Complex regional pain syndrome (previously known as reflex sympathetic dystrophy (RSD) or Sudeck atrophy) is a poorly understood condition which typically affects the extremities (arms and legs), causing severe pain, disability and sometimes swelling. It most commonly occurs after trauma, such as a fracture or sprain, but the trauma can be fairly trivial and in some cases no trauma at all is identified.

It is caused by sustained sympathetic activity, and characterised by symptoms that are out of proportion to any original injury.

It usually affects a single limb, but in 5-10% of cases it may spread to another limb.

Although very poorly understood, it is not a psychological disorder, although sometimes misinterpreted as such – especially as it is often associated with depression.

It can be divided into two types, although the type present does not affect the management:

• CRPS I – without an identified underlying nerve injury
• CPRS II – with an underlying identified nerve injury

It typically settles after time, but it can last for several years. Activity and mobility should be encouraged, and patients often require referral to the pain clinic.

Epidemiology

• Incidence of 25 per 100 000 per year
• Incidence increases with age
• 4x more common in women
• Arm: 60% of cases
• Leg: 40% of cases
• In children
  • Very rare before the age of 6
  • Tends to affect the lower limb
  • Even more common in females than in adults

Aetiology

• Fracture – 45% of cases
• Sprain – 20% of cases
• Elective surgery – 10% of cases
• Spontaneous – 10% of cases
• Other risk factors:
  • ACE-inhibitor use at the time of trauma
  • Limb immobilisation >4 weeks
  • Hx of migraine
  • Hx of asthma
  • Sibling of an affected child (genetic predisposition)
  • Smoking
  • Pre-existing anxiety or depression
  • Fibromyalgia

Pathology

• Not well understood
• An abnormal inflammatory response is thought to result in vasomotor dysfunction and alterations in neuroplasticity in the peripheral nerves
• There is some evidence that prophylactic vitamin C 500mg daily for 50 days reduces the incidence – in distal radius fractures, and foot and ankle surgery

Presentation

Typically presents within one month of traumatic event or immobilisation. In the early stages, there may be very few identifiable physical signs, which can make diagnosis difficult.

• Throbbing, burning pain which is usually worse at night
  • Out of proportion to the original injury
  • Pain often worsened by light touch or other sensations that do not usually cause pain (allodynia)
• Parasthesia (“pins and needles”)
• Spontaneous sweating
• Spontaneous formation of goosebumps
• Change in appearance of hand and skin
  • At first: red, warm, swollen hand or foot with dry skin
  • Later: cold, often cyanosed and mottled, moist skin
  • These changes are often demarcated by an obvious boundary line (very specific for complex regional pain syndrome)
• Muscle wasting
• Reduced strength and ROM of the hand – typically secondary to pain and swelling. Joint are also often described as being painful
• Loss of hair and nails in very advanced cases

Diagnosis

Diagnosis is made using the Budapest Criteria. These require:

• Pain that is out of proportion to any initial causative event PLUS
• At least ONE symptom from each of the THREE following categories AND at least ONE sign from at least TWO of the categories:
  • Sensory – hyperalgesia or allodynia
  • Vasomotor – temperature difference, skin colour changes / asymmetry
  • Oedema / abnormal sweating
  • Motor – reduced ROM, weakness, tremor, dystonia
• PLUS
• No other diagnosis is more suitable

The problem with these diagnostic criteria, is that signs must be present at the time the patient is seen, which often causes a delay in diagnosis.

Imaging studies are often completely normal.

• Occasionally patchy decalcification of bone may be seen on x-ray.
• Bone scan may show increased uptake and can assist diagnosis in some cases
• EMG / nerve conduction studies – may show changes in nerve conduction but are often too painful tome tolerated by the patient and not routinely adivised

Differential Diagnosis

• Improperly placed cast or splint
• Nerve entrapment
• DVT
• Carpal tunnel syndrome
• Psychiatric illness

Management

• Prompt diagnosis is associated with a better prognosis. 
• The most important factor is to keep using the affected limb. Prolonged periods of disuse are associated with a longer duration of illness and worse prognosis.
• Involve a multidisciplinary team – typically the GP, pain specialist and perhaps orthopaedics or rheumatology.
• Aim to improve function, and reduce fear about pain, particularly use-related pain.
• Multiple analgesics are often required. Consider use of the analgesia ladder, for example:
  • Paracetamol, plus
  • NSAID, plus
  • Neuropathic agent – e.g. amitriptyline, gabapentin plus
  • Opiates
• Consider the use of bisphosphonates in those with evidence of bone resorption. Has bene proven to improve pain in these patents.
• Avoid the use of capsaicin – which is often severely painful.
• Considering screening for and treating depression and anxiety which are associated with CRPS.
• Occasionally surgery may be indicated:
  • Surgical decompression – in cases where local nerve compression is implicated (most commonly if there is carpal tunnel involvement)
  • Surgical or surgical sympathectomy – stellate ganglion (upper limb) or lumbar spinal (lower limb)

Prognosis

• Pain will typically flare up and down during the duration of the illness. These are NOT a sign that the condition is progressing
• Rates of resolution vary widely from study to study
  • 75% at one year in one study
  • 35% at 6 years in another
• Good prognostic features
  • Upper limb
  • CRPS after fracture seems to have a better prognosis than other causes
  • Warm type CRPS (usually indicates an early diagnosis)
  • Children
• In severe cases CRPS can spread to all extremities and be completely disabling
• Be wary that many patients may develop opiate dependency after long periods of opiate treatment

Complications

• Mental health complications – such as anxiety and depression
• Immobilisation often makes the condition worse
• Skin infections are common

References

• Complex regional pain syndrome – patient.info
• Complex regional pain syndrome – orthobullets
• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy

Read more about our sources

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• Undescended testes (aka cryptorchidism, and sometimes maldescended testes) can be congenital or acquired
• Usually unilateral
• Congenital undescended testes affects approximately 3-6% of males at birth
  • <1% remain undescended by the age of 1 year
  • Up to 30% of premature infants
• Most resolve spontaneously within the first few months of life
• Testes are surgically descended usually around 6 months if they do not descend by themselves
• Leaving testes undescended increases the risk of malignancy and infertility
• Acquired undescended tests occurs between the age of 1 and 7, whereby the spermatic cord does not grow at the same rate as the child
• Can be confused for a retractile testes

Pathophysiology

• Testes normally descend in the 8th month of pregnancy
• Some boys have delayed testicular descent – but most will descend without intervention by the age of 6 months
• The axact cause is not known, but thought to be multifactorial
• Most are partially descended and found in the inguinal canal. Only rarely are they seen in the abdomen
  • Rarely they are also seen “ectopically” – i.e. not found along their normal path of descent, e.g. in the inguinal pouch. These testes are usually well developer and of normal appearance
• Growth of undescended testes may more slowly, due to the higher temperature within the abdomen
• The increased risk of malignancy in undescended testes only appears to affect testes in the abdominal cavity, and not those in the inguinal canal

Presentation

• Can be congenital, or acquired
• Congenital is often spotted on a new baby check or a 6 week baby check
• One or both testes will be absent from the scrotum
• 70% can be located (often in the inguinal canal)

Complications

• Increased risk of testicular torsion – which may present as abdominal pain
• Reduced fertility, but same paternity rate (for unilateral undescended testes)
• Reduced fertility and paternity rate (bilateral)
• 3-4x increased risk of testicular malignancy

Examination

• Examine the scrotum and inguinal canal for the testes
• Any testes not in the scrotum should be gently manipulated to see if it can be moved into the scrotum (see retractile testes below)
• In complete absence of the testes, examination under general anaesthetic (EUA) may be performed to assist locating it. If it still cannot be located, then laparoscopy is the procedure of choice. Imaging is not usually indicated

Retractile testes

Retractile testes is a normal variant, sometimes confused for an undescended tests. It a common finding in young boys, secondary to a strong cremasteric reflex, whereby the testicles can be retracted into the inguinal canal – often stimulated by examination of the genitals, cold or excitement. To differentiate this from true undescended testes, you should attempt to find the testes in the inguinal canal, or high up in the scrotum, and gently try to ‘milk’ it down into the scrotum. An undescended testes usually cannot be found, or if palpable in the inguinal canal, cannot be manually moved into the scrotum. A testicle that can be moved into the scrotum (even temporarily), is of normal size, and can reach the bottom of the scrotum is usually a retractile testes. Once placed in the scrotum, a retractile testes will usually remain there until the cremasteric reflex is activated again. A truly undescended testes may be able to be moved into the scrotum but will not stay there of its own accord.

Consider referral for retractile testes that does not resolve as occasionally these can become truly undescended. Monitor until puberty, after which time, ascension is rare.

Management

• Monitor up to 6 months of age
• If remains undescended after 6 months, then the child should be referred for surgical managements – orchidoplexy. This is usually performed at about the age of 9 months
• Orchidoplexy is usually a day procedure.
  • Palpable testes in the inguinal canal – Two incisions are made, one in the inguinal canal and one in the scrotum. The Testes is then pulled down into the scrotum and often fixed in place with sutures
  • Non-palpable testes –examination under anaesthetic followed by laparoscopy if still not located.
• Orchidoplexy is still a strongly debated topic amongst surgeons
• Treatment should be performed by 12-18 months to avoid sequelae of undescended testes
• Complications
  • Failure of procedure – a small percentage will require a second attempt
  • Testicular atrophy – if the testes was originally high up in the abdomen, or has a poor blood supply it can subsequently atrophy once placed in the scrotum

References

• Undescended Testes – pre-referral – RCH Melbourne
• Undescended Testes – RCH Melbourne
• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Undescended and Maldescended Testes – Patient.info

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Trauma is managed by teams in the Emergency Department. There is often a defined set of individuals on a ‘Trauma Team’. This might include:

• Team Leader – often an Emergency Physician / Registrar
• Anaesthetist
• Anaesthetic assistant
• Trauma (General) Surgeon / Registrar
• Orthopaedic Surgeon / Registrar
• Additional Emergency Doctors
• Radiographer
• Scribe
• Several Nursing Staff

Allocating Roles

Before the patient arrives then the roles of the team will usually be allocated. Often a ‘Trauma Code’ is sent out to the pagers of the members of the team with pre-defined roles once the message comes in from the ambulance that a trauma patient is expected.

Team leader, scribe, and other roles such as managing airway, circulation, taking blood will be discussed and allocated usually before the arrival of the patient.

Deaths in Trauma

Death in trauma can be divided into:

• Immediate – caused by major disruption or large blood vessels or body cavities
• Early – can occur in minutes to hours after the trauma. Caused by failure of oxygenation of the vital organs – often secondary to cardiovascular collapse.
• Late – occurs days to weeks after the injury. Often due to sepsis and multi-organ failure.

Training of critical care staff – such as with the ATLS (Advanced Trauma Life Support) and EMST (Early Management of Severe Trauma) protocols is aimed at reduced the number of deaths of the ‘late’ category.

The aims of the critical care team in severe trauma are to:

• Stabilise the trauma patient
• Identify life-threatening injuries
• Initiate organ saving interventions

Management of Trauma

Care in the emergency department usually begins with handover from the transporting team (usually ambulance crew). When taking this handover, you should think about the MIST pnemonic

• M – Mechanism
• I – Injury
• S – Symptoms
• T – Treatment

Primary Survey

This is based on the ABCDE approach – with an extra emphasis on the c-spine at the start of the survey. It is a very rapid assessment conducted as soon as the patient arrives in the Emergency Department designed to catch any immediately life-threatening injuries. The patient should be lying flat on their back in bed.

• C-Spine – is it immobilised? Does it need to be immobilised? Are there injuries that may have caused c-spine damage? If there is any doubt – assume c-spine injury
• A – Airway – can air pass in and out of the lungs? Is the patient conscious and breathing for themselves? Are there any visible obstructions (foreign body, vomit, secretions, patient’s tongue). Initiate airway management techniques as required – this might be anything from simple airway manoeuvres like chin lift (beware of head tilt in c-spine injury), to intubation or even performing a surgical airway!
• B – Breathing – the ability to ventilate. Is the patient breathing? Auscultate the chest. Check for chest rising and equal air entry. Look for gross chest wall defects or injuries. Check the trachea for any deviation. Be wary for pneumothorax or haemothorax – patients might need a chest drain. Flail chest segments often require mechanical ventilation.
• C – Circulation – check the BP and get an ECG if indicated. Make sure blood is sent, including FBC, Urea and Electrolytes, a blood gas, group and save and clotting. Check for signs of hypotension. Look for any signs of external bleeding. Check the heart sounds – think about cardiac tamponade. Check the abdomen for sources of bleeding, including palpating the abdomen for intra-abdominal bleeding. Try to get two large bore IV lines (if someone hasn’t done this already). Control any external bleeding with direct pressure until surgery. Consider a FAST scan to look for sources of intra-abdominal blood. Try to get two large bore cannulas into two large veins as soon as possible. 
• D – Disability – Check gross mental status. Do GCS. Check pupils. Quickly check for peripheral neurological signs
• E – Expose the patient – completely remove clothes and check for any injuries. Consider a log-roll to be able to check for spinal tenderness and rule out injuries on the back, the back of the head and the neck. You should also briefly check peri-anal sensation and anal tone. Once you have finished, make sure to put some blankets (or warmer) on the patient to avoid hypothermia.

Usually, whilst all this is going on, members of the team will be taking blood test, attaching leads for ECG, and getting IV access.

Don’t forget to repeat your survey frequently to keep on top of any changes in the patient’s condition.

Secondary Survey

This will vary a great deal depending on the condition of the patient – are they conscious and able to give a history? Is there a collateral history available?

You could base your history around the AMPLE acronym:

A – Allergies

M – Medications

P – Past History

L – Last meal – important for anaesthetic risk!

E – Event – how did it occur?

The physical examination is a full ‘top to toe’ examination

• Head – fully examine the soul and head for any evidence of injury. Examine the cranial nerves. Check the ears (haemotympanum for evidence of basal skull fracture) and nose for evidence of bleeding.
• C- Spine – check the c-spine for tenderness. Remove the collar for this, but make sure that the head is stabilised (usually by another member of staff) whilst you check the spine. Maintain full spinal precautions until the c-spine has been cleared. 
• Chest – palpate the chest wall checking for instability, rib fractures, areas of flail chest, evidence of subcutaneous emphysema. Listen again to the heart and lungs. Don’t forget to check the axilla and the back – especially in patients with any penetrating chest wounds. If any chest tubes have been places – make sure they are in place correctly and are having output. Make sure a CXR has been ordered +/- performed.
• Abdomen / Pelvis – palpate the abdomen. Check for tenderness or distension. If there is any suspicion of pelvic injury – apply a pelvic binder. Don’t forget to examine the genitals and anus for evidence of bleeding or other trauma.
• Limbs -check all 4 limbs for deformity or other evidence of injury. Split and/or reduce long bone fractures. Check for peripheral pulses. 
• Don’t forget to check the spine if it wasn’t; already done on in the primary survey
• Neurological examination – depending on the conscious level and injuries of the patient you should attempt to perform a neurological examination of the limbs
• Don’t forget to cover the patient up again at the end!

Your hospital may have a trauma pro forma that is filled in as part of the secondary survey (often with lots of diagrams and pictures to help injuries be described).

Fluids in Trauma

Be wary of giving large amounts of fluids – this can inadvertently increase the blood pressure and increase blood losses.

• Maintain a MAP (mean arterial pressure) of >65mmHg
• Aim for adequate BP – not normal BP
• Head injury patients should maintain a SBP (systolic blood pressure) of >90mmHg
• Be particularly cautious if there is internal bleeding
• Give small fluid boluses regularly as required – usually boluses of around 200mls. Avoid large amounts of fluid stat (if possible) – if parameters are maintained as above.
• If larger boluses are needed if BP drops – boluses of 10ml/Kg maximum are recommended

Haemorrhage

Defining haemorrhage is difficult. The American College of Surgeons Classification of Haemorrhagic Shock classifies haemorrhage shock in classes I – IV – with IV being the most severe.

• Blood pressure changes are late
• Pulse pressure changes are earlier
• Respiratory rate is an early change
• Mental state is an early change
• DON’T AIM FOR A ‘NORMAL’ BP
  • Aim for MAP >65mmHg
• Send a group and save and crossmatch request ASAP
  • O negative blood can be given immediately
  • Group specific blood takes about 10 minutes to be processed by the lab
  • Crossmatched blood takes about an hour to be process by the lab
• Give O negative blood as soon as possible if required
• Give blood products in the ratio of 1:1:1
  • 1 unit of RBCs
  • 1 unit of FFP (fresh frozen plasma)
  • 1 unit of platelets
• If there are signs of external bleeding – keep pressure on and don’t stop!

FAST Scan

This stands for Focused assessment Sonography in Trauma. The fast scan is an US scan performed at the bedside, usually by an Emergency Registrar or Consultant, or occasionally the Trauma Registrar or Consultant (Gen Surgery).

The scan is usually performed after the secondary survey.

The goals of the FAST scan are to find any intra-abdominal free fluid (which in this circumstance is most likely to be cause by bleeding), to check for cardiac tamponade, and to assess the lungs.

• Visualises three spaces: intra-abdominal, intra-thoracic and pericardial
• Can usually only detect blood if >200mls present
• Good pelvic views by a skilled sonographer in an easily viasulised (usually skinny person) abdomen can detect smaller amounts
• 7 Views in total
  • Subxiphoid 4 chamber (cardiac)
  • Transthoracic long axis
  • Abdominal and lower thoracic
  • Right coronal and intercostal oblique
  • Left coronal and intercostal oblique
  • Pelvic
  • Anterior thoracic

Other Imaging

• Chest XR
• Pelvic XR
• C-spine X-ray

These three scans are usually standard in most trauma patients. Other imaging should be requested based on clinical findings.

A “Pan Scan” is usually a CT scan from the Head to the Pelvis in cases of severe trauma with multiple indicated injuries.

Head Injury in Trauma

The use of fluids in head injury in trauma is a special case. In the absence of head injury – fluids should only be given if the MAP is <65mmHg.

In head injury, we give fluids to maintain a SBP of >90mmHg.

This is to prevent secondary brain injury. 

• Primary brain injury – occurs at the time of the trauma – nothing can be done to reverse this!
• Secondary brain injury – occurs in the hours after the injury and can be prevented by following the ABCDE principles
  • Often caused by hypoxia and hypotension
  • ALWAYS give oxygen and maintain SBP >90mmHg

Prognositc Indicators in Head Injury

• High energy trauma – e.g. fall from height, high speed MVA
• Low level of consciousness at presentation
• Anticoagulation
• Diffuse brain injury on CT
• Hypotension
• Age – worse prognosis in older patients

Disposition of the Trauma Patient

Obviously depends on many factors! Severe trauma will often go straight to theatre and then onto ICU.

Patients with mild trauma, especially those with head injury, will usually be admitted to the trauma ward for observation, and the following day a Tertiary Survey is usually performed.

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Presentation

• An erythematous ‘eczema-like’ rash, usually unilateral.
• Itchy, inflamed nipple
• Burning sensation
• Discharge from the affect area
  • May also be discharge from the nipple related to the underlying cancer
• Inverted nipple

Pathology

Investigations and treatment

• In the penis it is extremely rare
• Primary cases do exist – and are treated with local excision

• Paget’s typically starts at the nipple and works outwards
• Eczema starts at the periphery of the areolar and works inwards

References

• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy

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Introduction

Pancreatic cancers are 95% exocrine, adenocarcinomas. These affect the duct or surround the duct. The remaining 5% are neuroendocrine tumours e.g. insulinomas, glucagonomas (the former being the more common). This article pertains to adenocarincoma, with the latter briefly mentioned at the end.

Typically, the more common adenocarcinoma occludes the pancreatic duct or branches of it. 70% occur at the head, causing (an initial) painless jaundice as the obstructed bile cannot flow through the sphincter of Oddi and refluxes back up through the biliary tree and into the blood. Tail tumours are more likely to be neuroendocrine than head tumours.

These tumours nearly always present late and nearly always have a terrible prognosis, with mean survival from diagnosis of 6-10 months depending on the presence or absence of metastases respectively. >80% have metastasised at diagnosis.

Epidemiology

• Increasing in incidence rising 4% per decade
• Nearly 9000 new diagnoses yearly in the UK
• 10^th most common cancer
• 5% of all cancer deaths but only 3% of all cancer diagnoses
• In excess of 8,000 annual deaths (2011 data, Cancer research UK)
• 5 year survival <2%

>90% have KRAS mutations, and many other mutations besides.

Risk factors

• Age (above 60s, very rare below 40)
• Smoking (RR 1.7)
• Diabetes mellitus
• Helicobacter pylori infection status (may be subclinical, often is)
• Partial gastrectomy
• Family history and genetics (<5% of cases)
• Obesity
• Male sex (RR 1.3)

Dubious but commonly asked by patients: red meat consumption, sugar intake, poor vegetation intake.

Note: whilst chronic pancreatitis is associated, alcohol and gallstones (a known proponent of chronic pancreatitis) per se are not associated with pancreatic cancer: contrary to the Oxford handbook of clinical medicine. Chronic pancreatitis is thought to be required for the dysplastic transformation (personal communication on wards).

Symptoms

• Pain is found in 70% of presentations (similar to that seen in pancreatitis – epigastric radiating to the back. Remember the pancreas is retroperitoneal apart from the tail, found in the splenorenal ligament)
• Anorexia and nausea
• Diarrhoea
• Cachexia
• Jaundice (obstructive picture with pale stools and dark urine)
• Itch (due to peripheral bilirubin)

Symptoms of advanced disease

• Pulmonary emboli – SOB, chest pain
• Diabetes mellitus – polyuria, polydipsia
• Ascites – abdominal fullness

Courvoisier’s law: in the presence of painless jaundice, a palpable gallbladder is unlikely to be due to gallstones. I.e potentially pancreatic cancer; it’s spread to the gallbladder already. Whilst pain is the most common presentation, painless jaundice is always sinister.

Thrombophelbitis/Trousseau’s sign: uncommon but can occur e.g. portal venous thrombosis.

On examination

• Typically: cachectic, jaundiced old patient presenting with abdominal pain/breathlessness/diarrhoea.
• Masses may be felt in the epigastric region – either hepatomegaly or gallbladder
• Ascites

Blood tests

• Obstructive jaundice picture (raised bilirubin and alkaline phosphatase, may have hepatocellular dysfunction too with raised ALT and AST)
• Hyperglycaemia
• Anaemia
• Hypokalaemia (if vomiting or diarrhoea)
• Hypercalcaemia (may be related to chronic pancreatitis or Trousseau’s sign of latent malignancy)
• CA19-9 is a tumour marker is 77% sensitive and 87% specific if significantly raised and is more likely to be raised if the cancer has metastasised.

Investigations

Typically

• US – sensitive to masses in the biliary tree and pancreatic ducts
• CXR – Can determine lung involvement
• Endoscopic US or biopsy
• If there is a suspicious mass on US, endoscopy can help confirm the diagnosis. Histology is not normally required for formal diagnosis.
• CT/PET staging

Treatment

The mainstay of treatment is palliative with significant analgesia required. Many patients ask for or are recommended palliative endoscopic stenting to help control their symptoms. Bilirubin itch is debilitating, but endoscopic stenting can provide a good remedy. Patients will often be on PCA (patient-controlled analgesia) and may attend hospital for symptomatic ascites drainage. <20% have an operative option available.

Surgery

• Whipple’s procedure (head) – a massive operation and rarely done, but potentially curative. A Pancreatoduodenectomy.
• Distal pancreatectomy (tail)

Chemotherapy

• Gemtacitabine (weekly IV infusion) prolongs median survival and improves QoL in some, but many do not wish for chemotherapy.

Radiotherapy

• Mostly reserved for adjuvant usage in potentially ‘curable’ tumours

Prevention

Low dose aspirin for 5 years has been shown to reduce the risk of pancreatic cancer by around 75%.
(Effect of aspirin on long-term risk of death due to pancreatic cancer: analysis of individual patient data from randomised trials. Rothwell et al 2011, Lancet)

Neuroen​docrine tumours

Glucagonomas and insulinomas are much rarer.

They can be watchfully waited upon, have RF ablation, surgically excised and so on. These can be associated with MEN-1, particularly insulinomas

References

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Pancreatitis is a condition involving inflammation of the pancreas. It can be acute or chronic; acute pancreatitis can return to normal after resolution of the episode, conversely chronic pancreatitis, is continuing inflammation, often with irreversible structural changes.

Acute Pancreatitis

Aetiology

Gallstones and alcohol account for the vast majority of episodes. The severity varies from mild self-limiting to extremely severe with extensive pancreatic and peripancreatic necrosis as well as haemorrhage. In its most severe form the mortality can be between 40-50%, as damage can result in the release of is lytic enzymes into the blood, contributing to severe shock and digestion of surrounding tissue. The causes of pancreatitis can be remembered with the acronym GET SMASHED:

• G – Gallstones
• E – Ethanol (alcohol!)
• T – Trauma

• S – Steroids
• M – Mumps
• A – Autoimmune – e.g. SLE
• S – Scorpion bites (rare!)
• H – Hypercalcaemia, hypothermia, hyperlipiaemia
• E – ERCP
• D – Drugs – e.g. azathiaprin

Pathogenesis

Necrosis >> Autolysis >> Infection >> Pseuodycyst
A theory suggests that the final common pathway has marked ↑ in intracellular calcium which → activation of intracellular proteases. There is evidence that alcohol interferes with calcium homeostasis in pancreatic acinar cells. In severe inflammation, it becomes swollen and haemorrhagic. Proteases digest the walls of blood vessel → blood extravasation; amylase is released into the blood (but is a non-specific diagnostic marker). Released lipases (better diagnostic marker) cause fat necrosis within abdomen and subcutaneous tissue, can → discolouration of skin (Grey Turner’s sign). The released fatty acids can bind Ca²⁺ can → hypocalcaemia.Concomitant destruction of adjacent islets can → hyperglycaemia and thus cause Type  II diabetes. Also, formation of abscesses and cysts within the pancreas or adjacent tissues can occur.Infection secondary to pancreatic tissue damage does not always occur. Not all cases of infection lead to cyst / pseudocyst formation.
Pulmonary failure in acute pancreatitis is believed to be caused by circulating activated digestion enzymes (e.g. trypsin, phospholipase A2, etc.) leading to a loss of surfactant, atelectasis and irritation eventually leading to ARDS and pleural effusion. Cardiac depression and breakdown of the blood brain barrier can also occur in severe AP and are possibly due to the same etiology.

Clinical features

Upper abdominal pain, normally beginning in the epigastrium accompanied by nausea and vomiting. As inflammation spreads in peritoneal cavity pain → more intense, involvement of the retroperitoneum frequently → back pain. In severe cases the patient may have tachycardia, hypotension and be oliguric. Abdominal examination may show widespread tenderness with guarding; also reduced/absent bowel sounds. Also periumbilical bruising (Cullen’s sign) and Grey Turner’ sign (flank bruising) if present show severe necrotising pancreatitis. Left sided pleural effusion, if present, is indicative of poor prognosis.

Diagnosis

• Blood tests will show raised serum amylase (may be many times norm level, important indication of pancreatic inflammation), lipase, also with raised urinary amylase. Amylase is not prognostic, nor is the level related to the degree of tissue damage Lipase levels are more specific and may relate to the level of tissue damage, but levels do not rise until up to 8 hours after the onset of symptoms.
• CXR to exclude gastroduodenal perforation, which also ↑ serum amylase. May show gallstones or pancreatic calcification.
• Ultrasound scan (USS) → find gallstones (biliary cause of pancreatitis), may also sow pancreatic swelling and necrosis.
• Contrast-enhanced spiral CT → assess extent of pancreatic necrosis + to detect complications such as abscess dev, fluid collection and pseudocyst formation.
• MRI (MRCP) assesses degree of pancreas damage and finds gallstones, can differentiate between fluid and solid inflammation.
• ERCP (Endoscopic Retrograde Cholangiopancreatography) used to look at pancreatic duct for inflammatory fibrosis or tumours, and pancreatic juice can be collected and biochemically examined.
• Operative biopsies or needle aspiration cytology under USS.
• APACHE (acute physiology and chronic health evaluation score) is a means of assessing the severity of a wide spectrum of illness, adjusted for age + obesity and other health problems, has a high sensitively as early as 24 hours after symptom onset. A score of >8 indicates severe disease
• The Glasgow scoring system can also be used to asses the severity and prognosis of pancreatitis. The modified version of the score can be remembered with the acronym PANCREAS:

• PO₂ Oxygen < 60mmHg or 7.9kPa
• Age > 55
• Neutrophilia White blood cells > 15
• Calcium < 2 mmol/L
• Renal Urea > 16 mmol/L
• Enzymes Lactate dehydrogenase (LDH) > 600iu/L Aspartate transaminase (AST) > 200iu/L
• Albumin < 32g/L
• Sugar Glucose > 10 mmol/L

Treatment

• Replace lost fluids (IV) and a urinary catheter might be necessary
• Nasogastric suction to prevent abdominal distension and vomitus and hence ↓ risk of aspiration pneumonia. Continuous oxygen administration may be necessary, depending on sats.
• Prophylactic antibiotics, broad spectrum e.g. cefuroxime or aztreonam ↓ infection complications
• Analgesia, pethidine and tramadol administered under patient control system
• Enteral nutrition, via nasojejunal tubes.
• In patients with multiorgan failure → ventilation and renal support, mortality rate >80%.
• Complications of acute pancreatitis:
  • Within the first week, the morbidity and mortality reflect the systemic inflammatory response, which in turn results in multiple organ failure. After this, the prognosis is related to the extent of pancreatic necrosis. Extensive necrosis (> 50%) is associated with high risk of further complications, which frequently need surgical intervention. Infection of the necrotic pancreas can lead to sepsis, resection of infected areas of pancreas may be needed. Some fluid collections will be surrounded by granulation tissue → pseudocyst, larger ones (> 6cm) may become infected or → intraperitoneal bleeding, thus need to be drained surgically.

Prognosis – The vast majority of patients with mild or moderate acute pancreatitis will make a full recovery. Severe acute pancreatitis patients may become pancreatically insufficient with respect to exocrine (malabsorption) and endocrine function (diabetes).

Chronic Pancreatitis

Aetiology

Pathogenesis

Possibly, due to inappropriate activation of enzymes within the pancreas, this has been demonstrated in the case of hereditary pancreatitis, where genetic abnormalities of cationic trypsinogen and its inhibitory proteins have led to unopposed trypsin activity within the pancreas. Chronic alcohol intake is also believed to ↑ the level of trypsinogen relative to its inhibitor, and human trypsinogen has a tendency to auto-activate → unopposed activity → damage pancreas.  It is believed that the intrapancreatic enzyme activity → precipitation of proteins within the pancreatic duct lumen in the form of plugs. These form a starting point for calcification and also → ductal hypertension → further pancreatic damage. Cytokine activation and oxygen stress → perpetuate this process, via inflammation.  Clinical features Pain: usually epigastric often radiating through into the back, it may be episodic. Exacerbations may follow further alcohol excess. During periods of abdominal pain, weight loss may be severe. Malabsorption and diabetes by develop due to exocrine and endocrine insufficiency respectively. Jaundice secondary to common bile duct obstruction, may be a feature in a small number of patients.

Diagnosis

• ERCP (Endoscopic Retrograde Cholangiopancreatography) often shows distorted pancreatic ducts due to scar tissue resulting from chronic inflammatory process.
• X-Ray of upper abdomen often reveals flecks of calcification due to previous fat necrosis.
• Serum amylase and lipase levels are elevated.
• Faecal elastase levels will be abnormal in the majority of patients.
• PABA and pancreolauryl tests
• USS and contrast enhanced spiral CT, MRI with MRCP (magnetic resonance Cholangiopancreatography), which has replaced ERCP are used as in diagnosis of acute pancreatitis
•  Endoscopic ultrasound

Treatment

Combination of NSAIDs and opiate (tramadol) for pain relief. Trycyclic antidepressants e.g. amitriptyline are used for chronic pain. Oral pancreatic enzyme supplements reduce pancreatic stimulation (by -ve feedback) and hence intensity of pain. Pain does improve over time, after 6 to 10 years, 60% of patients are pain free. For patients with debilitating pain, surgical intervention is an option, with duct drainage and limited resection which can relieve pain in 80% of patients, but mortality of 5%. Endoscopic techniques can be used to improve pancreatic drainage. An acid suppressor (H₂-receptor antagonist or PPI) is also given, to compensate for decreased bicarbonate secretion. Despite this, a proportion of patients continue to malabsorb, due to inadequate mixing of pancreatic supplements with the food as well as the low pH in the duodenum.

Pancreatic enzyme supplements – pancreatin

Pancreatin consists of protease, lipase and amylase, which are inactivated by gastric acid and by heat. Supplements, therefore, must be taken with food (but not mixed with very hot food), and either concurrently with gastric acid suppression therapy (e.g. with cimetidine, a H₂-receptor antagonist or a proton pump inhibitor) or as enteric-coated formulations. Pancreatin preparations in clinical use are of porcine origin. Dosage is adjusted according to the size, frequency and consistency of stools.

Unwanted effects include irritation of the mouth and perianal skin, nausea, vomiting and abdominal discomfort. Some higher-strength formulations should be avoided in children under 15 years of age with cystic fibrosis, since they have been associated with the formation of large-bowel strictures. Thus, the amount of pancreatin given has to be balanced with the side effects. For example, to reduce the side effects, the amount of pancreatin given has to be reduced; which in turn means the amount of total dietary fat consumed has to also be reduced, to avoid steatorrhoea.

Complications

Same as acute pancreatitis, pseudocyst formation etc. Also, formation of ascites, accumulation of serous fluid in the peritoneal cavity and occasionally pleural effusions.

Steatorrhoea

Passage of fat in large amounts in the faeces (up to 30 mmol per 24 hours), due to failure to digest and absorb it, is associated with pancreatic insufficiency. This will usually improve with pancreatic enzyme supplements, e.g. pancreatin, and a low fat diet.

References

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• Hypertension
• Dyslipidaemia
  • High LDL and low LDL levels
• Diabetes
• Obesity
• FHx of arterial disease
  • Significant if a first degree relative had MI before the age of 55
• Smoking
• Age
• Male gender

Epidemiology

• Affects about 10-15% of the population
• Usually CAD (coronary artery disease) is also present. About 75% of patients will also have symptomatic CAD. In the other group of patients it is believed the CAD is masked by PVD, as the PVD prevents patients from exerting themselves to a degree which would initiate symptoms of CAD.

Presentation

The classical presentation involves:

• Pain in the calves on walking, relieved by rest
  • This pain is also known as claudication
  • The pain can occur anywhere along the leg, and down into the foot
  • Many patients do NOT present with classic claudication – often because they are not doing enough activity to induce the symptoms – particularly if they have another comorbidity that limits their activity.
• Pain may also occur when legs are raised (e.g. in bed), and abate when legs are lowered (e.g. by sitting)

The main differential is “spinal claudication” caused by impingement of the caudal equina by a spinal stenosis. This also classically causes pain in the back of the legs on exertion.

FUN FACT:

Claudication comes from the latin “to limp”, which itself derives from the Emperor Claudius – whom it was said walked with a limp

Examination

• Elevating the leg may cause it to go pale and cold, as well as causing pain.
  • Beuger’s angle <20’ – the leg will go pale and cold upon raising it 20’ off the couch.
• Increased vascular filling time – Upon lowering, the leg may become hot and red as reperfusion occurs. Perfusion time tends to be reduced (>15s)
• Oedema is not usually present
• There may be evidence of poor skin health due to poor perfusion, such as ulcers, dry scaly skin, cool peripheries and reduced capillary refill time
• Check the pulse in the foot (posterior tibial and dorsals pedis)
  • Palpable pulses indicate low likelihood of peripheral vascular disease
  • Absent pulses represent an increased chance of peripheral vascular disease
  • If you are unable to locate a pulse by hand, you can use a doppler probe to assess if significant blood flow is present in the artery
  • For more information, see Peripheral Vascular Exam

  

  An example of a doppler probe used for assessing peripheral pulses

Classification

Claudication – this is limb pain (inc aching, cramping and tired feeling of the legs) upon exertion. It most commonly occurs in the calves, but may also be present in the feet, thighs, buttocks and even arms. The distance a patient can walk before they experience symptoms is known as the claudication distance.

• Claudication could be thought of as ‘angina’ of the limbs
• Pain is usually relieved by rest
• As peripheral vascular disease progresses, the distance that a patient can walk reduces.

Can cause claudication / buttock pain at rest
Burning pain at night, due to elevation (which reduces limb perfusion), and is relieved by hanging the legs over the side of the bed (very poor prognostic sign!)
Patients may have:

• ‘Punched out’ ischaemic ulcers – usually on the toes and heels, rarely higher up the limb. These tend to occur after a localised traumatic event. They are often painful, but diabetic and alcoholic patients may not have pain.
• Gangrene – often black necrotic gangrenous tissue surrounds the punched out ulcer lesions. Infection of this areas can occur (wet gangrene).
• Reduced / absent peripheral pulses – start distally, and work your way up until you find the pulse
• Skin atrophy – in chronic disease
• Hair loss – in chronic disease
• Cyanosis
• Excessive sweating – due to overactivity of the sympathetic nerves
• Erectile Dysfunction – Leriche syndrome – the result of distal aortic disease. Other features of the syndrome are buttock pain, and pale, cold legs. Surgery may be useful to reduce symptoms in these patients
• Amputation – may be necessary in patients with very severe disease. Usually only performed in patients with severe unremitting leg pain + gangrene, to prevent sepsis. Amputation should be performed as distally as possible, ideally below the knee, as this provides the greatest flexibility with prosthetic replacement limbs, but must be high enough to provide sufficient perfusion to allow healing of the stump.  In many cases, above the knee amputation is likely to heal better.
  • Phantom limb pain is common, and usually treated with gabapentin. This is often used prophylactically, as this improves efficacy.

Investigations

The diagnosis can be made on the basis of a suggestive history and examination, in conjunction with an ABPI <0.9.

After diagnosis is made, typically a patient may be referred to the vascular team for further investigation, which would typically include a CT angiogram of the lower limb.

• Arterial duplex ultrasound is an alternative to CT angio but is highly dependent on operator skill

ABPI – Ankle-Brachial pressure index

This is a measure of the ratio of the blood pressure in the ankle vs the arm. As peripheral vascular disease affects the legs more than the arms, it can be used as an indicator of reduced arterial blood flow in the legs.

With the patient lying flat on the couch:

• Measure the blood pressure in both arms and take the highest value
• Measure the blood pressure in both ankles and take the highest value
  • Instead of the stethoscope, use a Doppler ultrasound probe to measure the pressure over the posterior tibial artery – record the pressure when your hear the first ‘whoosh’
• Using only systolic values, divide the ankle pressure by the brachial pressure
• A normal value is >1
• A value of <0.9 is pathological for limb ischaemia (PVD). The lower the number, the greater the degree of PVD
• Pain at rest – ABPI = <0.6
• High Risk of gangrene – ABPI – <0.3, or ankle systolic pressure <55mmHg
• CAUTION – in very severe arteriosclerosis the vessels are incompressible, and thus falsely high readings may be obtained (e.g. an ABPI >1.3)

Investigate for Diabetes

Bloods

• HbA1c
• Lipids
• U+E’s
• ESR/CRP – to exclude arteritis
• ECG – to check for cardiac involvement
• Platelets and clotting

Arterial imaging

• Should be performed to assess the extent of the disease
• E.g. CT angiography (aka arteriography), DSA (digital subtraction arteriography), colour duplex imaging

Differentials

The most likely differential diagnosis is a neurological cause – typically compression of the spinal cord due to spinal stenosis – sometimes referred to as neurogenic claudication. This can cause a similar pattern of pain on activity in the buttocks, radiating down the legs, alleviated by rest.

• PVD – pain starts in calf and typically radiates up the leg
• Neurogenic claudication – pain typically starts in the buttock and radiates down the leg

Management

A diagnosis of peripheral vascular disease is confirmation that the patient has cardiovascular disease. Thus, as well as treating the peripheral vascular disease, many of the treatments are aimed at reducing other complications of cardiovascular disease (such as stroke and MI).

The aim of PVD treatment is to improve the walking distance and lower limb circulation.

• There are no medications that are proven to improve the symptoms of intermittent claudication
• Walking therapies – can be as effective as surgery at improving symptoms

Medical management

All patients should be given:

• Statin (e.g. atorvastatin 40mg nocte) regardless of cholesterol levels
• Control hypertension – for example an ACE-inhibitor (e.g. ramipril 5mg daily) or a calcium channel blocker (e.g. amlodipine 5mg daily)
  • β-blockers should be avoided, but are typically safe unless PAD is very severe
• Antiplatelet agent –  aspirin 100mg daily or clopidogrel 75mg daily – can improve claudication distance and reduce other symptoms.

Lifestyle factors

• Stop smoking
• Lose weight – aim for BMI 18.5 – 24.9
• Increase exercise – e.g. 30-60 mins, 5x week – often undervalued as a treatment. May increase the claudication distance, and improve QoL. Thought to be beneficial by increasing collateral circulation, improved endothelial compliance (i.e. better vasodilation to overcome the lumen narrowing and improve blood flow), decreased blood viscosity.
  • May be as effective as surgery
  • Explain to patients to walk until limits by claudication, rest until symptoms resolve, and then try again
  • If patients find stopping in the street frequently embarrassing – try recommending they do their exercises at a shopping mall – where frequent stopping is more socially acceptable!
  • 1/3 of patients will improve
  • 1/3/ will stay the same
  • 1/3/ will get worse
• Symptom management
  • Raising the pillow 4-6 inches can help keep the legs below heart level and reduce leg pain at night
  • Avoid cold weather if possible
  • Foot care – encourage self inspection daily for lesions, with prompt treatment. Careful washing of the feet everyday with thorough drying

Control of risk factors

• Screen for and treat diabetes if present
• Patients with known cardiovascular disease are automatically considered high risk for diabetes

Surgical Interventions

Surgical treatments are typically reserved for patients with very severe symptoms or where tissue destruction is present.

Indications for specialist referral include:

• Lifestyle limiting claudication
• Pain at rest
• Gangrene

Percutaneous Transluminal angioplasty – PTA – is useful for short lesions (usually <5cm) in big arteries. A balloon is used to widen the artery, which in some cases, may be enough on its own. In many cases, a stent is also placed. Particularly useful in iliac artery disease (successful in 75-90% of patients), and also successful in 50-70% of thigh and calf disease patients.

• PTA is not good for long lesions. These are more likely to occur in diabetic patients.
• Selection of patients is usually based on arterial imaging.
• PTA can result in thrombus formation and subsequent embolisation
• Reccurrence is about 30% at 3 years

Surgery – thromboendarterectomy and bypass grafting

• Is suitable for some patients. These are usually those with an obvious blockage, where the distal vessel is still filled by collateral vessels (indicating that the distal vessel is still in good shape) – similar to the indications for PTA – however patients must be able to tolerate surgery. May be used in those in whom PTA was not successful.
• These patients may receive a bypass graft. These are usually made from venous tissue, but prosthetic structures are also used.
  • Aspirin improves the longevity / patency of prosthetic grafts
  • Warfarin may be required after graft surgery in venous grafts
• Sympathectomy may be used to relieve pain. This can be chemical or surgical, but as they are equally effective, and generally used in those who can’t tolerate other surgery, chemical sympathectomy is much more widely performed. Particularly useful in diabetic patients.

Other Interventions

Limb Compression

• May help those with severe disease who are not candidates for surgery.
• Inflatable cuffs are placed over the limb and inflated rhythmically for a period of 1-2 hours, several days per week
• This is thought to improve both venous and arterial flow, thus reducing symptoms, but evidence is poor

Flashcard

References

• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy
• Peripheral Vascular Disease – Health Pathways

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• introduce yourself
• wash your hands
• check you’ve got the right patient

Inspection

• Is the patient in any pain?
• Check around the bed
  • Mobility aids
  • O2
  • Cigarettes
  • Medication
• Look for any general signs – e.g. heart failure, cyanosis, pallor

Hands

• Tar staining
• Palmar xanthomas
• Capillary return – Press for at least 2-3 seconds – then check the return appears within 2 seconds
• Radial pulse – comment on the rate, rhythm and character. Also check for radio-radial delay – this is a sign of co-arctation of the aorta.
• Do the blood pressure in BOTH arms

Face

• Eyes – look for xanthelasma, arcus and conjunctival pallor
• Mouth – look for central cyanosis and angular stomatitis
• Caroitd pulse – check it and comment on the character!

Abdomen

• Look for obvious pulsations and masses
• Look for scars
• Check the AA – is it pulsatile (normal) or expansile (abnormal). The aorta bifurcates at approximately the level of the umbilicus

Leg inspection

• Swelling
• Discoloration
• Scars
• Dressings
• Pallor
• Missing hair / nails / toes
• Ulcers
• Dry skin
• Just have a good look and feel of the legs and toes. Make sure you look between the toes and lift up the feet.
• Compare the temperature with the back of your hand – do this at 3 separate places on each leg

Leg palpation

• Temperature – compare both legs using the back of your hand. Compare in several different places
• Sensation – ask the patient to close their eyes, and then touch them in a couple of different places on their feet. Ask them to say where/when they feel it
• Capillary refill – same as for the hands
• Pulses – check that these are normal / absent / reduced – comment on what you find
  • Dorsalis pedis
  • Posterior tibial
  • Popliteal – take the weight of the patients legt with both hands and feel into the popliteal fossa
  • Femoral

• Lift up the legs for 30s to 1 min, and see if they go pale
• If they do, then ask the patient to then sit up and drop the leg over the side of the bench. If the leg then turns red/purple then this is a positive test and the patients has reflex hyperaemia which is present when there is poor peripheral circulation
• Reflex hyperaemia occurs when there is dilation of the peripheral blood vessels when the leg is raised in response to the fall in bp. Then when the leg is lowered, the massively dilated blood vessels suddenly fill causing the leg to go a red/purple colour

Auscultation

• Renal bruit
• Femoral bruit
• Aortic bruit
• Carotid bruit

To finish

• Thank the patient
• Aks if they have any questions
• Allow them to re-dress in private
• Mention any further possible tests:
  • FBC – anaemia
  • U+E’s – renal failure
  • Blood sugar – diabetes

References

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• Change of Bowel habit – constipation, diarrhea, tenesmus
• Rectal bleeding
• Perianal symptoms e.g. pain/itching/discharge
• Urinary symptoms in men (for BPH)
• Assessment of anal tone in neurological exam

Introduction

• Introduce yourself, check you have the right patient, explain procedure; “will involve examining back passage with a finger”
• Explain WHY you are doing the procedure!
• Get verbal consent
• Alcohol gel hands!
• Get a chaperone if opposite sex and advised still if same sex.

Preparation

• Get patient to roll onto left hand side with knees up to chest. (Always examine from right hand side!)
• Collect equipment:
  1. Clean tray
  2. Gel (lubricant)
  3. Gloves
  4. Gauze (for wiping)

Inspection

• Put gloves on
• Look for…
• Fissures; normally at 6 o clock or 12 o clock position. Found in Crohn’s or constipation
• Fistula; consequence of abscess or a complication of Crohn’s.
• Discharge; mucus, blood, faeces
• Abscesses; red, painful, swollen
• Skin tags; can be normal or indicative of Crohn’s or previous hemorrhoids
• Hemorrhoids; 1^st degree- remain in rectum, 2^nd degree- prolapse through but spontaneously reduce, 3^rd degree- as for 2^nd but require digital reduction, 4^th degree- remain prolapsed persistently.
• Prolapse
• Cancer/polyps; on anal ring
• Excoriation; sore, red skin from mechanical abrasion (e.g. wiping!), perhaps in diarrhoea.
• Anal warts; STD

Examination

• Inform patient you are going to examine with your finger now
• Put blob of lubricant on finger
• With your left hand, raise up the patient’s right buttock.
• Insert finger, firstly assessing sphincter tone (hyper/hypotonic). If hypertonic and is difficult to insert finger, patient may be anxious and can ask patient to take a deep breath.
  • Hypertonic – Crohn’s disease, Fissure, stricture, nerves
  • Hypotonic – Old age, nerve damage, Muscle damage
• Insert whole of finger in. if you are having trouble, then ask the patient to take a deep breath, or to push, as if they are going to the toilet. If the patient lets out a gasp of pain, stop the examination! This is likely to indicate the presence of a fissure.
• Feel for what is in the rectum/anal canal; is it empty? Full of compact material?
• Feel posteriorly
• The feel each side systematically
• Feeling for any polyps; will feel soft and mobile or cancers; fixed, hard, irregular, lumpy. Describe according to site, size, shape, smoothness, surface, surroundings.
• To feel anterior part you must bend down! And twist finger round. Can feel prostate in men, cervix in women.
• Prostate; walnut sized, 2 lobes, separated by sulcus. In prostatic cancer you lose the sulcus.
• In a woman, you are likely to feel in the region of the cervix when you feel anteriorly.
• At the end, take out finger, and look at it; check if any blood, faeces, mucus
• Can take swab if necessary.
• Wipe the patients or ask them to wipe themselves (use your discretion).
• Take off glove, thank patient
• Wipe bottom with swab (if young just hand it to them to do themselves)
• THANK PATIENT! And WASH HANDS!

Likely Findings

• Faecal loading (lots of faeces in the rectum). This is often found in the elderly. You may experience soft faces, or have difficulty passing your finger through hard faeces. Sometimes, faeces may mimic a rectal tumor, but in the case of faeces, you should be able to separate the lump from the rectal wall.
• BPH
• Prostatic cancer
• Rectal carcinoma – this is normally quite obvious.

References

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Primary Sclerosing Cholangitis (PSC) is a chronic inflammatory condition that results in the fibrosis and destruction of intra-hepatic and extrahepatic bile ducts. This can lead to cholestasis, hypertension and liver failure.

Epidemiology

• 75% of cases are associated with IBD (usually ulcerative collitis). In fact, in some cases, it may present before other features of IBD.
  • 5-10% of UC will also have PSC
  • 1% of Crohn’s patients will have PSC
• Genetic component – associated with HLA A1-B8-DR3 variant. This variant is associated with other autoimmune diseases (e.g. autoimmune hepatitis).
• Male predominance (2:1)
• Average age of onset: 25–40

Presentation

• Pruritis (itch)
• Jaundice
• Fatigue
• RUQ pain
• Weight loss
• Acute cholangitis – rare but can occur, typically after a medical procedure involving insertion of equipment into the biliary tree (e.g. ERCP)
• Hepatomegaly / splenomegaly – approx 50% of patients

Investigations

• P-ANCA – a serum antibody is found in 60% of cases
• LFT’s: ↑ALP, ↑bilirubin
• MRCP / ERCP – are able to visualise bile ductal abnormalities. ERCP is more sensitive than MRCP but obviously more invasive. Small but still clinically significant lesions may be missed.
  • Irregularly shaped lumens of intra and extrahepatic ducts can be seen
• Liver Biopsy – histology used to confirm the diagnosis:
  • Inflammation
  • Scar tissue Classical ‘onion skin’ appearance of scars around the bile ducts
  • Wide range of changes depending on stage of the disease from mild inflammatory infiltrate, to cirrhosis. The condition is slowly progressive.
• Antibodies – ↑IgM in 50% of patients, ↑IgG in 30% of patients

Complications

• Cholangiocarcinoma – 20-30% of patients
• Osteoporosis – treated in the normal manner

Prognosis

• In symptomatic patients, presentation to death (or liver failure) is 12 years on average.
• Asymptomatic patients survive an average of 15 years
• The majority of patients die from liver failure. 30% die from bile duct carcinoma, and a small number die from colonic or UC complications.

Treatment

• Liver transplantation is the only curative treatment. 5 year survival is 80-90%. PSC can recur in the transplanted liver.
• Other options – in a small minority of patients, the disease is mostly confined to the extra-hepatic ducts, in which case, balloon dilatation and stenting can be done endoscopically to reduce further damage.
• UDCA – a hydrophilic bile acid, used to prevent liver damage by reducing the number of cholestatic liver enzymes. This alters the metabolism of cholesterol and micelles, and makes them break down more readily. The evidence for its use in CF is patchy, but it is thought to reduce cholestasis and aid bile acid reabsoprtion, which help increase liver function.
  • However – clinical trials have shown no statistically significant benefit on outcome or symptoms.
• Management of pruritis – cholestrymanine can be used – the dose can be increased until symptomatic relief is achieved.
• Cholangitis – is a major problem. It is often treated with a broad spectrum AB (e.g. ciprofloxacin) , but there is no benefit of antibiotic prophylaxis.
• Fat soluble vitamins – A, D, E, K – vitamin replacement therapy is required in jaundice therapy.

Secondary sclerosing cholangitis

• Previous bile duct surgery resulting in stricture
• Stones in the bile duct, resulting in cholangitis
• AIDS – probably due to CMV infection

References

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