Leg ulcer

Venous ulcers account for by far the majority (about 70%), with mixed arterial/venous (about 10%) and arterial (about 10%) most of the remainder. Pressure ulcers have become increasingly common because of the increase in elderly, frail, and relatively immobile patients. The other causes are relatively rare with the exception of neuropathic ulcers in patients with diabetes mellitus. Note that many leg ulcers may have a multifactorial aetiology, i.e. they may involve more than one of the pathologies listed in Figure 29.1. The first thing is to ask about the ulcer. You should consider: • Is the ulcer painful? ■ Venous ulcers are caused by venous stasis in the leg and are thus less painful when elevated and drained of blood. However, only about 30% of venous ulcers are painful. ■ Arterial (atherosclerotic) ulcers are caused by ischaemia to the leg and are thus more painful when elevated and drained of blood. Patients often say the ulcers are painful enough to wake them up at night and that they obtain relief by lowering their leg over the side of the bed. ■ Neuropathic ulcers are caused by loss of sensation (which predisposes to constant trauma) and are thus not painful. ■ Pressure ulcers are caused by, as the name suggests, prolonged pressure on the affected site. They tend to be exquisitely tender but not necessarily painful if no pressure is being applied. • How long has the ulcer been there? ■ Venous ulcers are less painful and can therefore present late. They often have a long and recurring history. ■ Arterial ulcers tend to present relatively early because of pain. They often occur secondary to trivial trauma. ■ Neuropathic ulcers are associated with a loss of sensation and thus often present late. ■ Pressure ulcers can develop surprisingly rapidly (e.g. days in immobile patients if they are not turned regularly during their admission, even hours in patients who suffer a long lie following a fall), but can have a more indolent course depending on how much pressure is put on for how long. Thus the time course is not especially helpful. ■ A long history should arouse suspicion of a Marjolin ulcer, which only occurs in long-standing ulcers.

Limb weakness

The definition of weakness is important, because many patients who self-describe a ‘weak limb’ will actually have a clumsy limb (ataxia), a numb limb (reduced sensation), or a limb that is too painful to move. The time course of the onset of the symptoms in general reflects the time course of the underlying pathology: • Sudden onset (seconds to minutes) usually implies either trauma (e.g. displaced vertebral fractures due to major trauma) or certain vascular insults (e.g. stroke, transient ischaemic attack (TIA)). • Subacute onset (hours to days) suggests a progressive demyelination (e.g. Guillain–Barre syndrome, multiple sclerosis) or a slowly expanding haematoma (e.g. subdural haematoma). • Chronic onset (weeks to months), is consistent with pathologies such as a slow-growing tumour or motor neuron disease (progressive degeneration of motor neurons). As only acute and subacute limb weakness will present acutely to generalists in hospital (chronic onset cases will most likely be referred to neurology from primary care), we have limited the chapter to these cases. Limb movement requires an intact pathway from the cerebral cortex, down the corona radiata, internal capsule, and pons, along the corticospinal tract of the spinal cord, out along a nerve root, and down a peripheral nerve to the neuromuscular junction and muscle itself. If a patient has limb weakness, there must be a lesion somewhere in this pathway. Figure 26.2 gives the differential diagnosis for limb weakness. Mr Walker has presented with rapid onset of left-sided arm weakness. Key clues in the history to elicit include: • Exact time of onset? This is critical in suspected strokes because the window of time in which to confirm the diagnosis and administer thrombolysis (if appropriate) is only 4.5 hours from onset of symptoms (after that, you risk doing more harm than good to the patient). If you suspect a stroke in a patient within that time frame, call the thrombolysis team immediately. In this case, all we can say is that the onset was at some point in the 7 hours between 11 p.m. (when he went to sleep) and 6 a.m. (when he woke up), so we cannot confidently say the onset was within 4.5 hours.

Poor urinary output

You should ask the nurse: • What the trend is in urine output—has it been gradually decreasing, or suddenly stopped? If the latter, have they checked if the urinary catheter is blocked by flushing it? This is a rapidly reversible cause of poor urinary output. • What the observations are for the patient. Ask for the heart rate, blood pressure, respiratory rate, oxygen saturations, and temperature, so you can get an idea of how unwell the patient is. This will help you prioritize how soon you need to see the patient. Healthy adults have a urine output of about 1 mL/kg/hour. Oliguria refers to a reduced urine output and is defined variously as <400 mL/day, <0.5 mL/kg/hour, or <30 mL/hour. Anuria refers to the complete absence of urine output. Decreased urine output should be taken very seriously as it may be the first (and only) sign of impending acute renal failure. Untreated, patients may die from hyperkalaemia, profound acidosis, or pulmonary oedema due to the kidneys not performing their usual physiological role. Normal urine output requires: • adequate blood supply to the kidneys • functioning kidneys, and • flow of urine from the kidneys, down the ureters, into the bladder, and out via the urethra. Pathology affecting any of these requirements can result in poor urine output, which is why the differential diagnosis for poor urinary output is often classified as shown in Figure 22.1. In practice, as a junior doctor you want to diagnose and treat the prerenal and postrenal causes. If you come to the conclusion that it is a renal cause (by exclusion), call the renal physicians for an expert opinion. This is crucial in determining the diagnosis: • Adequate intake? Remember that an adult of average size will require about 3 L of fluid intake per 24 hours (30–50 mL/kg/day). Febrile patients will require an extra 500 mL for every 1 °C above 37.0 °C to compensate for increased loss of fluids from evaporation and increased respiratory rate.

Diarrhoea

Strictly speaking, diarrhoea is an increase in the amount of stool passed daily to over 300 g of stool per day. This is usually accompanied by increased frequency and loosening of the stools. However, many patients will talk of ‘diarrhoea’ when they actually have melaena (dark, tarry stools from digested blood), steatorrhoea (pale, floating stools from undigested lipid), haematochezia (bright red stools from frank blood), or simply loose stools (soft faeces but no increase in frequency or quantity). Diarrhoea can be caused by: • Infection of the bowel (infectious diarrhoea) • Inflammation of the bowel (e.g. inflammatory bowel disease (IBD), diverticular disease) • Increased bowel motility (e.g. hyperthyroidism, anxiety, irritable bowel syndrome (IBS)) • Malabsorption of nutrients (e.g. coeliac disease, pancreatic insufficiency) • Obstruction overflow due to a mass allowing only liquid stool to pass beyond it (e.g. constipation—counterintuitively, hard faeces stuck in the bowel are a common cause of overflow diarrhoea in elderly people, colon cancer, ovarian cancer) • Medications (e.g. laxatives, colchicine, digoxin, metformin, thiazide diuretics, some antibiotics, etc.) For a young adult with acute diarrhoea, the most likely diagnoses are shown in Figure 20.1. Yes, it would. In elderly patients, neoplastic disease (villous polyps, colonic adenocarcinoma, pancreatic cancer), diverticular disease, overflow diarrhoea secondary to constipation, ischaemic colitis, microscopic colitis, and bacterial overgrowth (e.g. in patients with diabetes mellitus) are much more likely, whereas coeliac disease is less likely to present for the first time (as it tends to present in younger patients). Curiously, ulcerative colitis (UC) and Crohn’s disease are thought to have a bimodal distribution in incidence, with peaks at 15–25 and 50–80 years. • Airway, breathing, and circulation (ABC): always, always, always start the management of a patient with ABC. Although the ABCs will be obviously normal in a large number of patients presenting in a non-emergency setting, you should always keep this in mind when admitting patients to hospital. Note that hypotension is a late and worrying sign in young patients. • Dehydration: in a patient with a 3-day history of diarrhoea, one should be concerned about the possibility of dehydration (hypovolaemia).

Right iliac fossa pain

Note that certain diagnoses are going to be more likely in different patient groups. Children and elderly people are more likely to have a longer differential as symptoms are often less pronounced and non-specific. Intussusception is almost exclusively seen in children, and the vast majority of cases of mesenteric adenitis are also seen in children. By contrast, caecal pathology (tumours, volvulus, or a solitary mesenteric diverticulum) is usually associated with advancing age. An abdominal aortic aneurysm would be extraordinarily rare in a young adult but should be considered in anyone >50 years of age. You must of course consider gynaecological pathology, such as ectopic pregnancy, pelvic inflammatory disease/ salpingitis, torsion/haemorrhage/rupture of an ovarian tumour or cyst, mittelschmerz (mid-cycle pain corresponding to a ruptured ovarian follicle), threatened abortion, fibroid degeneration, or uterine dehiscence. In any woman of reproductive age you must perform a pregnancy test—this is not only to exclude particular diagnoses such as ectopic pregnancy, but is also essential to help weigh up the risk of radiation to the fetus against the diagnostic usefulness of the test. It is very useful to have an idea of the degree of abdominal tenderness before you even lay a hand on the patient. Remember that you will win no prizes (either in exams or with patients themselves) if you actually cause a patient pain. So, start by asking the patient to suck their tummy in as far as possible and then puff it out again (this is particularly useful in children). A patient with board-like abdominal rigidity secondary to generalized peritonism will only make very minor movements. Now ask the patient to cough: patients with inflammation of the parietal peritoneum will be reluctant to cough deeply and may well place their hands over the area of tenderness. Whether you palpate the abdomen in quadrants or nine zones, be sure to start in the opposite area to that which the patient states is most painful. Start by palpating gently and keep looking at the patient’s face for a reaction. Patients are likely to demonstrate guarding (involuntary muscular rigidity in tender areas of the abdomen).

Jaundice

The metabolism of bilirubin in humans is summarized in Figure 14.1 and can be divided into three sequential steps: 1 Production of unconjugated bilirubin. Red blood cells are broken down by macrophages (mainly in the spleen), which degrade haemoglobin into iron and unconjugated (water insoluble) bilirubin. The iron is stored inside transferrin proteins. Unconjugated bilirubin travels to the liver bound to albumin. In disease, unconjugated bilirubin can be produced by haemolysis of red cells intravascularly, rather than in the spleen. 2 Conjugation of bilirubin. Liver hepatocytes uptake unconjugated bilirubin and conjugate it to glucuronate, thus making water soluble, conjugated bilirubin. 3 Excretion of bilirubin. Once conjugated, bilirubin is secreted into the bile canaliculi. Conjugated bilirubin flows with bile down the bile ducts and into the duodenum. Inside the bowel, conjugated bilirubin is metabolized by bacteria into colourless products (urobilinogen, stercobilinogen). Some of these can be reabsorbed by the gut and excreted via the kidneys, but the vast majority are oxidized in the gut into coloured pigments (urobilin, stercobilin) which give faeces their brown colour. Consequently, if there is complete obstruction of the bile ducts there will be no flow of conjugated bilirubin into the gut, no conversion into urobilinogen, and therefore not even a trace of urobilinogen in the urine. The terminology is confusing because different people mean different things. If you are going to use this terminology, make sure that you and your colleagues agree on the definitions. Nonetheless, this is what people usually mean: • Prehepatic jaundice: this refers to jaundice caused by an excessive production of bilirubin. Remember that bilirubin is produced by the breakdown of haemoglobin in the blood vessels or the spleen, hence the term prehepatic. • Hepatic jaundice: for some people, this means any jaundice due to pathology in the liver (anatomically), such as points 3, 4, and 5 in Figure 14.1, and can thus include problems with hepatocytes (e.g. hepatitis) or with the bile canaliculi (e.g. primary sclerosing cholangitis, PSC).

Nausea and vomiting

The vomiting centre (mainly histamine and acetylcholine receptors) in the medulla oblongata can be activated by four main input systems shown in Figure 13.1: the vestibular system, the central nervous system, the chemoreceptor trigger zone (in the fourth ventricle of the brain), and cranial nerves IX and X. With these four inputs in mind, it becomes easier to understand some of the pathologies that can activate the vomiting centre and cause nausea and vomiting, as is shown in Figure 13.2. • Contents ■ Undigested: oesophageal disorders, e.g. achalasia, pharyngeal pouch ■ Partially digested: gastric outlet obstruction, gastroparesis (delayed stomach emptying, e.g. seen in diabetes mellitus) ■ Bile (green): small bowel obstruction (distal to the ampulla of Vater) ■ Faeculent: distal intestinal or colonic obstruction. Note: the only time you will see faecal (i.e. true faeces), as opposed to faeculent (i.e. foul looking), vomiting is in patients with a gastrocolonic fistula… or coprophagia ■ Blood/coffee-ground: haematemesis (see Chapter 5) ■ Large volume: less likely to be functional. • Timing ■ Early morning: classically in pregnancy and raised intracranial pressure. ■ Duration: this is useful in identifying the severity (patients with severe nausea and vomiting present early) and a longer time course makes acute pathologies such as bowel obstruction less likely, as untreated this will either deteriorate or resolve. • Association with eating? ■ Vomiting within an hour of eating suggests an obstruction high in the gastrointestinal (GI) tract proximal to the gastric outlet. If this is the case, you should ask about peptic ulcer disease (or a history of dyspepsia) as this can cause scarring and pyloric stenosis. ■ Vomiting after a longer postprandial delay is consistent with an obstruction lower in the GI tract, usually in the small bowel. ■ Early satiety, postprandial bloating, and abdominal discomfort together suggest gastroparesis or outlet obstruction. • Use the SOCRATES mnemonic to characterize the pain (see Chapter 12). • The site is indicative of certain pathologies (e.g. right upper quadrant suggests a hepatobiliary cause, epigastric suggests a pancreatic or gastroduodenal cause). However, localization of pain is far from accurate in abdominal pathology due to the neural wiring and embryology, and also anatomical variations.

Haematemesis

First of all, call for help. You cannot manage an emergency alone—it involves teamwork. Call for help and involve your seniors. Second, this patient has potentially lost a lot of blood. Start with ABCDE—Airway, Breathing, Circulation, Disability, Exposure. Airway: Ensure it is patent. Can he talk? Is there any gurgling or stridor? Beware of blood in the oropharynx in a patient with haematemesis. If necessary, use suction to remove the blood. Breathing: Are there any signs of respiratory distress (tachypnoea, use of accessory muscles, low saturations)? Circulation: Does he have a pulse? Is he in shock (tachycardia, narrow pulse pressure, hypotension, cold peripheries)? Disability: what is the patient’s Glasgow Coma Score (GCS)? Always calculate this in an emergency as a GCS ≤8 (or rapidly dropping towards that point) suggests that the patient may soon require intubation to protect their airway. If you can’t remember the components of a GCS in an emergency, use the AVPU score (patient is Alert, responds to Voice, responds to Pain or is Unresponsive), where an avPu score (i.e. a patient who is responding to painful stimuli but not voice) is roughly equivalent to a GCS = 8. Exposure: The patient may have suffered multiple trauma and/or have various sites of blood loss. Although it is unlikely, what the hostel staff perceived as drunken behaviour may in fact represent behaviour from an unwitnessed assault resulting in significant head injury, and the haematemesis may reflect a stab wound to the chest or abdomen. Always expose the patient or you will be caught out by unsuspected findings. Mr Tucker is in shock, often defined as a BP <90/60 mmHg. He needs fluid resuscitation: • Apply high flow oxygen (15 L/min). • Get intravenous (IV) access: insert a large-bore (14G–16G) cannula and if you can’t do it yourself, ask a senior to help. They may need to resort to ultrasound-guided peripheral vascular access, to intraosseus access or to central venous access. • Send bloods for: ■ Venous blood gas: this will give you a rapid estimate of the patient’s haemoglobin.

Neck lump

Considering the anatomy and associated pathology, the lump may represent: • Artery: carotid artery aneurysm, subclavian artery aneurysm, carotid body tumour (i.e. chemodectoma or paraganglioma of the carotid body) • Nerves: neurofibroma, schwannoma • Lymphatics: lymphatic malformations • Lymph nodes: infective, neoplastic (primary or metastatic), granulomatous • Salivary glands: infective, autoimmune, neoplastic • Larynx: laryngocele • Pharynx: pharyngeal pouch • Branchial arch remnant: branchial cyst/sinus/fistula • Skin/superficial subcutaneous: lipoma, epidermal cyst, abscess, dermoid cyst • Muscle/cartilage/bone: sarcomas (e.g. rhabdomyosarcoma, fibrosarcoma, osteosarcoma), cervical rib, torticollis The age of the patient has an enormous bearing upon the pathology you should expect to encounter: • In children, about 75% of neck lumps are benign. Congenital and inflammatory lumps are most common. Thus the differential diagnosis will be weighted in favour of branchial cleft cysts, lymphatic malformations, and lymphadenitis. If malignancy is diagnosed in paediatric neck lumps, it is usually a lymphoma or sarcoma, or sometimes a papillary thyroid carcinoma. • In adults over 40, as many as 75% of lateral neck lumps are malignant. Of the malignant neck lumps, about 80% are metastases and the rest are mostly lymphomas. In fact, ▲ in the absence of signs of infection, a lateral neck mass in an adult is lymphadenopathy due to metastatic carcinoma (usually squamous cell) until proven otherwise. • How long has the lump been there? ■ Less than a few weeks: most likely infective or inflammatory lymphadenopathy, although some patients will present with malignant neck lumps that have only been noticed within the last few days. ■ More than a few weeks: must exclude malignancy. ■ Years, with little change: most likely benign. ■ Note that congenital neck lumps, despite being ‘congenital’, may only ‘appear’ later in life as they may fluctuate in size (e.g. following an infection). • Has the lump got bigger, smaller, or stayed the same size? A lump that is gradually increasing in size must be regarded as a malignancy until proven otherwise. Remember that a progressive increase in size of a malignant neck lump may be reported as a sudden appearance by the patient.

Swollen calf

The main causes of an acutely swollen calf are shown in Figure 28.1. Note that it is possible for different pathologies to coexist: a patient may present with a deep vein thrombosis (DVT) and ruptured Baker’s cyst, for example. Also, many patients will get a swollen leg following surgery to that leg, but this shouldn’t present much of a diagnostic challenge (although you must obviously exclude DVT if the symptoms and signs warrant this) and therefore this is not included in the list in Figure 28.1. Yes, because most of the diseases listed in Figure 28.1 are local diseases and it would be highly unlikely for the patient to have two similar events in both legs at the same time. Instead, it would be more likely that the patient has either a systemic problem or a problem affecting central vessels. However, it is worth remembering that a DVT can arise in a patient with pre-existing bilateral leg oedema, so don’t rule out a DVT just because both legs are swollen. Figure 28.2 gives the main causes of bilateral swollen legs. • Are there any risk factors for venous thrombosis? Consider Virchow’s triad: ■ Hypercoagulable blood? Trauma, major surgery within the last 3 months, pregnancy and postpartum state (women are at increased risk of a venous clot for 6 weeks after birth and the risk is actually higher during the first few weeks after birth than during pregnancy itself), inflammatory bowel disease, active cancer, obesity (body mass index (BMI) >30 kg/m2), combined oral contraceptive pill or hormone replacement therapy (HRT), family history or past medical history of DVTs. ■ Stasis? Bed rest (>3 days) or long-haul travel (the actual length of flight that qualifies as ‘high risk’ is controversial). ■ Vessel injury? Trauma, surgery. • Has she felt breathless, had any chest pain, or coughed up any blood? If DVT is high on your differential list, it would be wise to enquire about symptoms of a possible pulmonary embolism (PE).