Introduction

Ruptured abdominal aortic aneurysm (AAA) kills 5000 people each year and is the 15th leading cause of death in the UK. With an incidence of 25–30/100 000 it is implicated in the death of 1.2% of men and 0.6% of women aged over 65 years. In the UK it is the indication for 7500 emergency operations per annum. Despite improved detection and perioperative care it remains a highly lethal pathology.

Definition

The presence of blood outside the lumen of an aneurysm affecting the abdominal aorta. It is usually associated with back, abdominal, flank or groin pain, in association with haemodynamic instability. The presence of one or both of these in a patient with an aortic aneurysm is an indication for immediate action.

Classification

Many classifications for aneurysms exist. The most frequently encountered are fusiform in shape and atherosclerotic in origin. Anatomically most are infrarenal (90%), juxta/supra-renal (9%), and thoracoabdominal (1%). Other aetiologies include inflammatory, mycotic, and false or anastomotic. The simplest method of classifying rupture is retroperitoneal (80%cases) which is usually to the left side and results in tamponade of the haematoma, or free (in traperitoneal – 20%) which is in the peritoneal cavity or nearby venous structures and usually results in sudden death or very poor outcome.

Management algorithm

Standard resuscitation guidelines should be followed, but with judicious use of colloids (or crystalloids) in maintaining an adequate (but not so high as to cause further bleeding) blood pressure.

Any cause for an acute abdomen can occur coincident with pregnancy, while others are specific to pregnancy.

History

1. ▪ Time of onset, duration, intensity and character of abdominal pain during pregnancy and associated symptoms need to be established.

2. ▪ Evaluation of gestational age is essential as aetiologies change with gestational age, and fetal viability also depends on this.

Examination

1. ▪ Peritoneal signs are often absent in pregnancy due to lifting and stretching of the anterior abdominal wall. Underlying inflammation has no direct contact with the parietal peritoneum, which precludes any expected muscular response such as guarding.

2. ▪ The uterus can obstruct and inhibit movement of the omentum to an area of inflammation, distorting the clinical picture.

3. ▪ Examination of patient in the right or left decubitus position may help distinguish extra-uterine tenderness from uterine tenderness.

4. ▪ Due to the gravid abdomen, the location of intra-abdominal contents will vary at different gestations.

Investigations

1. ▪ Blood tests are dependent on the suspected pathology. Some laboratory tests have altered reference ranges in pregnancy. For example, pregnancy can produce white blood cell counts of 6000–16000/mm3 in the second and third trimesters and 20000–30000/mm3 in early labour.

2. ▪ Ultrasound is the most frequently used non-invasive investigation for evaluating the pregnant abdomen.

Differential diagnoses related to pregnancy

Early pregnancy complications such as ectopic pregnancy or miscarriage. Consider rare possibility of a heterotopic pregnancy (1:7000–1:30000).

Always begin the examination by introducing yourself and ask the patient if they have any pain in the part of the body that you are about to examine. This avoids unnecessary patient discomfort.

Examination of the ischaemic arm

Exposure and positioning: expose and position the patient's arms and chest. Patient may be sitting or lying down.

INSPECTION

General inspection for:

1. ▪ Signs of cardiovascular disease

2. ▪ Respiratory rate (dyspnoea)

3. ▪ Scars from previous cardiovascular surgery

4. ▪ Pallor.

Inspect hands for:

1. ▪ Nicotine-stained nails

2. ▪ Clubbing

3. ▪ Vasculitic lesions

4. ▪ Finger pulp wasting

5. ▪ Skin changes

6. ▪ Colour (pallor, cyanosis).

PALPATION

1. ▪ Feel the temperature of both arms with the back of your hands.

2. ▪ Measure nail-bed capillary refill (normally < 2 s).

3. ▪ Feel radial pulses for rate, character, and rhythm. Look for radioradial delay (coarctation of aorta) and a collapsing pulse (aortic regurgitation) by raising the patient's armabove the level of their shoulder. Apply mild traction on shoulder to see if radial pulse collapses (indicates a cervical rib).

4. ▪ Feel brachial pulse.

5. ▪ Feel for axillary pulse (if palpable may be abnormal).

6. ▪ Feel for subclavian pulse in supraclavicular fossa (if palpable may be abnormal). Also you may feel a cervical rib here.

7. ▪ Feel the carotid pulses.

AUSCULTATION

Listen for bruits over carotid and subclavian arteries.

COMPLETE THE EXAMINATION

By:

1. ▪ Measuring the blood pressure in both arms

2. ▪ Performing a full neurological examination

3. ▪ Performing a full cardiovascular examination.

Introduction

The term priapism is derived from Priapus, the Greek god of fertility. If left untreated it may lead to irreversible penile ischaemia, necrosis and scarring of the intracavernosal erectile tissue.

Definition and classification

Penile erection that persists beyond, or is unrelated to sexual activity. Typically specialists have tried to define a time beyond which an erection is no longer ‘physiological’ four hours has been accepted in many definitions. It is classified as ischaemic (low flow) or non-ischaemic (high flow).

History

The peak incidence is bi-modal, occurring between 5 to 10 and 20 to 50 years.

Ischaemic priapism: the patient complains of a painful erection (pain may not be present in the first few hours). Fifty per cent of cases are idiopathic. Pharmacological causes include Viagra (sildenafil), the use of intracavernosal therapy (e.g. alprostadil), antipsychotics (e.g. chlorpromazine), antihypertensives (e.g. prazosin), anticoagulants (e.g. intravenous heparin), some antidepressants (e.g. trazodone), and recreational drugs (e.g. cocaine). Haematological diseases such as sickle-cell disease (or trait) and leukaemia are the commonest causes in the young. Rarer aetiologies include cerebrovascular disease, lumbar disk disease, and infiltrating prostate and bladder cancer.

Non-ischaemic priapism is less common and generally not associated with severe pain. Presentation may be delayed by days or months. Typically it is related to trauma to the penis, perineum or pelvis resulting in injury to the cavernosal artery, leading to increased arteriolar inflow of oxygenated blood.

Examination

In ischaemic priapism the patient will have a rigid painful erection, unlike a non-ischaemic priapism in which the penis is typically semierect and non painful. Perineal bruising may be indicative of trauma.

Skin grafts

Definition

These are living or preserved tissue transfers from a donor to a recipient site without their blood supply. The first record of a successful skin graft in humans was credited to Sir Astley Cooper (1817) even though the technique of free skin grafting may have originated some 3000 years ago in India.

CLASSIFICATION

Can be divided into autografts (same person), isografts (genetically identical e.g. twins), allografts (same species) or xenografts (different species). Can be further classified into split-thickness (SSG) (epidermis with partial-thickness dermis), full-thickness (FTSG) (epidermis with entire dermis) and composite (composed of two or more tissues e.g. skin and fat). They are indicated in cases where there is lack of adjacent tissue for coverage and are the third option on the reconstructive ladder (see Figure 156). Choice of donor site is influenced by scar visibility and skin colour match.

GRAFT HEALING

Known as graft ‘take’ this has five phases: adherence [fibrin mediated] (immediately), serum imbibition [graft nourished from serum nutrients] (1–2 days), inosculation [capillary re-anastomosis] (after 2 days), revascularization (3–7 days) and remodelling (weeks–months). Graft failure may arise because of: inadequate recipient site vascularization (avoid irradiated skin, exposed bone, cartilage or over-necrotic tissue), infection (especially β-haemolytic streptococci), fluid collection between the graft and the recipient surface (e.g. due to a haematoma or a seroma), shearing forces, co–morbidity (e.g. smoking, diabetes, vascular disease) and poor surgical technique (e.g. graft placed upside down). Other complications of skin grafting include skin colour mismatch and secondary contracture (especially with SSG).

Introduction: infective colitis is an inflammatory condition of the large bowel caused by the presence of pathogenic organisms, and may be primary or secondary.

Incidence: the incidence varies widely depending on the causative organism. The most common type, pseudomembranous colitis, occurs in up to 1%of hospitalized patients, and is almost exclusively associated with antibiotic use.

Causative organisms

A number of different organisms have been implicated, and these include:

1. ▪ Clostridium difficile. This organism is responsible for pseudomembranous colitis. It is associated with the use of antibiotics, particularly the macrolides. Clinically a patient who may have been steadily improving suddenly deteriorates, with tachycardia and signs of hypovolaemia. There is profuse diarrhoea which is characteristically green in colour. Blood tests show a rising white count and inflammatory markers. If dehydration is severe then renal function may become compromised. The inflammatory process causes a fibrinous pseudomembrane to develop over the colonic mucosa. Treatment is with oral metronidazole or vancomycin. Parenteral antibiotics are not effective. If treatment is delayed toxic megacolon and/or perforation may occur. Mortality is reported to be as high as 30%.

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Introduction

In 1862 Maurice Raynaud described an episodic digital ischaemia due to vasospasm of the small arteries and arterioles of the extremities, precipitated by cold or emotion. It consists of intense pallor (vasoconstriction), cyanosis (spasm relaxation with a trickle of blood flow causing rapid desaturation) and rubor (increased blood flow into dilated capillaries), with full recovery in 15–45 minutes. The fingers remain normal in between the episodes.

The term ‘Raynaud's phenomenon’ is used when the cause is unknown, and if underlying cause is identifiable, it is known as Raynaud's disease. However, the syndrome is better classified into spastic and obstructive type depending on the causative factor.

Incidence

The prevalence varies with climate and probably ethnic origin. In cooler countries (UK, Scandinavian) the prevalence varies from 20 to 25%. It affects all age groups but mainly young women. Around 40–80% of Raynaud's patients have associated disease, scleroderma being the most common.

Pathogenesis

Two types: obstructive and spastic.

Obstructive arterial disease causes a decrease in resting digital arterial pressure and, in these patients, even normal vasoconstrictive response to cold or emotion is sufficient to cause symptoms. Spastic type has normal resting digital pressure and symptoms are caused due to an increased intensity of cold-induced arterial spasm. Both α2 adrenoceptors and presynaptic βreceptors are implicated in its causation.

Raynaud's disease can be associated with autoimmune diseases (SLE, RA, Sjögren's syndrome, mixed connective-tissue disorders, scleroderma), haematological diseases (mixed cryoglobulinaemia, monoclonal gammopathies, leukaemia, cold agglutinins, thrombocytosis), trauma, vibrating tools, arteriosclerosis, frostbite, Buerger's disease, hypothyroidism, thoracic outlet obstruction, and drugs.

Speech

1. ▪ Assess the three components of speech production (phonation, articulation and language production).

2. ▪ You will already have heard the patient speak during the historytaking section. Are there any problems with phonation? (Dysphonia – reduced speech volume; aphonia – inability to produce sound.)

3. ▪ Now assess articulation by asking the patient to repeat the following phrases – ‘baby hippopotamus’, ‘West Register Street’ and ‘British Constitution’. Is there any dysarthria?

4. ▪ Assess language production centres by (1) Listening to the patient's spontaneous speech, (2) Assessing comprehension by observing responses to simple commands (for example ‘close your eyes’), (3) Assessing the patient's ability to identify and name simple objects, for example a pen or watch, and (4) Assessing the ability of the patient to repeat sentences (for example ‘no ifs, ands, or buts’). Note whether there is an expressive dysphasia, or a receptive dysphasia.

Mental state and higher cerebral functions

1. Consciousness –is the patient alert, confused, obtunded, stuporous,or comatose. Assess the level of consciousness more objectively using the Glasgow coma scale.

2. ▪ Appearance and behaviour – assess the patient's general demeanour, physical appearance and responses to your questions during history taking. Also look for any obvious evidence of self-neglect, which can often be seen in advanced dementia.

3. ▪ Affect – note the patient's affect.

4. ▪ Cognitive function – assess by using the mini-mental state examination.

5. ▪ Dyspraxia and apraxia – ask the patient to performsimple upper and lower limb tasks, for example for the upper limb, write a sentence, or do up his/her shoelaces).

Follow a step-wise system: inspect, palpate, percuss and auscultate (in that order). To ensure that the abdominal examination is thorough and that nothing is overlooked, expose the patient from ‘nipples to knees’. In the clinical setting try tomaintain the patient's dignity. Get the patient to relax – remember if the patient is tense, it will be difficult to feel anything within the abdomen. Ask the patient to lie down on the bed with the arms by the sides. Once you have ensured that the patient is suitably relaxed commence the examination.

1. Inspection:

1. ▪ Look for any general abnormalities, such as cachexia, frank jaundice or pallor.

2. ▪ Look for any obvious abdominal swelling/distension (Fat, Faeces, Flatus, Fluid, Fetus).

3. ▪ Look for skin lesions (e.g. spider naevi (liver disease), pigmentation (Addison's), tortuous veins (IVC obstruction), caputmedusae (portal hypertension), striations (pregnancy/Cushing's).

4. ▪ Look for scars – do they correlate with the surgical history?

5. ▪ Check abdominal movements on breathing – does the patient appear to find this uncomfortable/painful? If so, this may be suggestive of peritonitis.

6. ▪ Check hands – clubbing, palmar erythema, leuconychia, Dupuytren's contracture, liver flap.

7. ▪ Check radial pulse – rate and rhythm.

8. ▪ Check face – dehydration, pallor of conjunctivae, jaundiced sclerae, telangiectasia, stomatitis.

9. ▪ Gross inspection for hernias – ask the patient to lift their head off the pillowor cough. Look for incisional/paraumbilical/inguinal hernia.

2. Palpation:

1. ▪ Begin by palpating the areas you might otherwise overlook. Feel for supraclavicular lymphadenopathy (Virchow's node).

2. ▪ Nowposition yourself at the same height as the patient's abdomen. Ask the patient if they currently have any abdominal pain.

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