at the lesion site, then extravasation), and allows therapeutic embolization during bleeding—it detects bleeding >1mL/min. ct angiography offers a non-invasive alternative.
Treatment options:
Embolization, endoscopic laser electrocoagulation, resection.
In an acute attack colonoscopy should not be done.The need for surgery is reflected by the degree of infective complications:
Stage 1 | Pericolic or mesenteric abscess | Surgery rarely needed |
Stage 2 | Walled off or pelvic abscess | May resolve without surgery |
Stage 3 | Generalized purulent peritonitis | Surgery required |
Stage 4 | Generalized faecal peritonitis | Surgery required |
Stage 1 | Pericolic or mesenteric abscess | Surgery rarely needed |
Stage 2 | Walled off or pelvic abscess | May resolve without surgery |
Stage 3 | Generalized purulent peritonitis | Surgery required |
Stage 4 | Generalized faecal peritonitis | Surgery required |
For emergency colonic resection see p630.
The causes of rectal bleeding are covered else-where (minibox). Here let’s make an acute management plan for this common surgical event:
abc resuscitation, if necessary.
History and examination
Blood tests: fbc, u&e, lft, clotting, amylase (always thinking of pancreatitis), crp, group and save—await Hb result before crossmatching unless unstable and bleeding.
Imaging May only need plain axr, but if there are signs of perforation (eg sepsis, peritonism) or if there is cardiorespiratory comorbidity, then request an erect cxr. See angiodysplasia, p630, for more imaging options.
Fluid management Insert 2 cannulae (≥18g) into the antecubital fossae. Insert a urinary catheter if there is a suspicion of haemodynamic compromise—there is no absolute indication, but remember that you are weighing up the risks and benefits. Give crystalloid as replacement and maintenance ivi. Blood transfusion is rarely needed in the acute setting.
Antibiotics may occasionally be required if there is evidence of sepsis or perforation, eg cefuroxime 1.5g/8h iv + metronidazole 500mg/8h iv.
Keep bedbound The patient may feel the need to get out of bed to pass stool, but this could be another large bleed, resulting in collapse if they try to walk. Don’t allow them to mobilize and inform the nursing staff of this.
Start a stool chart to monitor volume and frequency of motions. Send a sample for mc&s (x3 if known to have compromising comorbidity such as ibd).
Diet Keep on clear fluids so that they can have something, yet the colon will be clear for colonoscopy (which is of little value until bleeding has stopped).
Surgery The main indication for this is unremitting, massive bleeding.
Around the anus
Pruritus ani
Itch occurs if the anus is moist/soiled; fissures, incontinence, poor hygiene, tight pants, threadworm, fistula, dermatoses, lichen sclerosis, anxiety, contact dermatitis (perfumed goods). Cause is often unknown.
℞:
Fissure-in-ano
Painful tear in the squamous lining of the lower anal canal—often, if chronic, with a ‘sentinel pile’ or mucosal tag at the external aspect. 90% are posterior (anterior ones follow parturition). ♂>♀.
Causes:
℞:
Fistula-in-ano
A track communicates between the skin and anal canal/rectum. Blockage of deep intramuscular gland ducts is thought to predispose to the formation of abscesses, which discharge to form the fistula. Goodsall’s rule determines the path of the fistula track: if anterior, the track is in a straight line (radial); if posterior, the internal opening is always at the 6 o’clock position.
Causes:
perianal sepsis, abscesses (see below), Crohn’s disease, tb, diverticular disease, rectal carcinoma, immunocompromise.
Tests:
℞:
Fistulotomy + excision. High fistulae (involving continence muscles of anus) require ‘seton suture’ tightened over time to maintain continence; low fistulae are ‘laid open’ to heal by secondary intention—division of sphincters poses no risk to continence.
Anorectal abscesses
usually caused by gut organisms (rarely staphs or tb). ♂:♀≈1:8. Perianal (∼45%), ischiorectal (≤30%), intersphincteric (>20%), supralevator (∼5%).
℞:
Incise & drain under ga.
Associations:
dm, Crohn’s, malignancy, fistulae.
Perianal haematoma
(aka thrombosed external pile—see p635). Strictly, it is actually a clotted venous saccule. It appears as a 2–4mm ‘dark blueberry’ under the skin at the anal margin. It may be evacuated under la or left to resolve spontaneously.
Pilonidal sinus
Obstruction of natal cleft hair follicles ∼6cm above the anus. Ingrowing of hair excites a foreign body reaction and may cause secondary tracks to open laterally ± abscesses, with foul-smelling discharge. (Barbers get these between fingers.) ♂:♀≈10:1. Obese Caucasians and those from Asia, the Middle East, and Mediterranean at ↑risk.
℞:
Rectal prolapse
Perianal warts
Condylomata acuminata (viral warts) are treated with podophyllotoxin or imiquimod or cryotherapy/surgical excision. Giant condylomata acuminata of Bushke & Loewenstein may evolve into verrucous cancers (low-grade, non-metastasizing). Condylomata lata secondary to syphilis is treated with penicillin.
Proctalgia fugax
Anal ulcers
are rare. Consider Crohn’s disease, anal cancer, tb, and syphilis.
Skin tags
seldom cause trouble but are easily excised.
It is necessary to have a chaperone present for the examination. Explain what you are about to do. Make sure curtains are pulled. Have the patient lie on their left side, with knees brought up towards the chest. Use gloves and lubricant. Part the buttocks and inspect the anus:
A gaping anus suggests a neuropathy or megarectum
Symmetry (a tender unilateral bulge suggests an abscess)
Prolapsed piles
A subanodermal clot may peep out
Prolapsed rectum (descent of >3cm when asked to strain, as if to pass a motion)
Anodermatitis (from frequent soiling). The anocutaneous reflex tests sensory and motor innervation—on lightly stroking the anal skin, does the external sphincter briefly contract?
Press your index finger against the side of the anus. Ask the patient to breathe deeply and insert your finger slowly. Feel for masses (haemorrhoids are not palpable) or impacted stool. Twist your arm so that the pad of your finger is feeling anteriorly. Feel for the cervix or prostate. Note consistency, size, and symmetry of the prostate. If there is faecal incontinence or concern about the spinal cord, ask the patient to squeeze your finger and note the tone. This is best done with your finger pad facing posteriorly. Note stool or blood on the glove and test for occult blood.
Wipe the anus. Consider proctoscopy (for the anus) or sigmoidoscopy (which mainly inspects the rectum).
300/yr.uk
Syphilis, anal warts (hpv 16, 6, 11, 18, 31 & 33 implicated), anoreceptive homosexuals (often young).
Squamous cell (85%); rarely basaloid, melanoma, or adenocarcinoma. Anal margin tumours are usually well-differentiated, keratinizing lesions with a good prognosis. Anal canal tumours arise above dentate line, are poorly differentiated and non-keratinizing with a poorer prognosis.
Tumours above the dentate line spread to pelvic lymph nodes; those below spread to the inguinal nodes.
may present with bleeding, pain, bowel habit change, pruritus ani, masses, stricture.
Perianal warts; leucoplakia; lichen sclerosis; Bowen’s disease; Crohn’s disease.
Anatomy of the anal canal. Perianal abscesses present as tender, inflamed, localized swellings at the anal verge. Ischiorectal abscesses are also tender but cause a diffuse, indurated swelling in the ischioanal fossa area. You will find your patient waiting anxiously for you, pacing about, or on the edge of their chair: avoiding all pressure is imperative. nb: Above the dentate line = visceral nerve innervation; below = somatic innervation (very sensitive to pain).
Haemorrhoids (piles)
Definition
Haemorrhoids are disrupted and dilated anal cushions. The anus is lined mainly by discontinuous masses of spongy vascular tissue—the anal cushions, which contribute to anal closure. Viewed from the lithotomy position, the 3 anal cushions are at 3, 7, and 11 o’clock (where the 3 major arteries that feed the vascular plexuses enter the anal canal). They are attached by smooth muscle and elastic tissue, but are prone to displacement and disruption, either singly or together. The effects of gravity (our erect posture), increased anal tone (?stress), and the effects of straining at stool may make them become both bulky and loose, and so to protrude to form piles (Latin pila, meaning a ball). They are vulnerable to trauma (eg from hard stools) and bleed readily from the capillaries of the underlying lamina propria, hence their other name, haemorrhoids (≈running blood in Greek). Because loss is from capillaries, it is bright red. nb: piles are not varicose veins.
As there are no sensory fibres above the dentate line (squamomucosal junction), piles are not painful unless they thrombose when they protrude and are gripped by the anal sphincter, blocking venous return.
Differential diagnosis
Perianal haematoma; anal fissure; abscess; tumour; proctalgia fugax. Never ascribe rectal bleeding to piles without adequate examination or investigation.
Causes
Constipation with prolonged straining is a key factor. In many the bowel habit may be normal. Congestion from a pelvic tumour, pregnancy, ccf, or portal hypertension are important in only a minority of cases.
Pathogenesis
There is a vicious circle: vascular cushions protrude through a tight anus, become more congested and hypertrophy to protrude again more readily. These protrusions may then strangulate. See table for classification.
1st degree | Remain in the rectum |
2nd degree | Prolapse through the anus on defecation but spontaneously reduce |
3rd degree | As for 2nd-degree but require digital reduction |
4th degree | Remain persistently prolapsed |
1st degree | Remain in the rectum |
2nd degree | Prolapse through the anus on defecation but spontaneously reduce |
3rd degree | As for 2nd-degree but require digital reduction |
4th degree | Remain persistently prolapsed |
Symptoms
Bright red rectal bleeding, often coating stools, on the tissue, or dripping into the pan after defecation. There may be mucous discharge and pruritus ani. Severe anaemia may occur. Symptoms such as weight loss, tenesmus and change in bowel habit should prompt thoughts of other pathology. In all rectal bleeding do:
An abdominal examination to rule out other diseases.
pr exam: prolapsing piles are obvious. Internal haemorrhoids are not palpable.
Proctoscopy to see the internal haemorrhoids.
Sigmoidoscopy to identify rectal pathology higher up (you can get no higher up than the rectosigmoid junction).
Treatment
Medical: (for 1st-degree haemorrhoids) ↑fluid and fibre is key ± topical analgesics & stool softener. Topical steroids for short periods only.
Non-operative: (for 2nd & 3rd degree, or 1st degree if medical therapy has failed). The best treatment is unknown as meta-analyses differ:
Rubber band ligation: A cheap treatment, but needs skill. Banding produces an ulcer to anchor the mucosa (se: bleeding, infection; pain). It has the lowest recurrence rate.
Sclerosants: (for 1st- or 2nd-degree piles) 2mL of 5% phenol in almond/arachis oil is injected into the pile above the dentate line. Recurrence is higher (se: impotence; prostatitis).
Cryotherapy (freezing) has a high complication rate and is not recommended. In all but 4th-degree piles, these measures may obviate the need for surgery.
Surgery:
Excisional haemorrhoidectomy is the most effective treatment (excision of piles ± ligation of vascular pedicles, as day-case surgery, needing ∼2wks off work). Scalpel, electrocautery or laser may be used.
Prolapsed, thrombosed piles are treated with analgesia, ice packs and stool softeners. Pain usually resolves in 2–3 weeks. Some advocate early surgery.
Internal and external haemorrhoids.
Gallstones
Pigment stones:
(<10%) Small, friable, and irregular. Causes: haemolysis.
Cholesterol stones:
Large, often solitary. Causes: ♀, age, obesity (Admirand’s triangle: ↑risk of stone if ↓lecithin, ↓bile salts, ↑cholesterol).
Mixed stones:
Faceted (calcium salts, pigment, and cholesterol).
Gallstone prevalence:
8% of those over 40yrs. 90% remain asymptomatic. Risk factors for stones becoming symptomatic: smoking; parity.
Acute cholecystitis
follows stone or sludge impaction in the neck of the gallbladder (gb), which may cause continuous epigastric or ruq pain (referred to the right shoulder—see p611), vomiting, fever, local peritonism, or a gb mass. The main difference from biliary colic is the inflammatory component (local peritonism, fever, wcc↑). If the stone moves to the common bile duct (cbd), obstructive jaundice and cholangitis may occur—see box for complications. Murphy’s sign: Lay 2 fingers over the ruq; ask patient to breathe in. This causes pain & arrest of inspiration as an inflamed gb impinges on your fingers. It is only +ve if the same test in the luq does not cause pain. A phlegmon (ruq mass of inflamed adherent omentum and bowel) may be palpable.
Tests:
Treatment:
Chronic cholecystitis
Chronic inflammation ± colic. ‘Flatulent dyspepsia’: vague abdominal discomfort, distension, nausea, flatulence, and fat intolerance (fat stimulates cholecystokinin release and gb contraction). us to image stones and assess cbd diameter. mrcp (p757) is used to find cbd stones.
℞:
Cholecystectomy. If us shows a dilated cbd with stones, ercp (p756) + sphincterotomy before surgery. If symptoms persist post-surgery consider hiatus hernia/ibs/peptic ulcer/relapsing pancreatitis/tumour.
Biliary colic
Gallstones are symptomatic with cystic duct obstruction or if passed into the cbd. ruq pain (radiates → back) ± jaundice.
℞:
ΔΔ:
The above may overlap as part of a spectrum of gallstone disease. Urinalysis, cxr, and ecg help exclude other diseases.
Other presentations
Cholangitis (bile duct infection) causing ruq pain, jaundice, and rigors (Charcot’s triad’, box). Treat with, eg cefuroxime 1.5g/8h iv and metronidazole 500mg/8h iv/pr.
Pancreatitis (p638).
Mucocoele/empyema: Obstructed gb fills with mucus (secreted by gb wall)/pus.
Gallbladder perforation: Rare because of dual blood supply (hepatic artery via cystic artery, and from small branches of the hepatic artery in the gb fossa).
Other: Causes of cholecystitis and biliary symptoms other than gallstones are rare. Consider infection (typhoid, cryptosporidiosis and brucellosis); cholecystokinin release; parenteral nutrition; anatomical abnormality; polyarteritis nodosa (p558).
In the gallbladder & cystic duct: | In the bile ducts: |
• Biliary colic • Acute and chronic cholecystitis • Mucocoele • Empyema • Carcinoma • Mirizzi’s syndrome | • Obstructive jaundice • Cholangitis • Pancreatitis In the gut: • Gallstone ileus |
In the gallbladder & cystic duct: | In the bile ducts: |
• Biliary colic • Acute and chronic cholecystitis • Mucocoele • Empyema • Carcinoma • Mirizzi’s syndrome | • Obstructive jaundice • Cholangitis • Pancreatitis In the gut: • Gallstone ileus |
ruq pain | Fever / ↑wcc | Jaundice | |
Biliary colic | ✓ | ✗ | ✗ |
Acute cholecystitis | ✓ | ✓ | ✗ |
Cholangitis | ✓ | ✓ | ✓ |
ruq pain | Fever / ↑wcc | Jaundice | |
Biliary colic | ✓ | ✗ | ✗ |
Acute cholecystitis | ✓ | ✓ | ✗ |
Cholangitis | ✓ | ✓ | ✓ |
Is it possible to perform double-blind rcts in surgery?
Acute pancreatitis
Symptoms
Gradual or sudden severe epigastric or central abdominal pain (radiates to back, sitting forward may relieve); vomiting prominent.
Signs
may be mild in serious disease! Tachycardia, fever, jaundice, shock, ileus, rigid abdomen ± local/general tenderness, periumbilical bruising (Cullen’s sign) or flanks (Grey Turner’s sign) from blood vessel autodigestion and retroperitoneal haemorrhage.
Tests
Amylase may be normal even in severe pancreatitis (levels starts to fall within the 1st 24–48h). Cholecystitis, mesenteric infarction, and gi perforation can cause lesser rises (usually). It is excreted renally so renal failure will ↑ levels. Serum lipase is more sensitive and specific for pancreatitis. abg to monitor oxygenation and acid-base status. axr: No psoas shadow (retroperitoneal fluid↑), ‘sentinel loop’ of proximal jejunum from ileus (solitary air-filled dilatation). Erect cxr helps exclude other causes (eg perforation). ct is the standard choice of imaging to assess severity and for complications—mri may be even better. us (if gallstones + ast↑). ercp if lfts worsen. crp >150mg/L at 36h after admission is a predictor of severe pancreatitis.Management
Severity assessment is essential (see box).
Nil by mouth, likely to need ng tube (decrease pancreatic stimulation). Set up ivi and give lots of 0.9% saline, to counter third-space sequestration, until vital signs are satisfactory and urine flow stays at >30mL/h. Insert a urinary catheter and consider cvp monitoring. Think about nutrition early on (p586).
Hourly pulse, bp, and urine output; daily fbc, u&e, Ca2+, glucose, amylase, abg.
ercp + gallstone removal may be needed if there is progressive jaundice.
Repeat imaging (usually ct) is performed in order to monitor progress.
ΔΔ
Any acute abdomen (p608), myocardial infarct.
Prognosis
See box.
Early complications
Shock, ards (p178), renal failure (give lots of fluid!), dic, sepsis, Ca2+↓, glucose↑ (transient; 5% need insulin).
Late complications
(>1wk) Pancreatic necrosis and pseudocyst (fluid in lesser sac, fig 1), with fever, a mass ± persistent ↑amylase/lft; may resolve or need drainage. Abscesses need draining. Bleeding from elastase eroding a major vessel (eg splenic artery); embolization may be life-saving. Thrombosis may occur in the splenic/gastroduodenal arteries, or colic branches of the sma, causing bowel necrosis. Fistulae normally close spontaneously. If purely pancreatic they do not irritate the skin. Some patients suffer recurrent oedematous pancreatitis so often that near-total pancreatectomy is contemplated. It can all be a miserable course.
Axial ct of the abdomen (with iv and po contrast media) showing a pancreatic pseudocyst occupying the lesser sac of the abdomen posterior to the stomach. It is called a ‘pseudocyst’ because it is not a true cyst, rather a collection of fluid in the lesser sac (ie not lined by epi/endothelium). It develops at ≥6wks. The cyst fluid is of low attenuation compared with the stomach contents because it has not been enhanced by the contrast media.
Gallstones(38%)
Ethanol(35%)
Trauma(1.5%)
Steroids
Mumps
Autoimmune (pan)
Scorpion venom
Hyperlipidaemia, hypothermia, hypercalcaemia
Ercp(5%) and emboli
Drugs
Also pregnancy and neoplasia or no cause found(10–30%)
3 or more positive factors detected within 48h of onset suggest severe pancreatitis, and should prompt transfer to itu/hdu. Mnemonic: pancreas.PaO2 | <8kPa |
Age | >55yrs |
Neutrophilia | wbc >15 x 109/L |
Calcium | <2mmol/L |
Renal function | Urea >16mmol/L |
Enzymes | ldh >600iu/L; ast >200iu/L |
Albumin | <32g/L (serum) |
Sugar | blood glucose >10mmol/L |
PaO2 | <8kPa |
Age | >55yrs |
Neutrophilia | wbc >15 x 109/L |
Calcium | <2mmol/L |
Renal function | Urea >16mmol/L |
Enzymes | ldh >600iu/L; ast >200iu/L |
Albumin | <32g/L (serum) |
Sugar | blood glucose >10mmol/L |
These criteria have been validated for pancreatitis caused by gallstones and alcohol; Ranson’s criteria are valid for alcohol-induced pancreatitis, and can only be fully applied after 48h, which does have its disadvantages. Other criteria for assessing severity include the Acute Physiology and Chronic Health Examination (apache)-ii, and the Bedside Index for Severity in Acute Pancreatitis (bisap).
Urinary tract calculi (nephrolithiasis)
Renal stones (calculi) consist of crystal aggregates. Stones form in collecting ducts and may be deposited anywhere from the renal pelvis to the urethra, though classically at
Pelviureteric junction
Pelvic brim
Vesicoureteric junction.
Prevalence
Common: lifetime incidence up to 15%. Peak age: 20–40yr. ♂:♀≈3:1.
Types
Calcium oxalate (75%)
Magnesium ammonium phosphate (struvite/triple phosphate; 15%)
Also: urate (5%), hydroxyapatite (5%), brushite, cystine (1%), mixed.
Presentation
Asymptomatic or:
uti can co-exist (↑risk if voiding impaired); pyelonephritis (fever, rigors, loin pain, nausea, vomiting), pyonephrosis (infected hydronephrosis)
Haematuria
Proteinuria
Sterile pyuria
Anuria.
Examination
Usually no tenderness on palpation. May be renal angle tenderness especially to percussion if there is retroperitoneal inflammation.
Tests
fbc, u&e, Ca2+, po43–, glucose, bicarbonate, urate.
Urine dipstick:
Usually +ve for blood (90%).
MSU:
mc&s.
Further tests for cause:
Urine pH; 24h urine for: calcium, oxalate, urate, citrate, sodium, creatinine; stone biochemistry (sieve urine & send stone).
Imaging:
Spiral non-contrast ct is superior to and has largely replaced ivu for imaging stones (99% visible) + helps exclude differential causes of an acute abdomen. A ruptured abdominal aortic aneurysm may present similarly. 80% of stones are visible on kub xr (kidneys+ureters+bladder). Look along ureters for calcification over the transverse processes of the vertebral bodies. ivu: radio-opaque contrast injected and serial films taken until contrast seen down to level of obstruction. Cannot be interpreted without a plain control. Abnormal findings: failure of contrast to flow to bladder, dense nephrogram (contrast unable to flow from kidney), clubbed/blunted renal calyces (back pressure), filling defects in the bladder. (ci: contrast allergy, severe asthma, pregnancy, metformin.) uss to look for hydronephrosis or hydroureter.
℞:
Initially:
Stones <5mm in lower ureter:
∼90–95% pass spontaneously. ↑fluid intake.
Stones >5mm/pain not resolving:
start at presentation. Most pass within 48h (>80% after ∼30d). If not, try extracorporeal shockwave lithotripsy (eswl) (if <1cm), or ureteroscopy using a basket. eswl: us waves shatter stone. se: renal injury, may also cause ↑bp and dm. Percutaneous nephrolithotomy (pcnl): keyhole surgery to remove stones, when large, multiple, or complex. Open surgery is rare.Indications for urgent intervention (delay kills glomeruli): Presence of infection and obstruction—a percutaneous nephrostomy or ureteric stent may be needed to relieve obstruction (p642); urosepsis; intractable pain or vomiting; impending arf; obstruction in a solitary kidney; bilateral obstructing stones.Prevention
General:
Drink plenty. Normal dietary Ca2+ intake (low Ca2+ diets increase oxalate excretion).
Specifically:
Calcium stones: in hypercalciuria, a thiazide diuretic is used to ↓Ca2+ excretion
Oxalate: ↓oxalate intake; pyridoxine may be used (p312)
Struvite: treat infection promptly
Urate: allopurinol (100–300mg/24h po). Urine alkalinization may also help, as urate is more soluble at pH>6 (eg with potassium citrate or sodium bicarbonate)
Cystine: vigorous hydration to keep urine output >3L/d and urinary alkalinization (as above). d-penicillamine is used to chelate cystine, given with pyridoxine to prevent vitamin b6 deficiency.
| Type | Causative factors | Appearance on xr |
|---|---|---|
Calcium oxalate (fig 1) | Metabolic or idiopathic | Spiky, radio-opaque |
Calcium phosphate | Metabolic or idiopathic | Smooth, may be large, radio-opaque |
Magnesium ammonium phosphate (fig 2) | uti (proteus causes alkaline urine and calcium precipitation and ammonium salt formation) | Large, horny, ‘staghorn’ radio-opaque |
Urate (p694) | Hyperuricaemia | Smooth, brown, radiolucent |
Cystine (fig 3) | Renal tubular defect | Yellow, crystalline, semi-opaque |
| Type | Causative factors | Appearance on xr |
|---|---|---|
Calcium oxalate (fig 1) | Metabolic or idiopathic | Spiky, radio-opaque |
Calcium phosphate | Metabolic or idiopathic | Smooth, may be large, radio-opaque |
Magnesium ammonium phosphate (fig 2) | uti (proteus causes alkaline urine and calcium precipitation and ammonium salt formation) | Large, horny, ‘staghorn’ radio-opaque |
Urate (p694) | Hyperuricaemia | Smooth, brown, radiolucent |
Cystine (fig 3) | Renal tubular defect | Yellow, crystalline, semi-opaque |
Diet: Chocolate, tea, rhubarb, strawberries, nuts and spinach all ↑oxalate levels.
Season: Variations in calcium and oxalate levels are thought to be mediated by vitamin d synthesis via sunlight on skin.
Work: Can he/she drink freely at work? Is there dehydration?
Medications: Precipitating drugs include: diuretics, antacids, acetazolamide, corticosteroids, theophylline, aspirin, allopurinol, vitamin c and d, indinavir.
For example:
Recurrent utis (in magnesium ammonium phosphate calculi).
Metabolic abnormalities:
Urinary tract abnormalities: eg pelviureteric junction obstruction, hydronephrosis (renal pelvis or calyces), calyceal diverticulum, horseshoe kidney, ureterocele, vesicoureteric reflux, ureteral stricture, medullary sponge kidney.1
Foreign bodies: eg stents, catheters.
↑risk of stones x 3-fold. Specific diseases include x-linked nephrolithiasis and Dent’s disease (proteinuria, hypercalciuria and nephrocalcinosis).
Is there infection above the stone?eg fever, loin tender, pyuria? This needs urgent intervention.
Calcium oxalate monohydrate.
Struvite stone.
Cystine stone.
Urinary tract obstruction
Urinary tract obstruction is common and should be considered in any patient with impaired renal function. Damage can be permanent if the obstruction is not treated promptly. Obstruction may occur anywhere from the renal calyces to the urethral meatus, and may be partial or complete, unilateral or bilateral. Obstructing lesions are luminal (stones, blood clot, sloughed papilla, tumour: renal, ureteric, or bladder), mural (eg congenital or acquired stricture, neuromuscular dysfunction, schistosomiasis), or extra-mural (abdominal or pelvic mass/tumour, retroperitoneal fibrosis, or iatrogenic—eg post surgery). Unilateral obstruction may be clinically silent (normal urine output and u&e) if the other kidney is functioning. Bilateral obstruction or obstruction with infection requires urgent treatment. See box p645.
Clinical features
Acute upper tract obstruction: Loin pain radiating to the groin. There may be superimposed infection ± loin tenderness, or an enlarged kidney.
Chronic upper tract obstruction: Flank pain, renal failure, superimposed infection. Polyuria may occur owing to impaired urinary concentration.
Acute lower tract obstruction: Acute urinary retention typically presents with severe suprapubic pain, often preceded by symptoms of bladder outflow obstruction (as below). Clinically: distended, palpable bladder, dull to percussion.
Chronic lower tract obstruction: Symptoms: urinary frequency, hesitancy, poor stream, terminal dribbling, overflow incontinence. Signs: distended, palpable bladder ± large prostate on pr. Complications: uti, urinary retention.
Tests
Blood:
u&e, creatinine.
Urine:
mc&s. Ultrasound (p758) is the imaging modality of choice. If there is hydronephrosis or hydroureter (distension of the renal pelvis and calyces or ureter), arrange a ct scan. This will determine the level of obstuction. nb: in ∼5% of cases of obstruction, no distension is seen on ultrasound. Radionuclide imaging enables functional assessment of the kidneys. mri also has a role.
Treatment
Upper tract obstruction:
Lower tract obstruction:
Insert a urethral or suprapubic catheter (p776). Treat the underlying cause if possible. Beware of a large diuresis after relief of obstruction; a temporary salt-losing nephropathy may occur resulting in the loss of several litres of fluid a day. Monitor weight, fluid balance, and u&e closely.
Periaortitis (retroperitoneal fibrosiset al)
Causes include idiopathic retroperitoneal fibrosis (rpf), inflammatory aneurysms of the abdominal aorta, and perianeurysmal rpf. Idiopathic rpf is an autoimmune disorder, where there is b-cell and cd4(+) t-cell associated vasculitis. This results in fibrinoid necrosis of the vasa vasorum, affecting the aorta and small and medium retroperitoneal vessels. The ureters get embedded in dense, fibrous tissue resulting in progressive bilateral ureteric obstruction. Secondary causes of rpf include malignancy, typically lymphoma.
Associations
Drugs (eg β-blockers, bromocriptine, methysergide, methyldopa), autoimmune disease (eg thyroiditis, sle, anca+ve vasculitis), smoking, asbestos.
Typical patient
Middle-aged ♂ with vague loin, back or abdominal pain, bp↑.
Tests
Blood:
↑urea and creatinine; ↑esr; ↑crp; anaemia.
Ultrasound:
dilated ureters (hydronephrosis). Then ct/mri: periaortic mass (biopsy under imaging guidance is used to rule out malignancy).
Treatment
| Common | Rare |
|---|---|
Stent-related pain | Obstruction |
Trigonal irritation | Kinking |
Haematuria | Ureteric rupture |
Fever | Stent misplacement |
Infection | Stent migration (especially if made of silicone) |
Tissue inflammation | Tissue hyperplasia |
Encrustation | Forgotton stents |
Biofilm formation |
| Common | Rare |
|---|---|
Stent-related pain | Obstruction |
Trigonal irritation | Kinking |
Haematuria | Ureteric rupture |
Fever | Stent misplacement |
Infection | Stent migration (especially if made of silicone) |
Tissue inflammation | Tissue hyperplasia |
Encrustation | Forgotton stents |
Biofilm formation |
ct scan of retroperitoneal fibrosis (rpf), with subsequent obstruction and dilatation of the ureters (thick arrows).
Urinary retention & benign prostatic hyperplasia
Retention means not emptying the bladder (due to obstruction or ↓detrusor power).
Chronic retention More insidious and may be painless. Bladder capacity may be >1.5L. Presentation: Overflow incontinence, acute on chronic retention, lower abdominal mass, uti, or renal failure (eg bilateral obstructive uropathy—see box). Causes: Prostatic enlargement is common, pelvic malignancy; rectal surgery; dm; cns disease, eg transverse myelitis/ms; zoster (s2–s4). Only catheterize patient if there is pain, urinary infection, or renal impairment. Institute definitive treatment promptly. Intermittent self-catheterization is sometimes required (p777). Catheters p776. Prostate carcinoma p646.
Benign prostatic hyperplasia (bph) is common (24% if aged 40–64; 40% if older).
Pathology:
Benign nodular or diffuse proliferation of musculofibrous and glandular layers of the prostate. Inner (transitional) zone enlarges in contrast to peripheral layer expansion seen in prostate carcinoma.
Features:
Lower urinary tract symptoms (luts) = nocturia, frequency, urgency, post-micturition dribbling, poor stream/flow, hesitancy, overflow incontinence, haematuria, bladder stones, uti.
Management:
Assess severity of symptoms and impact on life. pr exam.
Tests:
Lifestyle: Avoid caffeine, alcohol (to ↓urgency/nocturia). Relax when voiding. Void twice in a row to aid emptying. Control urgency by practising distraction methods (eg breathing exercises). Train the bladder by ‘holding on’ to ↑time between voiding.
Drugs are useful in mild disease, and while awaiting surgery.
α-blockers are 1st line (eg tamsulosin 400µg/d po; also alfuzosin, doxazosin, terazosin). ↓smooth muscle tone (prostate and bladder). se: drowsiness; depression; dizziness; bp↓; dry mouth; ejaculatory failure; extra-pyramidal signs; nasal congestion; weight↑.
5α-reductase inhibitors: can be added, or used alone, eg finasteride 5mg/d po (↓testosterone’s conversion to dihydrotestosterone).2 Excreted in semen, so warn to use condoms; females should avoid handling. se: impotence; ↓libido. Effects on prostate size are limited and slow.
Surgery:
Transurethral resection of prostate (turp) ≤14% become impotent (see box). Crossmatch 2u. Beware bleeding, clot retention and tur syndrome: absorption of washout causing hyponatraemia and fits. ∼20% need redoing within 10yrs.
Retropubic prostatectomy is an open operation (if prostate very large).
Transurethral laser-induced prostatectomy (tulip) may be as good as turp.
Ultrasound of an obstructed kidney showing hydronephrosis. Note dilatation of renal pelvis and ureter, and clubbed calyces.
Pre-op consent issues may centre on risks of the procedure, eg:
• Infection; prostatitis • Erectile dysfunction ∼10% • Incontinence ≤10% • Clot retention near strictures • Retrograde ejaculation (common) |
Avoid driving for 2 weeks after the operation.
Avoid sex for 2 weeks after surgery. Then get back to normal. The amount ejaculated may be reduced (as it flows backwards into the bladder—harmless, but may cloud the urine). It means you may be infertile. Erections may be a problem after turp, but do not expect this: in some men, erections improve. Rarely, orgasmic sensations are reduced.
Expect to pass blood in the urine for the first 2 weeks. A small amount of blood colours the urine bright red. Do not be alarmed.
At first you may need to urinate more frequently than before. Do not be despondent. In 6 weeks things should be much better—but the operation cannot be guaranteed to work (8% fail, and lasting incontinence is a problem in 6%; 12% may need repeat turps within 8yrs, compared with 1.8% of men undergoing open prostatectomy).
If feverish, or if urination hurts, take a sample of urine to your doctor.
In chronic urinary retention, an episode of acute retention may go unnoticed for days and, because of their background symptoms, may only present when overflow incontinence becomes a nuisance—pain is not necessarily a feature. After diagnosing acute on chronic retention and placing a catheter, the bladder residual can be as much as 1.5L of urine. Don’t be surprised to be called by the biochemistry lab to be told that the serum creatinine is 1500µmol/L! The good news is that renal function usually returns to baseline after a few days (there may be mild background impairment). Ask for an urgent renal us (fig 1) and consider the following in the acute plan to ensure a safe course:
Hyperkalaemia See p849.
Metabolic acidosis On abg there is likely to be a respiratory compensated metabolic acidosis. Concerns should prompt discussion with a renal specialist (a good idea anyway), in case haemodialysis is required (p292).
Post-obstructive diuresis In the acute phase after relief of the obstruction, the kidneys produce a lot of urine—as much as a litre in the first hour. It is vital to provide resuscitation fluids and then match input with output.
Fluid depletion rather than overload is the danger here.
Sodium- and bicarbonate-losing nephropathy As the kidney undergoes diuresis, Na+ and bicarbonate are lost in the urine in large quantities. Replace ‘in for out’ (as above) with isotonic 1.26% sodium bicarbonate solution—this should be available from itu. Some advocate using 0.9% saline, though the chloride load may exacerbate acidosis. Withhold any nephrotoxic drugs.
Infection Treat infection, bearing in mind that the wcc↑ and crp↑ may be part of the stress response. Send a sample of urine for mc&s.
Urinary tract malignancies 244
(OHOncol Ch20)
Renal cell carcinoma
(aka rcc, hypernephroma, Grawitz tumour) arises from proximal renal tubular epithelium.
Epidemiology:
Accounts for 90% of renal cancers; mean age 55yrs. ♂:♀≈2:1. 15% of haemodialysis patients develop rcc.
Features:
50% found incidentally. Haematuria, loin pain, abdominal mass, anorexia, malaise, weight loss, puo—often in isolation. Rarely, invasion of left renal vein compresses left testicular vein causing a varicocele. Spread may be direct (renal vein), via lymph, or haematogenous (bone, liver, lung). 25% have metastases at presentation.
Tests:
bp: ↑from renin secretion. Blood: fbc (polycythaemia from erythropoietin secretion); esr; u&e, alp (bony mets?). Urine: rbcs; cytology. Imaging: us (p758); ct/mri; ivu (filling defect ± calcification); cxr (‘cannon ball’ metastases).
℞:
Prognosis:
Transitional cell carcinoma (tcc)
may arise in the bladder (50%), ureter, or renal pelvis.
Epidemiology:
Age >40yrs; ♂:♀≈4:1.
Risk factors:
p648.
Presentation:
Painless haematuria; frequency; urgency; dysuria; urinary tract obstruction.
Diagnosis:
Urine cytology; ivu; cystoscopy + biopsy; ct/mri.
℞:
See Bladder tumours, p648.
Prognosis:
Varies with clinical stage/histological grade: 10–80% 5yr survival.
Wilms’ tumour
(nephroblastoma) is a childhood tumour of primitive renal tubules and mesenchymal cells.
Prevalence:
1:100,000—the chief abdominal malignancy in children. It presents with an abdominal mass and haematuria.
℞:
ohcs p133.
Prostate cancer
The commonest male malignancy.
Incidence:
↑with age: 80% in men >80yrs (autopsy studies).
Associations:
+ve family history (x2–3 ↑risk, p524), ↑testosterone. Most are adenocarcinomas arising in peripheral prostate. Spread may be local (seminal vesicles, bladder, rectum) via lymph, or haematogenously (sclerotic bony lesions).
Symptoms:
Asymptomatic or nocturia, hesitancy, poor stream, terminal dribbling, or obstruction. Weight↓ ± bone pain suggests mets.
dre exam of prostate:
May show hard, irregular prostate.
Diagnosis:
↑psa (normal in 30% of small cancers); transrectal uss & biopsy; x-rays; bone scan; ct/mri.
Staging:
Treatment:
Radical prostatectomy if <70yrs gives excellent disease-free survival (laparoscopic surgery is as good). The role of adjuvant hormonal therapy is being explored.
Radical radiotherapy (± neoadjuvant & adjuvant hormonal therapy) is an alternative curative option that compares favourably with surgery (no rcts). It may be delivered as external beam or brachytherapy.
Hormone therapy alone temporarily delays tumour progression but refractory disease eventually develops. Consider in elderly unfit patients with high-risk disease.
Active surveillance—particularly if >70yrs and low-risk. Metastatic disease:
Hormonal drugs may give benefit for 1–2yrs. lhrh agonists, eg 12-weekly goserelin (10.8mg sc as Zoladex la®) first stimulate, then inhibit pituitary gonadotrophin. nb: risks tumour ‘flare’ when first used—start anti-androgen, eg cyproterone acetate, in susceptible patients. The lhrh antagonist degarelix is also used in advanced disease.
Symptomatic ℞:
Analgesia; treat hypercalcaemia; radiotherapy for bone mets/spinal cord compression.
Prognosis:
10% die in 6 months, 10% live >10yrs.
Screening:
dre of prostate; transrectal uss; psa (see box).
Penile cancer
Epidemiology:
rare in uk, more common in Far East and Africa, very rare in circumcised. Related to chronic irritation, viruses, smegma.
Presentation:
chronic fungating ulcer, bloody/purulent discharge, 50% spread to lymph at presentation
℞:
radiotherapy & irridium wires if early; amputation & lymph node dissection if late.
(see also p534)
Many men over 50 consider a psa test to detect prostatic cancer. Is this wise?
The test is not very accurate, and we cannot say that those having the test will live longer—even if they turn out to have prostate cancer. Most men with prostate cancer die from an unrelated cause.
If the test is falsely positive, you may needlessly have more tests, eg prostate sampling via the back passage (causes bleeding and infection in 1–5% of men).
Only one in three of those with a high psa level will have cancer.
You may be worried needlessly if later tests put you in the clear.
If a cancer is found, there’s no way to tell for sure if it will impinge on health. You might end up having a bad effect from treatment that wasn’t needed.
There is much uncertainty on treating those who do turn out to have prostate cancer: options are radical surgery to remove the prostate (this treatment may be fatal in 0.2–0.5% of patients and risks erectile dysfunction and incontinence), radiotherapy, or hormones.
Ultimately, you must decide for yourself what you want.
A number of prognostic factors help determine if ‘watchful waiting’ or aggressive therapy should be advised:
Pre-treatment psa level
Tumour grade—as measured by its Gleason score. Gleason grading is from 1 to 5, with 5 being the highest grade, and carrying the poorest prognosis. A pathologist determines Gleason grades by analysing histology from two separate areas of tumour specimen, and adding them to get the total Gleason score for the tumour, from 2 to 10. Scores 8–10 suggest an aggressive tumour; 5–7: intermediate; 2–4: indolent.
Acute inflammation of the foreskin and glans. Associated with strep and staph infections. More common in diabetics. Often seen in young children with tight foreskins
Antibiotics, circumcision, hygiene advice.
The foreskin occludes the meatus. In young boys this causes recurrent balanitis and ballooning, but time (+ trials of gentle retraction) may obviate the need for circumcision. In adulthood presents with painful intercourse, infection, ulceration and is associated with balanitis xerotica obliterans.
Occurs when a tight foreskin is retracted and becomes irreplaceable, preventing venous return leading to oedema and even ischaemia of the glans. Can occur if the foreskin is not replaced after catheterization.
℞:Ask patient to squeeze glans. Try applying a 50% glucose-soaked swab (oedema may follow osmotic gradient). Ice packs and lidocaine gel may also help. May require aspiration/dorsal slit/circumcision.
May be acute or chronic. Usually those >35yrs. Acute prostatitis is caused mostly by S. faecalis and E. coli, also chlamydia (and previously tb).
utis, retention, pain, haematospermia, swollen/boggy prostate on dre.
Analgesia; levofloxacin 500mg/24h po for 28d. Chronic prostatitis may be bacterial or non-bacterial. Symptoms as above, but present for >3 months. Non-bacterial chronic prostatitis does not respond to antibiotics. Anti-inflammatory drugs, α–blockers and prostatic massage all have a place.
Bladder tumours
>90% are transitional cell carcinomas (tccs) in the uk. What appear as benign papillomata rarely behave in a purely benign way. They are almost certainly indolent tccs. Adenocarcinomas and squamous cell carcinomas are rare in the West (the latter may follow schistosomiasis). uk incidence ≈ 1:6000/yr. ♂:♀≈5:2. Histology is important for prognosis: Grade 1—differentiated; Grade 2—intermediate; Grade 3—poorly differentiated. 80% are confined to bladder mucosa, and only ∼20% penetrate muscle (increasing mortality to 50% at 5yrs).
Presentation
Painless haematuria; recurrent utis; voiding irritability.
Associations
Smoking; aromatic amines (rubber industry); chronic cystitis; schistosomiasis (↑risk of squamous cell carcinoma); pelvic irradiation.
Tests
Cystoscopy with biopsy is diagnostic.
Urine: microscopy/cytology (cancers may cause sterile pyuria).
ct urogram is both diagnostic and provides staging.
Bimanual eua helps assess spread.
mri or lymphangiography may show involved pelvic nodes.
Staging
See table.
Tis | Carcinoma in situ | Not felt at eua |
Ta | Tumour confined to epithelium | Not felt at eua |
T1 | Tumour in lamina propria | Not felt at eua |
T2 | Superficial muscle involved | Rubbery thickening at eua |
T3 | Deep muscle involved | eua: mobile mass |
T4 | Invasion beyond bladder | eua: fixed mass |
Tis | Carcinoma in situ | Not felt at eua |
Ta | Tumour confined to epithelium | Not felt at eua |
T1 | Tumour in lamina propria | Not felt at eua |
T2 | Superficial muscle involved | Rubbery thickening at eua |
T3 | Deep muscle involved | eua: mobile mass |
T4 | Invasion beyond bladder | eua: fixed mass |
eua = examination under anaesthetic
Treating tcc of the bladder
The patient should have all these options explained by a urologist and an oncologist.T4: Usually palliative chemo/radiotherapy. Chronic catheterization and urinary diversions may help to relieve pain.
Follow-up
History, examination, and regular cystoscopy:
High-risk tumours: Every 3 months for 2yrs, then every 6 months;
Low-risk tumours: First follow-up cystoscopy after 9 months, then yearly.
Tumour spread
Local → to pelvic structures; lymphatic → to iliac and para-aortic nodes; haematogenous → to liver and lungs.
Survival
This depends on age at surgery. For example, the 3yr survival after cystectomy for T2 and T3 tumours is 60% if 65–75yrs old, falling to 40% if 75–82yrs old (in whom the operative mortality is 4%). With unilateral pelvic node involvement, only 6% of patients survive 5yrs. The 3yr survival with bilateral or para-aortic node involvement is nil.
Complications
(See also p527)
Dipstick tests are often done routinely for new admissions. If non-visible (previously microscopic) haematuria is found, but the patient has no related symptoms, what does this mean? Before rushing into a barrage of investigations, consider:
Asymptomatic non-visible haematuria is the sole presenting feature in only 4% of bladder cancers, and there is no evidence that these are less advanced than malignancies presenting with macroscopic haematuria.
When monitoring those with treated bladder cancer for recurrence, non-visible-haematuria tests have a sensitivity of only 31% in those with superficial bladder malignancy, in whom detection would be most useful.
Urinary incontinence
Think twice before inserting a urinary catheter.
Carry out rectal examination to exclude faecal impaction.
Is the bladder palpable after voiding (retention with overflow)?
Is there neurological co-morbidity: eg ms; Parkinson’s disease; stroke; spinal trauma?
Anyone might ‘wet themselves’ on a long bus ride (we all would if it was long enough). Don’t think of people as dry or incontinent, but as incontinent in some circumstances. Attending to these is as important as the physiology. Get good at treating incontinence and you will do wonders for quality of life. See p64 for symptoms.
Incontinence in men
Enlargement of the prostate is the major cause of incontinence: urge incontinence (see below) or dribbling may result from partial retention of urine. turp (p644) & other pelvic surgery may weaken the bladder sphincter and cause incontinence. Troublesome incontinence needs specialist assessment.
Incontinence in women
Often under-reported with delays before seeking help.
Functional incontinence, ie when physiological factors are relatively unimportant. The patient is ‘caught short’ and too slow in finding the toilet because of (for example) immobility, or unfamiliar surroundings.
Urge incontinence/overactive bladder syndrome The urge to urinate is quickly followed by uncontrollable and sometimes complete emptying of the bladder as the detrusor muscle contracts. Urgency/leaking is precipitated by: arriving home (latchkey incontinence, a conditioned reflex); cold; the sound of running water; coffee, tea or cola; and obesity. Δ: urodynamic studies. Cause: detrusor overactivity, eg from central inhibitory pathway malfunction or sensitization of peripheral afferent terminals in the bladder; or a bladder muscle problem. Check for organic brain damage (eg stroke; Parkinson’s; dementia). Other causes: urinary infection; diabetes; diuretics; atrophic vaginitis; urethritis.
In both sexes incontinence may result from confusion or sedation. Occasionally it may be purposeful (eg preventing admission to an old people’s home) or due to anger.
Management
Check for:
uti; dm; diuretic use; faecal impaction; palpable bladder; gfr.
Urge incontinence: The patient (or carer) should complete an ‘incontinence’ chart for 3 days to define the pattern of incontinence. Examine for spinal cord and cns signs (including cognitive test, p70 & p85); and for vaginitis (if postmenopausal). Vaginitis can be treated with topical oestrogen therapy for a limited period. Bladder training1 (may include pelvic floor exercises) and weight loss are important. Drugs may help reduce night-time incontinence (see box) but can be disappointing. Consider aids eg absorbent pad. If ♂ consider a condom catheter.
Do urodynamic assessment (cystometry & urine flow rate measurement) before any surgical intervention to exclude detrusor overactivity or sphincter dyssynergia.
| Agents for detrusor overactivity | Notes |
|---|---|
Topical oestrogens | Post-menopausal urgency, frequency + nocturia may occasionally be improved by raising the bladder’s sensory threshold. |
β3 adrenergic agonist: mirabegron 50mg/24h; se tachycardia; ci: severe htn; Caution if renal/hepatic impairment. | Consider if antimuscurinics are contraindicated or clinically ineffective, or if se unacceptable. |
Intravesical botulinum toxin (Botox®) | Consider if above medications ineffective. |
Percutaneous posterior tibial nerve stimulation (ptns). (A typical treatment consists of x12 weekly 30 min sessions.) | Consider if drug treatment ineffective and Botox® not wanted. ptns delivers neuromodulation to the s2–s4 junction of the sacral nerve plexus. |
Sacral nerve stimulation inhibits the reflex behaviour of involuntary detrusor contractions. | |
Modulation of afferent input from bladder | |
Hypnosis, psychotherapy, bladder training1 | (These all require good motivation.) |
Surgery (eg clam ileocystoplasty) | Reserved for troublesome or intractable symptoms. The bladder is bisected, opened like a clam, and 25cm of ileum is sewn in. |
| Agents for detrusor overactivity | Notes |
|---|---|
Topical oestrogens | Post-menopausal urgency, frequency + nocturia may occasionally be improved by raising the bladder’s sensory threshold. |
β3 adrenergic agonist: mirabegron 50mg/24h; se tachycardia; ci: severe htn; Caution if renal/hepatic impairment. | Consider if antimuscurinics are contraindicated or clinically ineffective, or if se unacceptable. |
Intravesical botulinum toxin (Botox®) | Consider if above medications ineffective. |
Percutaneous posterior tibial nerve stimulation (ptns). (A typical treatment consists of x12 weekly 30 min sessions.) | Consider if drug treatment ineffective and Botox® not wanted. ptns delivers neuromodulation to the s2–s4 junction of the sacral nerve plexus. |
Sacral nerve stimulation inhibits the reflex behaviour of involuntary detrusor contractions. | |
Modulation of afferent input from bladder | |
Hypnosis, psychotherapy, bladder training1 | (These all require good motivation.) |
Surgery (eg clam ileocystoplasty) | Reserved for troublesome or intractable symptoms. The bladder is bisected, opened like a clam, and 25cm of ileum is sewn in. |
nb: desmopressin nasal spray 20µg as a night-time dose has a role in ↓urine production and ∴ nocturia in overactive bladder, but is unsuitable if elderly (se: fluid retention, heart failure, Na+↓).
is a condition in which the bladder neck does not open properly during voiding. Studies in men and women with voiding dysfunction show that it is common. The cause may be muscular or neurological dysfunction or fibrosis.
Video-urodynamics, with simultaneous pressure-flow measurement, and visualization of the bladder neck during voiding.
This may follow trauma or infection (eg gonorrhoea)—and frequently leads to voiding symptoms, uti, or retention. Malignancy is a rare cause.
Retrograde urethrogram or antegrade cystourethrogram if the patient has an existing suprapubic catheter.
incorporate themselves into the wall of the urethra and keep the lumen open. They work best for short strictures in the bulbar urethra (anterior urethral anatomy, from proximal to distal: prostatic urethra→posterior or membranous urethra→bulbar urethra→penile or pendulous urethra→fossa navicularis→meatus).
Lumps in the groin and scrotum
Testicular lump = cancer until proved otherwise.
Acute, tender enlargement of testis = torsion (p654) until proved otherwise.
Diagnosing scrotal masses
(fig 2):
Can you get above it?
Is it separate from the testis?
Cystic or solid?
Diagnosis of scrotal masses. (*=transilluminates: position of pen torch shown in image)
Cannot get above ≈ inguinoscrotal hernia (p616) or hydrocele extending proximally
Separate and cystic ≈ epididymal cyst
Separate and solid ≈ epididymitis/varicocele
Testicular and cystic ≈ hydrocele
uss testis. Heterogeneity suggests tumour (ΔΔ: chronic inflammation).
Epididymal cysts
usually develop in adulthood and contain clear or milky (spermatocele) fluid. They lie above and behind the testis. Remove if symptomatic.
Hydroceles
(fluid within the tunica vaginalis). Primary (associated with a patent processus vaginalis, which typically resolves during the 1st year of life) or secondary to testis tumour/trauma/infection. Primary hydroceles are more common, larger, and usually in younger men. Can resolve spontaneously. ℞: aspiration (may need repeating) or surgery: plicating the tunica vaginalis (Lord’s repair)/inverting the sac (Jaboulay’s repair) Is the testis normal after aspiration? If any doubt, do uss.
Epididymoorchitis
Causes:
Chlamydia (eg if <35yrs); E. coli; mumps; N. gonorrhoea; tb.
Features:
℞:
Varicocele
Dilated veins of pampiniform plexus. Left side more commonly affected. Often visible as distended scrotal blood vessels that feel like ‘a bag of worms’. Patient may complain of dull ache. Associated with subfertility, but repair (via surgery or embolization) seems to have little effect on subsequent pregnancy rates.
Haematocele
Blood in tunica vaginalis, follows trauma, may need drainage/excision.
Testicular tumours
Signs:
Typically painless testis lump, found after trauma/infection ± haemospermia, secondary hydrocele, pain, dyspnoea (lung mets), abdominal mass (enlarged nodes), or effects of secreted hormones. 25% of seminomas & 50% of nsgcts present with metastases.
Risk factors:
Undescended testis; infant hernia; infertility.
Staging:
No evidence of metastasis.
Infradiaphragmatic node involvement (spread via the para-aortic nodes not inguinal nodes).
Supra-diaphragmatic node involvement.
Lung involvement (haematogenous).
Tests:
℞:
Radical orchidectomy (inguinal incision; occlude the spermatic cord before mobilization to ↓risk of intra-operative spread). Options are constantly updated (surgery, radiotherapy, chemotherapy). Seminomas are exquisitely radiosensitive. Stage 1 seminomas: orchidectomy + radiotherapy cures ∼95%. Do close follow-up to detect relapse. Cure of nsgct, even if metastases are present, is achieved by 3 cycles of bleomycin + etoposide + cisplatin. Prevention of late presentation: self-examination (see p655). 5yr survival >90% in all groups.
(see also p617)
Psoas abscess—may present with back pain, limp and swinging pyrexia
Neuroma of the femoral nerve
Femoral artery aneurysm
Saphena varix—like a hernia, it has a cough impulse
Lymph node
Femoral hernia
Inguinal hernia
Hydrocele or varicocele
Also consider an undescended testis (cryptorchidism)
Torsion of the testis
If in any doubt, surgery is required. If suspected refer immediately to urology.
Symptoms:
Sudden onset of pain in one testis, which makes walking uncomfortable. Pain in the abdomen, nausea, and vomiting are common.
Signs:
ΔΔ:
The main one is epididymo-orchitis (p652) but with this the patient tends to be older, there may be symptoms of urinary infection, and more gradual onset of pain. Also consider tumour, trauma, and an acute hydrocele. nb: torsion of testicular or epididymal appendage (the hydatid of Morgagni—a remnant of the Müllerian duct)—usually occurs between 7–12yrs, and causes less pain. Its tiny blue nodule may be discernible under the scrotum. It is thought to be due to the surge in gonadotrophins which signal the onset of puberty. Idiopathic scrotal oedema is a benign condition usually between ages 2 and 10yrs, and is differentiated from torsion by the absence of pain and tenderness.
Tests:
Doppler uss may demonstrate lack of blood flow to testis, as may isotope scanning. Only perform if diagnosis equivocal—do not delay surgical exploration.
Treatment:
Ask consent for possible orchidectomy + bilateral fixation (orchidopexy)—see p570. At surgery expose and untwist the testis. If its colour looks good, return it to the scrotum and fix both testes to the scrotum.
Undescended testes
Incidence
About 3% of boys are born with at least one undescended testis (30% of premature boys) but this drops to 1% after the first year of life. Unilateral is four times more common than bilateral. (If bilateral then should have genetic testing.)
Cryptorchidism: complete absence of the testicle from the scrotum (anorchism is absence of both testes).
Retractile testis: the genitalia are normally developed but there is an excessive cremasteric reflex. The testicle is often found at the external inguinal ring. ℞: Reassurance (examining whilst in a warm bath, for example, may help to distinguish from maldescended/ectopic testes).
Maldescended testis: may be found anywhere along the normal path of descent from abdomen to groin.
Ectopic testis: most commonly found in the superior inguinal pouch (anterior to the external oblique aponeurosis) but may also be abdominal, perineal, penile and in the femoral triangle.
Complications of maldescended and ectopic testis
Treatment of maldescended and ectopic testis
restores (potential for) spermatogenesis; the increased risk of malignancy remains but becomes easier to diagnose.
Surgery:
Orchidopexy, usually dartos pouch procedure, is performed in infancy: testicle and cord are mobilized following a groin incision, any processus vaginalis or hernial sac is removed and the testicle is brought through a hole made in the dartos muscle into the resultant subcutaneous pouch where the muscle prevents retraction.
Hormonal:
Hormonal therapy, most commonly human chorionic gonadotrophin (hcg), is sometimes attempted if an undescended testis is in the inguinal canal.
Regularly; at least once a month. Ideally in the shower/bath when the muscle in the scrotum is relaxed.
Gently feel each testicle individually. You should feel a soft tube at the top and back of the testicle. This is the epididymis which carries and stores sperm. It may feel slightly tender. Don’t confuse it with an abnormal lump. You should be able to feel the firm, smooth tube of the spermatic cord which runs up from the epididymis.
Feel the testicle itself. It should be smooth with no lumps or swellings. It is unusual to develop cancer in both testicles at the same time, so if you are wondering whether a testicle is feeling normal or not you can compare it with the other.
Remember—if you do notice a change in size/weight or find any abnormal lumps or swellings in your testicle, make an appointment and have it checked by your doctor as soon as possible.
Note—most abnormalities are not cancer but collections of fluid, infection, or cysts. Cancer usually starts as a small hard painless lump. Even if it is cancer, treatment is often effective. In more than 9 in 10 cases, treatment can result in a complete cure. However, the earlier it is detected the easier it is to treat. More than a third of people with this cancer consult their doctor after the cancer has spread, which makes treatment more difficult. Often this is because of unfounded fears, or just hoping it will go away.
Adapted from www.cancerhelp.org.uk.
Aneurysms of arteries
An artery with a dilatation >50% of its original diameter has an aneurysm; remember this is an ongoing process. True aneurysms are abnormal dilatations that involve all layers of the arterial wall. False aneurysms (pseudoaneurysms) involve a collection of blood in the outer layer only (adventitia) which communicates with the lumen (eg after trauma). Aneurysms may be fusiform (eg most aaas) or sac-like (eg Berry aneurysms; fig 2 p483).
Common sites
Aorta (infrarenal most common), iliac, femoral and popliteal arteries.
Complications
Rupture; thrombosis; embolism; fistulae; pressure on other structures.
Screening
Ruptured abdominal aortic aneurysm (aaa)
Death rates/year from ruptured aaas rise with age: 125 per million in those aged 55–59; 2728 per million if over 85yrs.
Symptoms & signs:
Intermittent or continuous abdominal pain (radiates to back, iliac fossae, or groins—don’t dismiss this as renal colic), collapse, an expansile abdominal mass (it expands and contracts: swellings that are pulsatile just transmit the pulse, eg nodes overlying arteries), and shock. If in doubt, assume a ruptured aneurysm.
Unruptured aaa
Definition:
>3cm across.
Prevalence:
Symptoms:
Often none, they may cause abdominal/back pain, often discovered incidentally on abdominal examination (see box).
Monitoring:
bp↑
Smoker
Female
Strong family history. Modify risk factors if possible at diagnosis.
Elective surgery:
Stenting (evar):
Atheroma
Trauma
Infection, eg mycotic aneurysm in endocarditis, tertiary syphilis (esp. thoracic aneurysms)
Connective tissue disorders (eg Marfan’s, Ehlers–Danlos)
Inflammatory, eg Takayasu’s aortitis (p726)
Thoracic aortic dissection
Blood splits the aortic media with sudden tearing chest pain (± radiation to back). As the dissection extends, branches of the aorta occlude sequentially leading to hemiplegia (carotid artery), unequal arm pulses and bp or acute limb ischaemia, para-plegia (anterior spinal artery), and anuria (renal arteries). Aortic valve incompetence, inferior mi and cardiac arrest may develop if dissection moves proximally. Type A (70%) dissections involve the ascending aorta, irrespective of site of the tear, whilst if the ascending aorta is not involved it is called type B (30%) All patients with type A thoracic dissection should be considered for surgery: get urgent cardiothoracic advice. Definitive treatment for type B is less clear and may be managed medically, with surgery reserved for distal dissections that are leaking, ruptured, or compromising vital organs.
Management:
Crossmatch 10u blood;
ecg & cxr (expanded mediastinum is rare).
Summon a vascular surgeon and an experienced anaesthetist; warn theatre.
Do an ecg, and take blood for amylase, Hb, crossmatch (10–40u may eventually be needed). Catheterize the bladder.
Gain iv access with 2 large-bore cannulae. Treat shock with ORh−ve blood (if desperate), but keep systolic bp ≤100mmHg to avoid rupturing a contained leak (nb: raised bp is common early on).
Take the patient straight to theatre. Don’t waste time on x-rays: fatal delay may result, though ct can help in a stable patient with an uncertain diagnosis.
Give prophylactic antibiotics, eg cefuroxime 1.5g + metronidazole 500mg iv.
Surgery involves clamping the aorta above the leak, and inserting a Dacron® graft (eg ‘tube graft’ or, if significant iliac aneurysm also, a ‘trouser graft’ with each ‘leg’ attached to an iliac artery).
The bomb inside you?!
A wise doctor might reframe a patient’s fear of an unexploded bomb inside them to deepen their view of his or her own health: health is not simply a question of being of sound body and mind, but entails a process of adaptation to changing environments, to growing up, to ageing, and to healing when damaged (ohcs, p470).
Peripheral arterial disease 290
Acute ischaemia—see box
Peripheral arterial disease (pad) occurs due to atherosclerosis causing stenosis of arteries via a multifactorial process involving modifiable and non-modifiable risk factors. 65% have co-existing clinically relevant cerebral or coronary artery disease. Cardiovascular risk factors should be identified and treated aggressively. The chief feature of pad is intermittent claudication (= to limp). Prevalence = 10%.
Symptoms
Fontaine classification for peripheral arterial disease:
Asymptomatic
Intermittent claudication
Ischaemic rest pain
Ulceration/gangrene (critical ischaemia).
Signs
Absent femoral, popliteal or foot pulses; cold, white leg(s); atrophic skin; punched out ulcers (often painful); postural/dependent colour change; a vascular (Buerger’s) angle1 of <20° and capillary filling time >15s are found in severe ischaemia.
Tests
Exclude dm, arteritis (esr/crp). fbc (anaemia, polycythaemia); u&e (renal disease); lipids (dyslipidaemia); ecg (cardiac ischaemia). Also do thrombophilia screen and serum homocysteine if <50 years.
Ankle–brachial pressure index (abpi):
Normal = 1–1.2; Peripheral arterial disease = 0.5–0.9; Critical limb ischaemia <0.5 or ankle systolic pressure <50mmHg. Beware falsely high results from incompressible calcified vessels in severe atherosclerosis, eg dm.
Imaging
Colour duplex uss is 1st line (non-invasive and readily available). If considering intervention mr/ct angiography (fig 2) is used to assess extent and location of stenoses and quality of distal vessels (‘run-off’). It has largely replaced digital subtraction angiography.
(right) ct angiogram showing (a) normal lower limb vasculature and (b) heavily diseased arteries with previous left femoral anterior tibial bypass.
℞
Management of claudication:
Supervised exercise programmes reduce symptoms by improving collateral blood flow (2h per week for 3 months). Encourage patients to excercise to the point of maximal pain.
Vasoactive drugs, eg naftidrofuryl oxalate, offer modest benefit and are recommended only in those who do not wish to undergo revascularization and if exercise fails to improve symptoms.
If conservative measures have failed and pad is severely affecting a patient’s lifestyle or becoming limb threatening, intervention is required.
Percutaneous transluminal angioplasty (pta) is used for disease limited to a single arterial segment (a balloon is inflated in the narrowed segment). 5-year patency is 79% (iliac) and 55% (femoral). Stents can be used to maintain artery patency.
Amputation
Future therapies:
(left) Leg arteries.
Surgical emergency requiring revascularization within 4–6h to save the limb. May be due to thrombosis in situ (∼40%), emboli (38%), graft/angioplasty occlusion (15%), or trauma. Thrombosis more likely in known ‘vasculopaths’; emboli are sudden, eg in those without previous vessel disease; they can affect multiple sites, and there may be a bruit. Mortality: 22%. Amputation rate: 16%.
Symptoms and signs: The 6 ‘p’s of acute ischaemia: pale, pulseless, painful, paralysed, paraesthetic, and ‘perishingly cold’. Onset of fixed mottling implies irreversibility. Emboli commonly arise from the heart (af; mural thrombus) or aneurysms. In patients with known pad, sudden deterioration of symptoms with deep duskiness of the limb may indicate acute arterial occlusion. This appearance is due to extensive pre–existing collaterals and must not be misdiagnosed as gout/cellulitis.
This is an emergency and may require urgent open surgery or angioplasty. If diagnosis is in doubt, do urgent arteriography. If the occlusion is embolic, the options are surgical embolectomy (Fogarty catheter) or local thrombolysis, eg tissue plasminogen activator (t-pa, p339), balancing the risks of surgery with the haemorrhagic complications of thrombolysis. Anticoagulate with heparin after either procedure and look for the source of emboli. Be aware of possible post-op reperfusion injury and subsequent compartment syndrome.
2–3% risk of stroke and death within 30 days; hypoglossal nerve injury. nb: there is no benefit in treating completely occluded vessels.
Varicose veins (vvs)
(OHClinSurg p594)
vvs are long, tortuous & dilated veins of the superficial venous system.
Pathology
Symptoms
“My legs are ugly”. Pain, cramps, tingling, heaviness, and restless legs. But studies show these symptoms are only slightly commoner in those with vvs.
Signs
Oedema; eczema; ulcers; haemosiderin; haemorrhage; phlebitis; atrophie blanche (white scarring at the site of a previous, healed ulcer); lipodermatosclerosis (skin hardness from subcutaneous fibrosis caused by chronic inflammation and fat necrosis). On their own varicose veins don’t cause dvts (except possibly proximally spreading thrombophlebitis of the long saphenous vein).
Examination
See box.
Treatment
nice guidelines suggest that the criteria for specialist referral of patients with vvs should be: bleeding, pain, ulceration, superficial thrombophlebitis, or ‘a severe impact on quality of life’ (ie not for cosmetic reasons alone). In the uk funding for nhs treatment is usually via special funding panels.
Treat any underlying cause.
Education: Avoid prolonged standing and elevate leg(s) whenever possible; support stockings (compliance is a problem); lose weight; regular walks (calf muscle action aids venous return).
Endovascular treatment: (less pain and earlier return to activity than surgery.)
Before surgery and after venous mapping, ensure that all varicosities are indelibly marked to either side (to avoid tattooing if the incision is made through inked skin).
Saphena varix
Dilatation in the saphenous vein at its confluence with the femoral vein (the sfj). It transmits a cough impulse and may be mistaken for an inguinal or femoral hernia, but on closer inspection it may have a bluish tinge.
Unknown
Congenital valve absence (very rare)
Obstruction: dvt, fetus, ovarian tumour
Valve destruction: dvt
Arteriovenous mal-formation (↑pressure)
Constipation
Overactive muscle pumps (eg cyclists)
(Start with the patient standing.)
Inspect for: ulcers usually above the medial malleolus (varicose ulcers, ohcs p410) with deposition of haemosiderin causing brown edges, eczema, and thin skin. Inspect the legs from anterior thigh to medial calf (long saphenous vein) and the back of the calf (short saphenous vein). Palpate veins for tenderness (phlebitis) and hardness (thrombosis). If ulceration is present palpate pulses to rule out arterial disease.
Feel for cough impulse at the saphenofemoral junction (sfj) (≈incompetence). Percussion test: Tap vvs distally and palpate for transmitted impulse at the sfj (interrupted by competent valves).
Auscultate over varicosities for a bruit, indicating arteriovenous malformation.
For completion, examine the abdomen, the pelvis in females and external genitalia in males (for masses).
Doppler ultrasound probes listen for flow in incompetent valves, eg the sfj, or the short saphenous vein behind the knee (the calf is squeezed: flow on release lasting over ½–1 second indicates significant reflux). If incompetence is not identified and treated, varicosities will return.
Special tests: Trendelenburg’s test assesses if the sfj valve is competent. Doppler uss has largely consigned this and other examination methods (eg Tourniquet and Perthes’ test) to the history books.
The superficial veins of the leg.
When do varicose veins become an illness?We adopt the sickness role when we want sympathy. Somatization is hard to manage: here is one approach to consider:Give time; don’t dismiss these patients as ‘just the “worried well” ‘.
Explore factors perpetuating illness behaviour (misinformation, social stressors).
Agree a plan that makes sense to the patient’s holistic view of themself.
Treat any underlying depression (drugs and cognitive therapy, ohcs p374).
Gangrene and necrotizing fasciitis
Definitions
Necrotizing fasciitis is a rapidly progressive infection of the deep fascia causing necrosis of subcutaneous tissue. Prompt recognition (difficult in the early stages) and aggressive treatment is required. In any atypical cellulitis, get early surgical help. There is intense pain over affected skin and underlying muscle. Group a β-haemolytic streptococci is a major cause, although infection is often polymicrobial. Fournier’s gangrene is necrotizing fasciitis localized to the scrotum and perineum. ℞ Radical debridement ± amputation; iv antibiotics, eg benzylpenicillin and clindamycin.
Skin ulcers
ohcs, p604
Ulcers are abnormal breaks in an epithelial surface. Leg ulcers affect ∼2% in developed countries.
Causes
History
Ask about number, pain, trauma. Go over comorbidities—eg varicose veins, peripheral arterial disease, diabetes, vasculitis. Is the history long or short? Is the patient taking steroids? Is the patient a bit odd? (remember self-induced ulcers: dermatitis artefacta). Has a biopsy been taken?
Examination
Note features such as site, number, surface area, depth, edge, base, discharge, lymphadenopathy, sensation, and healing. If in the legs, note features of venous insufficiency or arterial disease and, if possible, apply a bp cuff to perform ankle–brachial pressure index (abpi). See box.
Tests
Skin and ulcer biopsy may be necessary—eg to assess for vasculitis (will need immunohistopathology) or malignant change in an established ulcer (Marjolin’s ulcer = scc presenting in chronic wound). If ulceration is the first sign of a suspected systemic disorder then further screening tests will be required.
Management
Managing ulcers is often difficult and expensive. Treat the cause(s) and focus on prevention. Optimize nutrition. Are there adverse risk factors (drug addiction, or risk factors for arteriopathy, eg smoking)? Get expert nursing care. Consider referral to specialist community nurse or leg ulcer/tissue viability clinic:
Surgery, larval therapy and hydrogels are used to debride sloughy necrotic tissue (avoid hydrogels in diabetic ulcers due to ↑ risk of wet gangrene).
Venous
Arterial
Large vessel
Small vessel
Neuropathic
Diabetic
Neuropathic, arterial or both
Lymphoedema
Vasculitic
Malignant (p598)
Infective
tb, syphilis
Traumatic (pressure)
Pyoderma gangrenosum
Drug induced
Above the medial malleolus (‘gaiter’ area) is the favourite place for venous ulcers (mostly related to superficial venous disease, but may reflect venous hypertension via damage to the valves of the deep venous system, eg 2° to dvt). Venous hypertension leads to the development of superficial varicosities and skin changes (lipodermatosclerosis = induration, pigmentation, and inflammation of the skin). Minimal trauma to the leg leads to ulceration which often takes many months to heal. Ulcers on the sacrum, greater trochanter, or heel suggest pressure sores (ohcs p605), particularly if the patient is bed-bound with suboptimal nutrition.
The ulcer and surrounding tissues are cold in an ischaemic ulcer. If the skin is warm and well perfused then local factors are more likely.
Draw a map of the area to quantify and time any healing (a wound >4 weeks old is a chronic ulcer as distinguished from an acute wound).
Shelved/sloping ≈ healing; punched-out ≈ syphilis or ischaemic; rolled/everted ≈ malignant; undermined ≈ tb.
Any muscle, bone, or tendon destruction (malignancy; pressure sores; ischaemia)? There may be a grey-yellow slough, beneath which is a pale pink base. Slough is a mixture of fibrin, cell breakdown products, serous exudate, leucocytes and bacteria—it need not imply infection, and can be part of the normal wound healing process. Granulation tissue is a deep pink gel-like matrix contained within a fibrous collagen network and is evidence of a healing wound.
If not uncomfortable for the patient (eg in neuropathic ulceration) a probe can be used to gauge how deep the ulceration extends.
Culture before starting any antibiotics (which usually don’t work). A watery discharge is said to favour tb; bleeding can ≈ malignancy.
suggests infection or malignancy.
Decreased sensation around the ulcer implies neuropathy.
Healing is heralded by granulation, scar formation, and epithelialization. Inflamed margins ≈ extension.
Risk of mortality from elective surgery is currently about 1 : 100,000 to 1 : 150,000.
In agreeing to a blood test, the patient understands that it may be an uncomfortable experience, but he also knows that the results of the test may help you in making a diagnosis and hopefully restore him to full health. But grey areas exist everywhere: when he extends his arm towards you, does he know that you could accidentally injure an artery or nerve, with all the complications that follow—does he need to know…?
Futher reading: Consent: patients and doctors making decisions together. General Medical Council (2008).
Reference guide to consent for examination or treatment. Department of Health (2009).
Give 1mg/kg every 5min iv—up to 10mg/kg in total (ohcs p628).
Not to be confused with hyoscine hydrobromide; used for drying secretions and in motion sickness.
For an in-depth guide to nutrition see Manual of Dietetic Practice, 4e, Briony Thomas, Blackwell.
Enteral feeding promotes integrity of the gut mucosal barrier, thus preventing bacterial and endotoxin translocation across the gut wall, which can lead to multiple organ dysfunction syndrome (mods) and perpetuation of a systemic inflammatory response—even when the gut is not the primary source of pathology.
Other palm rashes: Stevens–Johnson syn.; hand, foot & mouth dis.; palmar erythema; palmoplantar pustulosis.
us is more accurate at detecting invasive breast cancer, though mammography remains most accurate at detecting ductal carcinoma in situ (dcis). mri is used in the assessment of multi-focal/bilateral disease and patients with cosmetic implants who are identified as high risk.
Nodal status is scored 1–3: 1 = node −ve; 2 = 1–3 nodes +ve; 3 = >3 nodes +ve for breast cancer. Histological grade is also scored 1–3.
Give antibiotics if peritonitic, eg cefuroxime 1.5g/8h iv + metronidazole 500mg/8h iv/pr.
The omphalos is the centre-stone at the Temple of Apollo in Delphi, centre of the ancient world—hence its umbilical association. Here Apollo persuaded Pan (the god of wild places, music, and syrinxes, p520) to reveal the art of prophesy, without which we would be without our most mysterious tool: prognosis.
For a useful exposition on imaging in pancreatitis see www.emedicine.com/radio/topic521.htm.
Medullary sponge kidney is a typically asymptomatic developmental anomaly of the kidney mostly seen in adult females, where there is dilatation of the collecting ducts, which if severe leads to a sponge-like appearance of the renal medulla. Complications/associations: utis, nephrolithiasis, haematuria and hypercalciuria, hyperparathyroidism (if present, look for genetic markers of men type 2a, see p215).
αfp is not ↑ in pure seminoma; may also be ↑ in: hepatitis, cirrhosis, liver cancer, open neural tube defect.
Leg goes pale when raised, eg by 20° off the couch; compare sides.
’The first sign of his approaching end was when one of my old aunts, while undressing him, removed a toe with one of his old socks’. Graham Greene, A Sort of Life, 1971, Simon & Schuster.
