Scabies, Lice and Infestations

Insect bites

Presentation

  • Variable presentation depending on the insect, location etc and can vary from small papulo-urticaria to larger bullae.  Most are itchy and some may be painful.
  • May appear in a linear/regional distribution (linear- e.g. bed bugs; exposed regions- e.g. outdoor insects e.g. midges) where the insect has had access
  • At the extreme end, bites can induce an allergic reaction and/or can become infected

bites

A quick note about tick bites: see also Lyme Disease

Management

  • Try and identify the source and avoid that if possible.  Alternatively, use repelling creams/sprays.  Make sure household pets are treated, and that bed linen is clean.
  • Topical steroids and antihistamines may be used short term for symptomatic relief.

Scabies (Sarcoptes Scabiei)

Pathophysiology

  • Note that the symptoms of scabies is actually most likely an allergic reaction (mostly type IV, some type I) to saliva, mites, eggs, faeces.
    • As a result, most patients are asymptomatic for the first 6 weeks of infestation
  • Most infestations only composed of 10-12 mites in a patient who maintains hygiene (can be 100s if neglected)
  • The female mites burrow through the keratin layer at around 2mm/day, laying eggs as they go.
  • Scabies is highly contagious (skin-skin), so it is not uncommon for an entire household to get it

Presentation

  • Generalised itching (particularly when hot/warm)
  • Widespread eruption of inflammatory papules
    • Burrows may also be visible and tracks may also be seen
      • These are often fine, wavy, grey, dark or silvery lines with a minute speck (mite) at the end
    • Scabetic nodules may develop on the elbows, nipples, web spaces, wrists, axillae, penis or scrotum.  They are firm, dull red/brown, intensely itchy and may persist after treatment (they are not a sign of active infestation but the delayed reaction to an infestation)
    • Note that an eczematous reaction may also occur which can confuse the clinical picture with eczema.  Fissures/infection risk is also a possibility.
  • May have a contact history with someone with scabies

Investigations

  • Skin scraping with a blunt scalpel or needle.  KOH staining usually confirms whether a mite (which should adhere to the implement) is present
  • NB Scrapings are not very sensitive- the diagnosis will always be clinical based on history and examination.

Management

  • Permathrin cream top to toe for 8 hours (30g will cover average adult); twice, one week apart
  • Treat all in household and close contacts at the same time if possible (just once- the first treatment)
  • Prescribe mild-moderate topical steroid for secondary eczema/itch (may take a while to resolve)
  • Wash all clothes and linen at 50°C at first treatment
  • If permathrin is not appropriate (some patients may be allergic), then malathion aqueous liquid

Headlice (pediculosis capitis)

  • Infestation with pediculus capitis– which lives on the scalp of humans (cannot survive more than 3 days off the head.  Female may lay up to 10 eggs/day onto the hair shaft.

Pediculus_humanus_development

  • More common in girls aged 4-11 (i.e. primary school age) with longer hair
  • Symptoms (itchy scalp) may not develop til 2 weeks after initial infestation
  • Diagnosing lice can be done simply by fine combing the scalp (wet or dry).  If it is diagnosed in one member of the family, the rest of the family should be checked.

Management

  • If an infestation is confirmed, it can be eradicated with a combination of
    • Dimeticone 4% lotion or Malathion 0.5% aqueous liquid.  (both applied twice with a week between applications)
    • Active combing (Bugbuster comb)

Lyme Disease

An infection of the spirochete called Borrelia burgdorferi, which are transmitted to humans via tick bites.

There are 3 stages of the disease

  1. Erythema chronicum migrans (ECM) is first and occurs within one month of the bite.
    1. Usually a solitary macule, or annular lesion which can vary in size
      1. may have a target like appearance
      2. usually expands over days to weeks
      3. usually larger than 5cm
    2. Other lesions may be present if there has been spirochetaemia/lymphatic spread
      1. around 40% will have lymphadenopathy too, and may have flu-like symptoms (fever, headache, tiredness, nausea, vomiting, arthralgia, myalgia etc)
  2. Borrelia Lymphocytoma
    1. Firm, bluish/red swelling on the earlobes of children/nipple in adults
    2. Tender, local lympadenopathy
    3. Flu-like symptoms +/- numbness, facial paralysis, meningitis, arrythmia
  3. Acrodermatitis Chronica Atrophicans
    1. Characteristic blue/red discolouration progressing to atrophy
    2. 6 months – 8 years post initial infection
    3. Has an early, treatable, inflammatory stage and a late, atrophic, resistant stage
    4. Arthritis, neurological problems and chronic pain

Investigation

  • Serology for Lyme antibodies
    • (NB must wait 4 weeks after the onset of symptoms to avoid false negative results)

Management

  • If symptomatic (i.e. suspected Lyme’s, not just a tick bite)
    • Doxycycline 200-300mg daily
    • Amoxicillin 500mg daily (both 14 days)
      • Cefuroxime 500mg BD if contraindication to above
  • If severe, consider admission with IV penicillin/ceftriaxone.
  • NB 15% of patients will exhibit Jarisch Herxheimer reaction in 1st 24 hours of treatment (death of many organisms and release of toxins)

Urticaria

Superficial swelling of the skin that results in a red, raised, itchy rash.  It can be localised or generalised.

 

Pathophysiology

 

  • Release of a variety of inflammatory mediators (including histamine, bradykinin, leukotrienes, prostaglandins) cause close-by vessels to become leaky.  Leakage of plasma causes the classic oedema/wheal whilst histamine causes an itch.
  • Can either be immune mediated on ‘non-immune’ urticaria
    • Immune-mediated urticaria
      • Can be associated with a type I (immediate allergic IgE-mast cell response e.g. to latex, cosmetics); type II (cytotoxic T cell mediated causing an urticarial vasculitis (e.g. hereditary angioedema) and type III (immune-complex diseases e.g. SLE that can cause urticaria).
    • Non-immune mediated
      • Normally complement mediated in viral/bacterial infections but can also be due to transfusion reactions (technically IgE mediated), opioids and other drugs, physical stimulation etc
    • Note Idiopathic urticaria and chronic urticaria
      • Some patients exhibit chronic urticaria for which there is no known cause/pathogenesis.  About a 1/3 of chronic cases are thought to be immune mediated.

 

English: Uriticaria
English: Uriticaria (Photo credit: Wikipedia)

Presentation

  • Classic urticarial weals (small, raised areas 1-2cm that develop suddenly and usually last <24 hours, but may reappear again within hours) with itch
    • Acute <6weeks vs Chronic >6weeks
    • It is important to ask about:
      • the possibility of food allergy (new food/prev allergy)
      • drug history (particularly NSAIDs/aspirin, OTC medications, supplements, penicillins, ACE inhibitors) as there may be an allergy.  Note also any PMHx.
      • Any recent viral/bacterial infections (acute or chronic)?
      • Where the hives caused by physical stimuli (hot/cold/pressure etc)?
      • Any bites/insect manifestations?
      • Also take an extensive occupational/hobbies history.

Investigations

  • You might (based on the history) want to do FBC/U&E/LFTs and or blood cultures if you suspect a more systemic cause (e.g. urticarial vasculitis where urticaria is painful and persistent).
  • You might also want to do RAST if there is a specific allergen that you think could be causing the urticaria.

Management

  • Where possible, avoid the trigger
  • For severe acute urticaria, consider using a short course of prednisolone (40mg/day 3-5 days) in addition to a non-sedating anti-histamine e.g. (cetirizine, fexofenadine, loratidine)
  • Antihistamines are the main treatment otherwise (other than treatment of the underlying cause)
    • sedating anti-histamines may be useful for patients who have problems with nocturnal itching (not uncommon)
    • cooling agents e.g. menthol/calamine may also be of benefit
  • consider referral to a specialist if symptoms persist >6 weeks and are not responding to treatments

Contact Dermatitis

Inflammatory skin reaction (dermatitis) to an external agent.  This can either be an irritant or an allergen.

  • Allergic contact dermatitis is a type IV (delayed) hypersensitivity reaction that occurs after sensitization and subsequent re-exposure

  • Irritant contact dermatitis occurs after damage to the skin, usually by chemical irritation.

     

Epidemiology

  • Accounts for around 6% of all dermatology consultations.  Many are referrals from occupational health.  Around 80% are irritant dermatitis.

Aetiology

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Mechanism of type IV allergic reaction

http://highered.mcgraw-hill.com/sites/0072507470/student_view0/chapter22/animation__delayed__type_iv__hypersensitivity.html

This animation from America, is better than I can explain it.

Presentation/Assessment

  • There may be a few differences between allergic and irritant dermatitis (in reality, this can be more difficult to distinguish and both can present in the same way)
    • Irritant contact dermatitis can be burning, stinging, sore; whereas allergic dermatitis mainly present with redness and itching (and scaling).
    • Irritant dermatitis is usually well demarcated in the acute phase (less so with allergic forms)
    • Depending on the suspected cause, the pattern of distribution of the dermatitis may tend towards a diagnosis of either irritant or allergic pathology
      • e.g. the neck/face are commonly affected in cosmetic allergies, whereas the hands are often exposed more to irritants
    • Irritant contact dermatitis can also be associated with atopic eczema (unlike allergic)Pioneer11-male
  • In general, both can present with
    • red skin; a vesicular/papular rash; crusting/scaling; itch, pain or burning
    • if exposure and the reaction is chronic, then fissures, lichenification and hyperpigmentation may also be present
  • The patient history is very important
    • Any triggers/exacerbating/alleviating factors?  Are there times when the symptoms are worse/better? Describe the onset, progression etc?
    • Occupation/hobbies?
    • Any young children?
    • Any changes in perfume/washing detergent etc?
    • Any pre-existing skin disease?
    • Any other medical conditions/drugs/allergies?
    • Any family hx of skin disease/allergy?
  • NB If anything does stand out in the history, always ask more about this.

Investigations

  • Patch-testing is the gold standard and should be done in cases with
    • chronic, recurring, or unrelenting eczematous or lichenified dermatitis (occupational or otherwise) despite appropriate avoidance measures and corticosteroid treatment
    • features suspicious of contact dermatitis but no clear history of relevant exposure

Management

  • Avoidance of the the trigger stimulus should be advised
    • Sometimes it is not possible to completely remove the stimulus
  • Advise the frequent use of emolients to maintain skin hydration, and try to avoid soap by substituting with aqueous cream
  • Topical steroid may be used to reduce symptoms (strength should be appropriate to the severity/duration/location of the symptoms)
  • Whilst antihistamines aren’t recommended by NICE, they may help some patients with severe itch.
  • Light therapy (PUVA) and non-steroid immunomodulation is rarely required and should only be considered by a specialist after conventional measures have failed.

Constipation

Definition

Defecation that is unsatisfactory because of infrequent stools, difficult stool passage or seemingly incomplete defecation.  Stools may be dry/hard and may be abnormally large/small.

NB This definition is somewhat subjective.  It is always important to know what is normal and what is abnormal for a patient.  It should also be noted that ‘constipation’ alone is a symptom.  (Functional constipation may be considered a disorder in itself).

Epidemiology

  • Constipation is a common problem at all ages
    • 16% population prevalence worldwide
    • more common in women and the elderly and in pregnancy

Types of constipation

  • Functional (Primary/Idiopathic) Constipation
    • No known cause
    • Can be classified as either normal transit constipation (most common- can be sometimes classed as IBS-C); slow transit constipation or pelvic floor dysfunction
  • Secondary (organic) constipation
    • Caused by a drug or medical condition
  • Faecal loading/impaction
    • retention of the faeces to the extent that spontaneous evacuation becomes unlikely.  Retained faeces may be palpable on examination of the abdomen or per rectally.
  • Overflow incontinence
    • leakage of (usually very) loose stools around impacted faeces

0912_Gambert_Table

Assessment

  • Make sure you understand what the patient considers to be normal.  From there, assess when and how things changed
    • Consistency; size; discomfort/ straining/ bleeding/ incontinence of loose material; have they had to use any manual measures (usually a sign of severe impaction but may be a sign of rectocele/ulcer)
    • Are there any associated symptoms?
      • Nausea; vomiting; abdo pain; loss of appetite; weight loss;abdo distension; pain when passing stools

FWFWFEWF

  • Ask about past medical and drug histories
  • Social history is particularly important
    • Diet history is important: ask about fibre intake (fruit, veg, fluids, cereals etc)
    • Also ask about other social factors that may influence toilet habits e.g. if they are in a job where they cannot go to the toilet always when they need to (any holding in)
    • Have there been any big changes in lifestyle recently?

Presentation/Investigation/Diagnosis

  • Presentation depends on the suspected cause, but if constipation is the only presenting symptom, and the patient is troubled by it, then a management plan will be required.
    • NB In the elderly, constipation may present as/with confusion; diarrhoea (overflow); abdominal pain; urinary retention; nausea/anorexia
  • Functional Constipation
    • ROME criteria (of functional GI disorders)
      1. Must include 2 of the following for last 3 months and beginning at least 6 months ago:
        • Straining during at least 25% of defecations
        • Lumpy or hard stools in at least 25% of defecations
        • Sensation of incomplete evacuation for at least 25% of defecations
        • Sensation of anorectal obstruction/blockage for at least 25% of defecations
        • Manual maneuvers to facilitate at least 25% of defecations
        • ❤ defecations / week
      1. 2. loose stools are rarely present without the use of laxatives and insufficient criteria for IBS
  • Generally, investigations aren’t required for primary/functional constipation but any secondary causes should be appropriated investigated (often an FBC can be done to check for any anaemia).  Note that any red-flag symptoms will require investigation.

Investigations

  • Blood tests may be useful
  • Scope tests and scans/x-rays may be of benefit if ‘red-flag’ symptoms are present and you suspect a more sinister cause of constipation

Differential Diagnosis

  • Mechanical
    • Cancer; stricture; rectocele/sigmoidocele/enterocele; Intussusception; rectal prolapse; megacolon; anal fissure
  • Metabolic
    • Diabetes mellitus; Hypothyroidism; Hyperparathyroidism; Hypercalcaemia; Hypokalaemia; Hypomagnesaemia; Uraemia; Depression
  • Neuropathies
    • Hirschsprung disease; Parkinson’s disease; MS
  • Other
    • Scleroderma; Amyloidosis
  • Medications
    • Antacids; Iron; calcium; opioids; anticholinergic agents; calcium channel blockers; diuretics; NSAIDs; sympathomimetics; TCAs

Management

  • Treat any underlying cause
    • If this is due to poor diet, advice on diet is particularly important (high fibre diet and fluids)
    • If due to medications, adjust where possible.  If this is opioid-induced, avoid bulk-forming laxatives but rather use osmotic laxatives e.g. lactulose
  • Drugs (laxatives) should aim to be used short-term
    • Bulk-forming laxatives (e.g. Ispaghula husk/methylcellulose) should be used in the first instance
    • Osmotic laxatives can be considered if this doesn’t help soften stools
    • Add a stimulant laxative if the patient is having trouble pass soft stools
  • The dose of laxative can be titrated up as required.  Do not suddenly withdraw high-dose laxatives, as there may be a rebound reaction.
  • Consider suppository treatments and enemas in faecal loading.

Special case:

  • Prucalopride is a serotonin agonist that has been approved by NICE as almost a ‘last resort’ medical treatment for women with chronic, refractory constipation for which there is no known cause.  It has dramatic effects on bowel motility and thus can cause diarrhoea and other side effects.  It should only be prescribed by a specialist after unsuccessful trial of at least 2 laxative treatments- or if surgical management is being considered.

Breast lump

Breast lumps are very common, the majority of which will be benign.  However, given that 1 in 9 women will develop breast cancer at some stage in their life, an accurate and organised assessment of any abnormality in the breast is very important.

Breast Screening (Scotland) (http://www.nsd.scot.nhs.uk/services/screening/breastscreening/breastfaqs.html)

  • Offered to all women over the age of 50-70.  NB Appointments can also be made by patients or by GPs.
  • Mammography
  • Any patients with suspicious results will be sent to the one-stop clinic within 3-weeks for further assessment

One-stop clinic

  • Consultant breast surgeon will see every patient for history and examination
  • Imaging
    • If >40, a mammogram is the modality of choice
    • If <35, an ultrasound is the modality of choice
    • If <40 and >35, both may be required.
      • All results are reviewed by a radiologist during the clinic
  • Pathology
    • Most commonly, a core biopsy will be taken during the clinic and sent to pathology for assessment (this will take 1-3 weeks for results) as this will give a definitive diagnosis
    • Occasionally, fine needle aspiration will be done there and then in the clinic (As far as I know, they don’t routinely do this in Tayside)
  • Based on these results, further testing (MRI) may be required.

Presentation

  • History
    • Most patients present with a palpable mass.  Ask about duration, speed of growth etc
    • It is important to ask about any association symptoms
      • Pain; nipple discharge; skin dimpling; inflammation; nipple inversion
    • A family history of breast cancer is important.  It is also important to ask about menstrual and obstetric history.
  • Examination of the breast
    • Important points
      • ALWAYS offer a chaperone
      • Try and use appropriate language (examine not feel)
      • Allow the patient to undress and prepare in private (or with chaperone if they wish)
    • Inspection
      • Inspect first with the patient’s hands by their side:
        • look for any nipple abnormality (inversion/discharge etc) and any skin changes (Peau d’orange; tethering; rash) and any visible lumps
        • check symmetry (NB most breasts are not completely symmetrical, though if there is a gross abnormality that could be of concern, it is appropriate to ask the patient whether this is new)
      • Also inspect with the patient with her hands on her hips, squeezing inwards (may bring out any abnormalities in deeper tissue)
      • Also with her hands behind her head.  (also look into the axilla)
      • Remember to inspect under the breast
    • Palpation
      • Ask if there is any pain and examine this area last.
      • Examine all of the areas of the breast (either divided into quadrants + tail or as a clock face + tail)
        • Do NOT use the fingertips but the flat pads of the fingers/hand
        • Remember also to examine under the nipple
        • NB the breast can feel a bit lumpy- if you feel a lump, carry on to finish the examination, then come back to this at the end for a more detailed assessment
      • Repeat on the other breast
    • Lymph node exam
      • If you are examining the right axilla, support the patient’s arm with your right hand/arm and examine with the left (opposite) hand, and vice versa
      • You would also examine the subclavicular nodes
  • Record
    • Size; location; shape; surface; texture; mobility

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Haemorrhoids

Abnormally swollen vascular mucosal cushions that are present in the anal canal.

Anatomy

  • NB Haemorrhoids are NOT varicose veins, but rather they are clusters (cushions) of vascular tissue (i.e. containing arterioles, cappillaries and venules), smooth muscle and connective tissue lined by the normal epithelium of the anal canal.  Bleeding coming from haemorrhoids actually comes from the perisinusoidal arteries (haemorrhoid=sinusoid).
  • They lie along the anal canal in 3 columns
    • left lateral (3 o’clock)
    • right posterior (7 o’clock)
    • right anterior (11 o’clock)
  • Haemorrhoids play an important role in adjusting anal tone during increased abdominal pressure (e.g. coughing) and may be important in distinguishing between faeces and flatus.
  • Haemorrhoids can be classified as either
    • External
      • located below the dentate line
      • drain via inferior rectal veins to pudendal vessels to internal iliac
      • covered by squamous cell epithelium
      • has somatic sensory innervation (pudendal nerve)
    • Internal
      • lie above the dentate line
      • drain via middle rectal veins to internal iliac
      • covered by columnar epithelium
      • has visceral sensory innervation (not usually felt)
      • Can further be classified based on location
        1. 1st degree protrude into the anal canal
        2. 2nd degree prolapse outside of the canal but reduce spontaneously
        3. 3rd degree prolapse outside of the canal but require manual reduction
        4. 4th degree prolapse outside of the canal and are irreducible.

Pathophysiology

  • There are two main theories as to how haemorrhoids develop (the first is a pressure problem, the second more likely explains the increased incidence with age).
    1. Long-standing straining/constipation causes increased pressure within the anal canal and increased engorgement of the anal cushions.  If this eventually becomes great enough to interfere with venous return, engorgement may not resolve.  Repetition of this cycle leads to enlarged haemorrhoids.  It is known that a low-fibre diet and constipation are risk factors.
    2. Sliding anal canal lining suggests that haemorrhoids develop when the supporting tissues of the anal cushions deteriorate.  Here, venous dilatation is a consequence of a downward ‘sliding’ of anal cushions (rather than the cause).  It is thought that inflammatory processes may be involved in this.

Presentation

  • History
    • PR bleeding
      • Usually painless (see below)
      • Bright red (fresh arterial)
      • Associated with defecation
      • Amount can vary- from streaks on toilet paper to in the bowl, never mixed with stool (consider another cause if this is the case)
    • Anal itch
    • Prolapse
      • usually with bowel movement; often described like fullness, incomplete evacuation or a lump at the end of going to the toilet.
    • Pain
      • Pain is not normally relevant but may be present in 3rd/4th degree haemorrhoids if the haemorrhoid becomes strangulated
      • In external haemorrhoids, the haemorrhoid can thrombose and cause severe pain/discomfort then
      • Discomfort is more common (rather than acute pain)
    • Mucus/faeculant discharge
  • Examination
    • May be normal (if grade I)
    • The perineum may appear irritated from chronic discharge
    • If visible, the haemorrhoids usually appear at the anal verge (on coughing) as bluish, soft bulging vessels covered by mucosa (or if external they may be covered by skin)
    • Digital rectal examination should be performed to rule out any other causes of rectal bleeding and to check for any other haemorrhoids and for their reducibility

Investigations

  • Protoscopy may be useful if initial examination was difficult/inconclusive
  • FBC (anaemia/infection)

Management

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  • *  Advise about a high fibre diet; fluid intake; weight loss and perianal hygiene.  Discourage straining and ‘holding in’ (i.e. advise to go to the toilet as soon as the urge comes).
  • **   Prescribe a laxative if the patient is constipated (bulk-forming is the preferred choice; stimulant laxatives are not recommended as they may worsen the haemorrhoids).  Prescribe pain relief where appropriate.  Topical creams (e.g. steroid/local anaesthetic creams) may be used in the short term ONLY.  Long-term use is not advised.
  • Rubber band ligation
    • A band is applied to the base of the haemorrhoid. The strangulated haemorrhoid becomes necrotic and sloughs off.  Up to 3 can be treated at once.  Minor complications include thrombosis, bleeding and ulceration.
  • Sclerotherapy
    • Phenol in oil is injected at the base of the haemorrhoids to induce a fibrotic reactions and cutting off the blood supply.  The haemorrhoids with atrophy, but can recur.
  • Haemorrhoidectomy
    • Only recommended for grade III/IV symptomatic haemorrhoids as there is a risk of incontinence
    • Other complications include post-operative urinary retention, bleeding, anal stricture, abscess, fistula, infection
  • Stapled haemorrhoidopexy
    • Staples are used to lift the haemorrhoids up back into the canal.

Diverticular Disease, Diverticulitis, and Abdominal Abscess

Diverticula

Sac-like herniations of mucosa through the smooth muscular colonic wall, often in natural openings created by the vasa recta or vessels.

  • Around 50% of the population have diverticula by age 50 and 70% by age 80.

Diverticulosis

Diverticula present without any symptoms.

  • Around 75% of people with diverticula are asymptomatic.

Diverticular Disease

Condition where diverticula cause intermittent pain, but without any signs of acute infection or inflammation

Diverticulitis

Infection and inflammation of the diverticula, usually causing marked pain, fever and malaise.  It can be complicated by abscess formation, perforation or fistula.

  • Of the 25% of people with diverticula who develop symptomatic disease, 75% will have at least one episode of diverticulitis

Pathophysiology

  • The vasa recta that penetrate the bowel wall create areas of weakness through which a portion of colonic mucosa and submucosa can herniate.
  • The sigmoid colon is commonly affected, probably due to its small diameter and thus higher intraluminal pressures.
  • The pathophysiology that causes symptoms is poorly understood
    • Damage to the vasa recta vessels may result in inflammation
    • It has also been thought that obstruction of the diverticula with faecal matter can cause an acute inflammatory reaction.
    • It has also been suggested that microperforation of diverticula could be a cause of diverticular disease symptoms (i.e. without causing an acute diverticulitis)
    • In any case, acute diverticulitis is thought to be a result of a perforated diverticulum.
    • Abscess formation is not uncommon

Presentation

  • Diverticulosis, by definition, is asymptomatic and is usually an incidental finding on investigation
  • Diverticular disease
    • Intermittent pain in the (left) lower abdomen, which is tender on examination.  Pain may be brought on with eating and may be relieved by bowel movements
    • Altered bowel habit- commonly constipation but diarrhoea can be a symptom
    • Bloated feeling
    • mucus discharge
    • PR bleeding- usually fresh or mixed with the stool (haematochezia); can be substantial and will often be the presenting complaint
      • NB diverticular bleeding is usually a single (or infrequent) episode- if frequent/continuous, the cause is unlikely to be diverticular (even if this has been diagnosed)
  • Diverticulitis
    • Constant, severe abdominal pain that may localise to the left iliac fossa.  Tender on examination.
    • Fever is a typical feature (distinguishing from diverticular disease)
    • Nausea, vomiting and anorexia may also be present
    • Urinary symptoms may also be present due to subsequent inflammation of urinary structures.  It is important to ask about this

Investigations

  • Bloods- FBC should be done to check for degree of blood loss (Hb) and inflammatory response (WCC raised in diverticulitis)
  • Flexible sigmoidoscopy/colonoscopy will diagnose diverticulosis (the others are clinical diagnoses)
    • Rarely will a barium enema be used to diagnose diverticular disease (more often a barium study will identify diverticulosis as an incidental finding)
    • CT will also identify diverticula (and is more suitable if the patient has signs of peritonism) but is not first line

Management

  • Diverticulosis does not require any treatment, although a high fibre diet is advised
  • Diverticular disease can usually be managed conservatively with pain relief (avoid NSAIDs and opioids if at all possible due to risk of bleeding and further constipation)
    • Any blood loss should be managed appropriately (usually warranting admission) with fluid resuscitation
  • Diverticulitis
    • People with mild, uncomplicated diverticulitis can be managed at home with pain relief (paracetamol); clear fluids; and oral antibiotics (co-amoxiclav or, if allergic, ciprofloxacin and metronidazole) for at least 7 days
      • Advise clear fluids only (no hard diet) until symptoms improve.  If symptoms don’t improve/worsen, consider admission
    • Arrange admission if:
      • Pain is not managed with paracetamol
      • Hydration cannot be maintained with oral fluids or oral antibiotics not tolerated
      • There is significant co-morbidity likely to affect their recovery
      • If there is bleeding that might require transfusion
      • Perforation/peritonitis
      • Any evidence of a fistula (e.g. faecal discharge via waterworks)
      • Any swelling suggestive of an intra-abdominal abscess
    • Management in hospital is similar i.e. with fluid resuscitation and antibiotics (IV amoxicillin, metronidazole +/- gentamycin)
    • Surgery is rarely offered for removal of diverticula, but may be required for the drainage/removal of abscesses, repair of fistulae, and management of peritonitis

Abdominal Abscess

  • Most commonly caused by perforated appendicitis/diverticulitis or perforated peptic ulcer
    • Other causes include gangrenous cholecystitis; mesenteric ischaemia with infarction; and pancreatitis or pancreatic necrosis
    • Occasionally, an abscess may be iatrogenic (post-surgery)
  • Infective organisms that cause the abscess are mixed (aerobic/anaerobic)- most commonly E coli and Bacteroides
  • Pain is usually a feature.  Signs of infection (particularly a spiking fever, but also other signs of SIRS/Sepsis e.g. hypotension, tachycardia etc may also be present)
    • Occasionally change in bowel habit (important to ask)
    • Also ask about urinary symptoms (pelvic abscess) and chest symptoms (subphrenic) e.g. hiccuping, pleuritic pain
  • A tender, hot mass may (or may not) be palpable on examination
  • CT scan and/or ultrasound should be carried out to localise the abscess.  FBC/U&E/cultures should also be taken.
  • Drainage depends on clinical severity.  In either case broad spectrum antiobiotic treatments will also be needed (see above)

Anal Fissure

Tear or ulcer in the lining of the anal canal, immediately within the anal margin.

Classification

  • Acute (<6 weeks) vs Chronic (>6 weeks)
  • Primary (no underlying cause) vs Secondary (underlying cause)

Aetiology and Pathophysiology

  • Primary
    • Thought to be due to increased anal tone after an initial fissure injury caused by the passage of a hard stool.  The increased tone impairs healing by impairing blood flow to the area, worsening ischaemia.  The result is painful passage of stools- the pain of which can last several hours.
  • Secondary
    • NB Not associated with increased tone or ischaemia
    • Causes include
      • Constipation
      • IBD
      • Malignancy of the anorectal canal

Presentation

  • Often classic history of severe pain when passing stools, and it may be that the patient doesn’t like going (this only worsens the cycle, by increasing anal tone further)
  • Bleeding (usually fresh blood) may be present upon defaecation
  • Some may have a history of constipation
  • On examination
    • Most fissures occur in the posterior midline (12 o’clock position) with the remainder commonly in the anterior midline (6 o’clock position)
    • If a tear can be seen clearly (well-defined), this is more likely to be acute.  Chronic fissures commonly appear a bit scarred, wider or deeper with muscle fibres visible or there may be a skin tag overlying the area.
    • NB PR examination is often very painful and not suitable.

Anal fissures are often a clinical diagnosis so investigation are no required.  If there is suspicion over the cause or concerns about blood loss, then further investigations may be appropriate.

Management

  • Ensure soft, easily passed stool
    • Laxatives (lactulose- osmotic laxatives) are recommended in children
    • Bulk-forming laxatives e.g. ispaghula husk, are recommended for adults
    • Similarly, increasing dietary fibre intake should be advised.
      • Fruit/veg/grains etc
      • Adequate fluids too
      • Aim between 18-30g of fibre
  • Pain relief- paracetamol and/or ibuprofen
  • Consider GTN ointment or topical diltiazem in those who cannot be managed with other conservative measures (particularly in patients with large fissures at initial presentation)
  • Surgery (sphincter dilatation or, more commonly, lateral internal sphincterotomy) may be offered to patients with chronic or unresolved symptoms/signs after 6-8 weeks (if asymptomatic 12-16 weeks)

Acute Pancreatitis

An acute inflammatory process of the pancreas.

Epidemiology

  • Occurs in 56.5/100,000/year (i.e. 0.05%)
  • It has significant mortality- 10-15%
    • <1% in mild; up to 11% in sterile severe cases; up to 25% in infective severe; up to 50% if organ failure for >48hrs

Aetiology

  • Most cases are associated with either gallstones or alcohol excess
  • The remainder can be
    • a complication of ERCP investigation
    • trauma (either accidental or surgical)
    • drugs (there are many drugs that are associated with acute pancreatitis- steroids; azathioprin)
    • rarer causes include infection (mumps); hereditary (gene mutations in CFTR (cystic fibrosis)); other causes of obstruction e.g. tumours; autoimmunity; hypercalcaemia (almost always secondary to hyperparathyroidism); hypothermia; hyperlipidaemia

Presentation

  • History
    • Classically with severe, continuous, boring, sudden-onset pain in the epigastric/ left upper quadrant region
      • Generalised pain and signs of peritonism may indicate severe disease
      • The pain can often radiate to the back; is worse when lying flat
      • In alcohol-related pancreatitis, the onset may be more gradual and occur 6-12 hours after a binge.  Gall-stone related pancreatitis is usually very sudden.
    • Nausea/vomiting
  • Examination
    • Fever is important (may be an early sign of SIRS); Hypotension
    • Abdominal tenderness (may be localised or generalised)
    • Abdominal distension (leakage of fluid into the retroperitoneum in trying to dilute enzymes-> abdominal contents pushed forward)
    • Cullen’s sign (a bluish discolouration around the umbilicus) or Grey-Turner’s sign (the same in the flank)
      • NB these are usually late signs
    • Look for signs of rarer causes e.g. hyperlipidaemia

Investigations

  • Bloods
    • Serum amylase >3x the normal (normal reference range is 30-110U/l; so anything above 300U/l is suggestive; most cases of clear acute pancreatitis will be around 600-800)
      • NB Amylase can also be raised in mesenteric ischaemia; appendicitis; malignancy; macroamylasaemia etc
    • Serum lipase (if available)- more sensitive/specific
    • CRP- often raised but may be low in drug induced pancreatitis
    • Calcium- check for hypocalcaemia (even though its rare)
    • LFTs- raised Alk Phos/bilirubin are suggestive of gallstone disease
    • FBC and U&Es should be done to check for any abnormalities that may require management
  • Imaging
    • Whilst these patients may get abdo x-ray/ CXR/ USS (e.g. may show gall stones), these may not be entirely helpful and the key imaging required is a CT abdo, which will show the extent/severity of disease. 
      • NB A CT is only really justified in patients with (mod-)severe disease
  • Grading Severity
    • General
      • Mild
        • No organ failure and no local/systemic complications (i.e. problem free recovery)
      • Moderately severe
        • Organ failure that resolves within 48 hours
        • Local/systemic complications without persistent organ failure
      • Severe
        • Persistent organ failure (>48 hours)
        • Single or multiple organs
    • Scoring systems
    • Glasogw
    • A score ❤ indicates mild disease; >=3 more severe disease
    • The RANSON Criteria is another scoring system that also includes developments within the first 48 hours (e.g. fall in haematocrit; rise in urea; base deficit; fluid loss; etc.)
    • The Apache II Score is often used in critically ill patients to predict mortality and severity of disease.  It is often used in patients with acute pancreatitis to assess severity.

Management

  • Mild cases can often be managed on a general ward with simple fluid resuscitation and conservative management
    • Antibiotic treatment is only indicated if there are signs of infection
    • Pain control
  • Severe disease may require more intensive management in ICU/HDU
    • Essentially still fluid resuscitation and supportive tx
    • Likely enteral nutrition
    • Surgery is only ever indicated when there is infection/necrosis

Complications

  • Occur in around 15-20%
  • Local complications
    • Pancreatic necrosis (necrotizing pancreatitis) +/- infections
      • Inflammatory mediators released in acute pancreatitis induce thrombosis and haemorrhage leading to pancreatic necrosis.  Necrosis also affects the surrounding tissues (particularly fat) and can spread retroperitoneally behind the colon and into the small bowel mesentery
      • The necrosed tissue commonly becomes infected by bacteria from the gut
    • Pseudocyst
      • Ischaemia and inflammation of the pancreas causes disruption of the pancreatic ducts.  This leads to collections of pancreatic fluid in so called pseudocysts.
        • NB there aren’t always connections between the duct and pseudocysts
    • Abscess
      • Pancreatic abscess usually follows an infections of a limited area of pancreatic necrosis and may develop several weeks after initial infection.
    • Fistulae
      • to the peritoneal cavity (ascites); pleural cavity (pleural effusion); bowel; skin (more common after intervention)
    • Vascular problems
      • Pre-hepatic portal hypertension (involving splenic vein to cause segmental portal hypertension)
      • Erosion and haemorrhage of the pancreatic, splenic or peri-pancreatic arteries or veins
      • Formation of an arterial pseudoaneurysm (i.e. one that does not involve all the layers of the vessel)
  • Systemic complications
    • SIRS

Prognosis

  • About one third of patients can develop diabetes, maldigestion/malabsorption
    • Creon is important if pancreatic function is significantly impaired