Surgery conditions Flashcards
Causes of peritonitis
Acute perf appendicitis (commonest under 45)
Acute perf diverticular (commonest elderly)
Upper Gi perf - peptic ulcer, carcinoma, traumatic (fish bone), ischaemic (gastric vulvulus)
Perforated tumour
Ischaemic bowel e.g. adhesion
Acute panc
Peritoneal dialysis
Post surgical intervention e.g. leak or injury
Can be primary via strep in blood stream ,(rare)
Management of peritonitis
Resuscitation
• Establish large calibre IV access.
• Catheterize and place on a fl uid balance chart.
• Send blood for FBC (Hb, WCC), U&E (Na, K), CRP, amylase, group
and save.
• ABGs if shocked or ischaemic bowel/pancreatitis suspected.
Establish a diagnosis
Most causes of acute peritonitis require surgery to correct them, but surgery
is contraindicated in most cases of acute pancreatitis.
Diagnostic investigations are indicated if the patient would otherwise be
a candidate for surgical intervention.
Blood investigations may show neutrophilia, i CRP.
• Raised amylase may suggest pancreatitis.
• Abdominal CT scanning is the investigation of choice for diagnosis.
It should reliably exclude acute pancreatitis and often locate the
probable source of the pathology.
• Laparoscopy is occasionally useful in patients where a formal
laparotomy should be avoided if possible.
If still unsure abdo CT
Early IV abx if no clear diag e.g. metroidazole and cefuroxime
Management of condition
Diverticular, perforated tumor - operation to remove affected part
Causes of a right hypochondriac acute abdomen
• Right lower lobe pneumonia/ embolism • Cholecystitis • Biliary colic • Hepatitis
Causes of an epigastric acute abdomen
• Pancreatitis • Gastritis • Peptic ulcer • Myocardial infarction
Causes of left hypochondriac acute abdomen
• Left lower lobe pneumonia/ embolism • Large bowel obstruction
Causes of right flank acute abdomen
- Renal colic
* Appendicitis
Causes of umbilical acute abdomen
• Intestinal obstruction • Intestinal ischaemia • Aortic aneurysm • Gastroenteritis • Crohn’s disease
Causes of left flank acute abdomen
• Renal colic
• Large bowel
obstruction
Causes of right iliac fossa pain
• Appendicitis
• Crohn’s disease
• Right tubo-ovarian
pathology (abcess, PID, ectopic)
Hypogastric/ suprapubic pain causes
- Cystitis
- Urinary retention
- Dysmenorrhoea
- Endometriosis
Causes of left iliac fossa pain
• Sigmoid
diverticulitis
• Left tubo-ovarian
pathology
Severe pain out of proportion to clinical findings
Ischaemic pain
Abdo injuries from blunt trauma
Most frequent injuries are spleen (45%), liver (40%), and
retroperitoneal haematoma (15%). Blunt trauma may cause:
• Compression or crushing, causing rupture of solid or hollow
organs.
• Deceleration injury due to differential movement of fi xed and
non-fi xed parts of organs, causing tearing or avulsion from their
vascular supply, e.g. liver tear and vena caval rupture.
• Blunt abdominal trauma is very common in RTAs where:
• There have been fatalities.
• Any casualty has been ejected from the vehicle.
• The closing speed is >50mph.
Abdo injuries from penetrating trauma
stab wounds commonly involve the liver
(40%), small bowel (30%), diaphragm (20%), colon (15%).
small bowel (50%), colon (40%), liver (30%), and vessels (25%).
Initial management of abdo trauma primary survey
• Any patient persistently hypotensive despite resuscitation, for whom
no obvious cause of blood loss has been identifi ed by the primary
survey, can be assumed to have intra-abdominal bleeding.
• If the patient is stable, an emergency abdominal CT scan is indicated.
• If the patient remains critically unstable, an emergency laparotomy is
usually indicated.
Pertinant history questions abdo trauma - secondary survery
• Obtain from patient, other passengers, observers, police, and
emergency medical personnel.
• Mechanism of injury. Seat belt usage, steering wheel deformation,
speed, damage to vehicle, ejection of victim, etc. in automobile
collision; velocity, calibre, presumed path of bullet, distance from
weapon, etc. in penetrating injuries.
• Prehospital condition and treatment of patient.
Investigations in acute abdominal trauma
Blood and urine sampling Raised serum amylase may indicate small bowel
or pancreatic injury.
Plain radiography Supine CXR is unreliable in the diagnosis of free intraabdominal
air.
Focused abdominal sonography for trauma (FAST)
• It consists of imaging of the four Ps. Morrison’s pouch, pouch of
Douglas (or pelvic), perisplenic, and pericardium.
• It is used to identify the peritoneal cavity as a source of signifi cant
haemorrhage.
• It is also used as a screening test for patients without major risk
factors for abdominal injury.
Diagnostic peritoneal lavage (DPL)
• Mostly superseded by FAST for unstable patients and CT scanning in
stable patients. Useful, when these are inappropriate or unavailable, for
the identifi cation of the presence of free intraperitoneal fl uid (usually
blood).
• Aspiration of blood, GI contents, bile, or faeces through the lavage
catheter indicates laparotomy.
Catheter 1/3 below umbilicus to public sympysis
1L of saline injected then drained.
CT
• The investigation of choice in haemodynamically stable patients in
whom there is no apparent indication for an emergency laparotomy.
• It provides detailed information relative to specifi c organ injury and its
extent and may guide/inform conservative management.
Indications for resuscitative laparotomy (trauma)
Blunt abdominal trauma.
Unresponsive hypotension despite adequate resuscitation and no other
cause for bleeding found.
Indication for urgent laparotomy (trauma)
• Blunt trauma with positive DPL or free blood on ultrasound and an
unstable circulatory status.
• Blunt trauma with CT features of solid organ injury not suitable for
conservative management.
• Clinical features of peritonitis.
• Any knife injury associated with visible viscera, clinical features of
peritonitis, haemodynamic instability, or developing fever/signs of
sepsis.
• Any gunshot wound.
Gastric outlet obstruction Causes
PUD (scarring)
TB
Pyloric steonosis
Pancreatic pseudocyst
Gastric cancer any
Treatment gastric outlet obstruction
Medical
-PUD - oedema will settle with conserv so nasogastric suction, PPI, fluid and Es
Endoscopic baloon dilation
Pyloroplasty (+/-vagotomy (vagus nerve)) or partial gastrectomy
Signs and symptoms gastric outlet obstruction
Vomiting devoid of bile History of peptic ulcers or weigt loss Wasting and dehydration Visible peristalsis Succussion splash in LUQ
Causes of small bowel obstruction
Adhesions
Hernia
Large bowel cancer
CD
Rarer Volvulus Intersussception Mesenteric infarction Gallstone ileus
Symptoms of small bowel obstruction
Absolute constipation
Abdominal distension
Abdominal pain
+/- vomiting (faeculent)
Signs of small bowel obstruction
Visible peristalsis Visible hernias Tinkling dehydration Tachycardia Hypotension Fever Tenderness Scars Think cause
Investigations into small bowel obstruction
CT
Barium meal
Colonoscopy
Management small bowel obstruction
Medical
Resusictation - fluids and Parenteral nutrition
NBM
Urinary catheter
60-70% of adhesional obstructions resolve spontaneously
Operative - fever, peritonitis, failure to resolve, hernia
How is presentation of large bowel obstruction different from small bowel?
Rarely vomiting unless ileocaecal valve dysfunction
Interval between pain is longer
Causes of large bowel obstruction
Cancer
Diverticulitis
Sigmoid vulvulus - constipation, hypothyroidism, congential abnormality
Caecal volvulus - development failure with adhesion or mass
Causes upper GI haemorrhage
Peptic ulcer Oesophageal varices Oesophgeal ulceration Oesophageal trauma (Mallory- Weiss tear) Vascular malformation (Dieu La Foy) - tortuous stomach artery that erodes and bleeds Gastric carcinoma Aortienteric fistula (fatal)
Upper GI haemorrhage emergency management
Resuscitation
• Establish large calibre IV access; give crystalloid fl uid up to 1000mL if
tachycardic or hypotensive. Only use O –ve blood if the patient is in
extremis; otherwise wait for cross-matched blood if transfusion needed.
• Catheterize and place on a fl uid balance chart if hypotensive.
• Send blood for FBC (Hb, WCC), U&E (Na, K), LFTs (albumin), crossmatch
(at least 3U if haematemesis large), clotting.
• Always consider alerting HDU/ITU if very unwell.
• Monitor pulse rate, BP, and urine output (urinary catheter).
• Insertion of a Sengstaken–Blakemore gastro-oesophageal tube may be
a life-saving resuscitation manoeuvre.
Establish a diagnosis
• Urgent OGD is the investigation of choice (at least within 24h).
• May require ongoing resuscitation with anaesthetist present.
• Allows diagnosis and biopsy if appropriate.
• May allow therapeutic interventions including adrenaline injection,
heater probe coagulation, banding of varices, clipping vessel.
• Angiography.
• Occasionally suitable for active bleeding due to invasive
intervention done in radiology department.
• May allow selective embolization in some patients with recurrent
bleeding.
Early treatment of upper GI haemorrhage
• Give IV PPI (e.g. omeprazole 40mg IV); stop all NSAIDs.
• Blood transfusion if large volume haematemesis or drop in Hb.
• Ensure the appropriate surgical team knows of the patient in case
surgical intervention is required.
• Known or suspected liver disease—consider FFP to correct clotting.
• Surgery may be required if:
• Massive haemorrhage requiring ongoing resuscitation.
• Failed initial endoscopic treatment with ongoing bleeding.
• Rebleeding not suitable for repeated endoscopic treatment.
Score for predicting mortality of acute upper GI bleed
Rockall score 0 1 2 Age (y) <60 60–79 >80 Shock None HR >100bpm Systolic BP <100mmHg Comorbidities None Cardiac Hepatorenal disease Carcinoma
Commonest causes of rectal bleeding/ lower GI bleed
Piles UC Cancer Anorectal fissure Angiodysplasia Diverticular disease Ischaemic collitis Meckles Intersusseption Massive Upper GI bleed CD trauma
Anorectal Bright red blood, on the surface of the stool and paper, after defecation. • Haemorrhoids. • Acute anal fi ssure. • Distal proctitis. • Rectal prolapse. Rectosigmoid Darker red blood, with clots, in surface of stool and mixed. • Rectal tumours (benign or malignant). • Proctocolitis. • Diverticular disease. Proximal colonic Dark red blood mixed into stool or altered blood. • Colonic tumours (benign or malignant). • Colitis. • Angiodysplasia. • NSAID-induced ulceration.
Emergency management rectal bleeding
Resuscitation
• Establish large calibre IV access; give crystalloid fl uid up to 1000mL
if tachycardic or hypotensive.
• Catheterize and place on a fl uid balance chart if hypotensive.
• Send blood for FBC (Hb, WCC), U&E (Na, K), LFTs (albumin), group
and save, clotting.
Establish a diagnosis
• Rigid proctosigmoidoscopy should be performed in all cases to
exclude a simple anorectal cause.
• Urgent fl exible sigmoidoscopy and colonoscopy may be undertaken. It
is higher risk than elective endoscopy, but may confi rm an origin and
may allow therapeutic intervention (adrenaline injection, heater probe
coagulation, argon plasma coagulation (APC)).
• Urgent selective mesenteric arteriography for obscure or persistent
bleeding; needs active bleeding of 0.5mL/min.
• Urgent gastroscopy should be used to exclude massive upper GI
bleeding if suspected.
Early treatment Consider blood transfusion if major bleed (persisting
haemodynamic instability despite resuscitation, Hb <8g/dL).
Definitive management of rectal bleed from anorectal, acute colitis, diverticular disease, angiodysplasia, undiagnosed
Anorectal causes Most can be controlled by local measures, such as
injection, coagulation, or packing.
Acute colitis
• IV or PO metronidazole if thought to be infective until organism
identifi ed.
• IV hydrocortisone 100mg qds if thought to be ulcerative or Crohn’s
colitis.
• Surgery may be necessary whatever the aetiology if bleeding persists
(subtotal colectomy and ileostomy formation).
Diverticular disease
• IV antibiotics (cefuroxime 750mg tds + metronidazole 500mg tds).
• Angiographic embolization if bleeding fails to stop and patient not
critically unstable for time in radiology.
• Surgery is high risk, but may be unavoidable. If the location is known,
a directed hemicolectomy may be performed (on-table colonoscopy
may be used). If not, a subtotal colectomy is safest.
Angiodysplasia
• Colonoscopic therapy (injection, heater probe, APC) is ideal.
• Angiographic embolization may be possible.
• Right hemicolectomy is occasionally unavoidable.
Undiagnosed source
Rarely, the patient remains unstable with active bleeding and no cause can
be reliably confi rmed. Surgical options to deal with this include:
• On-table colonoscopy with washout via colostomy to locate bleeding
source.
• Formation of mid-transverse loop colostomy and subsequent targeted
hemicolectomy.
• ‘Blind’ hemicolectomy (left if signifi cant diverticular disease present;
right if no other cause obvious and angiodysplasia is likely).
Acute lower limb ischaemia definition
Any sudden decrease in limb perfusion that causes a \
potential threat to viability.
Causes of acute limb ischaemia
Acute thrombosis in a vessel with pre-existing atherosclerosis
(60% of cases)
• Predisposing factors are: dehydration, hypotension, malignancy,
polycythaemia, or inherited prothrombotic states.
• Features suggestive of thrombosis are:
• Previous history of intermittent claudication.
• No obvious source of emboli (see below).
• Reduced or absent pulses in the contralateral limb.
Emboli (30% of cases)
• Eighty per cent have a cardiac cause (AF, MI, ventricular aneurysm).
• Arterial aneurysms account for 10% of distal emboli and may be from
the aorto-iliac, femoral, popliteal, or subclavian arteries.
• Rarely, acute thrombosis in pre-existing atherosclerosis (see above)
will embolize.
• Commonest sites of impaction are the brachial, common femoral,
popliteal, and aortic bifurcation (‘saddle embolus’).
• Features suggestive of embolism are:
• No previous history of claudication.
• Presence of AF or recent MI.
Rare causes
• Aortic dissection, trauma, iatrogenic injury, peripheral aneurysm
(particularly popliteal), and intra-arterial drug use.
Symptoms of acute limb ischaemia and complications
Six Ps:
• Pain, pallor, pulselessness, paraesthesia, paralysis, perishingly cold.
death (20)
Loss of limb
Management of acute limb ischaemia
Remember, patients will usually have coexisting coronary, cerebral, or
renal disease.
Resuscitation
• Give 100% O2.
• Get IV access and consider crystalloid fl uid up to 1000mL if
dehydrated.
• Take blood for FBC, U&E, troponin, clotting, glucose, group and save.
• Request CXR and ECG (look for dysrhythmias).
Give opiate analgesia (5–10mg morphine IM).
• Call for senior help.
Establish degree of urgency
• Limb viability assessment. Involve senior help early.
• Irreversible. Fixed mottling of skin, petechial haemorrhages in skin,
woody hard muscles.
• Immediate treatment needed. Muscles tender to palpation/swollen,
loss of power, loss of sensation.
• Prompt treatment after investigation. Pulseless, pale, cold, reduced
capillary refi ll.
Treatment of all patients
Give heparin (5000IU unfractionated heparin IV bolus and start an infusion
of 1000IU/h) if there are no contraindications (e.g. aortic dissection,
multiple trauma, head injury).
• Recheck APTT in 4–6h.
• Aim for a target time of 2–2.5 x the normal range.
Defi nitive management
Depends on the severity of ischaemia (as above) and there are three
broad categories.
• Irreversible (non-salvageable limb). Amputation is inevitable and urgent
(but not emergency).
• Immediate treatment needed (to prevent the systemic complications
of muscle necrosis—hyperkalaemia, acidosis, acute renal failure, and
cardiac arrest). Consider amputation if ischaemic changes advanced
and life-threatening. Surgery to revascularize limb and perform
fasciotomies (to prevent or treat compartment syndrome).
• Prompt treatment after investigation. Continue heparinization.
Angiogram (stop heparin 4h before) or duplex/CT angio to determine
cause/location of disease. Thrombolysis, angioplasty, arterial surgery,
or combination. Limb may remain viable and functional after period of
heparinization alone.
Cause of carotid artery disease
Colour duplex scan (all patients with stroke)
If it fails then MRA or CTA
Presentation of carotid artery disease
Stroke/ TIA
Crescendo TIA - rappidly recurring with increased frequency due to unstable plaque with ongoing platelet aggregation and small emboli
Completed stroke - the stable end result of an acute stroke lasting over 24hours
Stroke in evolution - progressive deficit over hours/ days.
Amaurosis fugax - transient monocular visual loss - curtain coming down lasting a few seconds or minutes to being permanent.
Hemianopia
Poor correlation between bruit and degree of stenosis or risk. No always present
Diagnosis
Colour duplex scan
If it fails then MRA or CTA
Treatment of carotid artery disease
Medical management
• Best medical therapy is an antiplatelet agent (e.g. aspirin,
dipyridamole), smoking cessation, optimization of BP and diabetes
control, and a statin (e.g. simvastatin 40mg daily) for cholesterol
lowering, irrespective of baseline cholesterol.
• Acute thrombolysis in CT-proven ischaemia indicated in specialized
units if detected early.
Surgery
Carotid endarterectomy (CEA)
• Offered to patients with symptomatic >70% stenosis of the ICA (not sig under 70%) or
>50% stenosis if recent TIA/CVA and high ABCD2 risk score (age, BP,
clinical, duration, diabetes).
• Urgent CEA within 2 weeks now considered for all patients presenting
of acute TIA/CVA.
Details of carotid end arterectomy
• Increasingly undertaken under local (LA) block.
• Incision anterior to sternomastoid.
• Carotid vessels controlled after dissection.
• IV heparin prior to trial clamp (if patient awake).
• Cerebral circulation protected in 10% of awake patients with a
shunt (Pruitt/Javed) (without an intact circle of Willis, there is not
enough collateral blood fl ow from the contralateral carotid).
• Shunt in GA patients, depending on surgeon preference and
cerebral monitoring (stump pressure of 50mmHg or transcranial
Doppler monitoring of middle cerebral artery blood fl ow).
• Patch closure of the arteriotomy common. Eversion
endarterectomy technique may avoid the need for a patch.
• Post-operatively, close monitoring of BP and neurological state.
Complications
Complications. • Death or major disabling stroke, 1–2%. • Minor stroke with recovery, 3–6%. • MI. • Wound haematoma. • Damage to hypoglossal nerve (weak tongue, moves to side of damaged nerve), glossopharyngeal nerve (diffi culty swallowing), facial numbness.
Predisposing features to mesenteric ischaemia
Age CVS factors Cocaine AF Emboli
Features mesenteric Ischaemia
Sudden pain (often at splenic fecture) - with eating and N/V
Rectal bleeding
Vomiting
Diarrhoea
Investigation mesenteric ischaemia
CT angio
MR angio
Transfermoral digital subtraction angio/aortogram
Assessment renal function, coronary circ, aneurysmal disease
COmplications mesenteric ischaemia
Acute intestinal ischaemia is less common due to the development of
collaterals although, if undiagnosed, loss of all visceral vessels results in
eventual pan-intestinal infarction.
• Chronic ischaemic strictures due to focally severe ischaemia.
Treatment of mesenteric ischaemia
Medical
• Stop smoking.
• Control of hypertension; treatment of any hyperlipidaemia.
• Aspirin 75mg od to prevent thromboembolic events.
• Control diabetes if present.
• Treatment of autoimmune disease if present.
Interventional
Commonest treatment for large vessel stenosis is radiologically guided
stenting. Risks converting stenosis to acute occlusion with the risk of precipitating
emergency surgery. Not possible if the stenosis is at the aortic
ostium of the vessel affected.
Surgical
• Rarely indicated. Commonest procedure is external iliac to ileocolic
artery side-to-side bypass.
• Overall prognosis is poor as the underlying disease process is often
widespread and progressive.
AAA epidemiology
Male
Associated with hypertension, tobacco smoking, and family history (all
associated with atherosclerosis).
AAA symptoms
asympto
True aneurysm vs false and causes
• True aneurysms. Contain all three layers of artery wall. May be fusiform
(symmetrical dilatation) or saccular. Underlying cause is usually
atherosclerosis-related, but may be associated with infective causes
(‘mycotic aneurysm’), Marfan’s and Ehlers–Danlos syndromes (collagen
and elastin abnormalities).
• False aneurysms. Do not contain all three layers of vessel wall and
often only lined by surrounding connective tissue or adventitia. Usually
secondary to penetrating trauma, including iatrogenic injury (e.g.
femoral cannulation, surgery).
Where are most AAAs
Ninety-fi ve per cent start below the origin of the renal arteries
(‘infrarenal’).
• Fifteen per cent extend down to involve the origins of the common
iliac arteries.
AAA screening programme
Men aged 65 US One off Small AAA then monitor yearly (3-4.4) (diatary advice can slow) Medium 4.5-5.4 then 4monthly Large then surgery
When is surgery indicated
• AP diameter >5.5cm in fi t individuals.
• Rapid increase in diameter on serial surveillance scans, e.g. >0.5cm
in 6 months.
Types of AAA repair and advantages/disadvantages
Elective surgery
• Open repair by inlay synthetic graft. May be ‘straight’ if aneurysm
confi ned to aorta or ‘bifurcated/trouser’ if there are common iliac
aneurysms as well; 3–7% operative mortality.
• Laparoscopic repair may offer earlier return to normal function and
reduced hospital stay.
Endovascular repairs
• Endovascular aneurysm repair (EVAR) with a stent graft. Percutaneous
insertion of covered stent to exclude the aneurysmal segment from
arterial pressure.
• Advantages. Percutaneous technique, reduced early mortality.
• Disadvantages. High early re-intervention rate, requires lifelong
surveillance, no long-term survival benefi ts over open repair shown to
date.
ruptured AAA symp
Symptoms
• Severe/sudden onset epigastric and/or back/loin pain.
• History of sudden ‘collapse’, often with transient hypotension.
• May have history of AAA under surveillance.
Signs
• Cardinal signs are unexplained rapid onset hypotension, pain, and
sweating.
• A pulsatile abdominal mass is not always easy to feel (due to pain and
abdominal wall rigidity).
Less than 50% reach hospital alive
mortality 75-96%
Emergency management
Resuscitation
• If the diagnosis is seriously considered, call for senior surgical
assistance immediately. Transfer to theatre may be required even as
resuscitation continues.
• ‘Permissive hypotension’. Do not ‘chase’ a ‘normal’ systolic BP to
reduce the risk of worsening the rupture.
• If the patient is critically hypotensive, consider calling a peri-arrest
cardiac emergency.
• IV access via two large bore cannulae, catheterize, cross-match blood
(10U), order FFP and platelets.
• High fl ow O2 via non-rebreathing mask.
• Give modest doses of analgesia (morphine 5–10mg).
• Alert anaesthetist, theatres, ITU.
• Witnessed verbal consent for surgery may be the only practical way
and is acceptable here.
Establish a diagnosis
• If patient stable and diagnosis uncertain, request contrast CT.
• If going to CT, ensure blood is sent for cross-match and IV access has
been established before going.
Principles of surgery for rupture
• Go straight to the operating table, not anaesthetic room.
• If unstable, muscle relaxation/anaesthesia is not started until patient is
prepared/draped and surgical team ready to go.
• If haemodynamically stable, central line and arterial line sited while
waiting for blood to arrive and surgical team in theatre.
• Give antibiotic prophylaxis.
• Proximal neck is controlled rapidly with aortic cross-clamping. Full
fl uid expansion with blood can now safely begin.
• Distal outfl ow of aneurysm is controlled.
• The sac is opened and lumbar vessels and inferior mesenteric artery
are oversewn to control back bleeding.
• Dacron/Gore-Tex® graft is sewn to proximal neck and tested.
• Distal anastomosis performed next and tested.
• Sequential reperfusion is undertaken accompanied with volume
expansion to minimize post-declamping shock. Ideally the systolic BP
should be maintained over 85mmHg.
• Blood products at this stage may be required to correct coagulopathy
(e.g. platelets and FFP).
• The sac is closed over the graft to reduce the risk of aortoenteric
fi stula.
Post-operative care
• Transfer to ITU.
• Normalize core temperature.
• Correct clotting and maintain Hb >10g/dL.
• Adequate analgesia and accurate fl uid balance.
• Attention to cardiac/renal/pulmonary dysfunction.
Complications of AAA rupture
- Death (overall up to 50% of operated cases).
- MI.
- Renal failure.
- Lower limb embolism.
- Gut ischaemia/infarction.
- Abdominal compartment syndrome.
Haemorrhoids pathophys/ epi
Low fibre, constipation, pregancy, develop in young adult, long time on toilet, exercise
What are haemorrhoids?
Normal cushions that help contain stool
Types and symptoms of haemorrhoids
Asymptomatic
INternal - perianal itch, bleeding, painless, mucous discharge and fecal incontinence possile. May prolapse requiring reduction
External - pain on defication/ wiping if thrombosed, swelling. May leave a skin tag. Rarely itching (hygiene related)
Location compared to dentate line
Management of haemorrhoids
Fibre, hydration, exercise, dont strain. Softner laxatives
topical analgesia (or oral NSAID) and coolants, supportive, rarely do surgery due to overexcision of anal tissue. Bed rest. Can do anal dilation under GA
Banding especially if prolapse (internal only)
Dilute phenol injections
HALO - haem arterial ligation. Doppler US guided. - vessels sutured
Stapled anopexy (PPH proceedure for)
Diagnosis of haemorrhoids
• Diagnosis is usually by rigid sigmoidoscopy and proctoscopy.
• Flexible sigmoidoscopy or colonoscopy may be appropriate if there
is concern about the cause of symptoms; remember—haemorrhoids
rarely start over the age of 55y and it is often best to assume another
cause until proven otherwise in these cases.
Complications from an ileostomy
Volume depletion
Lactic acdosis
Electrolyte imbalance
Social
What is a total mesorectal excision and why is it neccessary?
In the rectum a 2cm distal clearance margin is required and this may also impact on the procedure chosen. In addition to excision of the rectal tube an integral part of the procedure is a meticulous dissection of the mesorectal fat and lymph nodes (total mesorectal excision/ TME).
Which bowel cancer can get radiation therapy and why?
Rectal - extraperitoneal
Palliative options for cancer causing blockage?
Stent or defunction with a proximal loop stoma
Perianal fissure epidemiology and path
Spasming of the internal anal sphincter
Constipation, prolonged fiarrhea
Laterally: TB, occult abscess, leukemic infiltrates, carcinoma, AIDS, IBD
Childbirth
Anal sex
CD
UC
Treatment fissure
Topical diliazem or GTN
Injection of botulinum toxin into anal sphincter
High fibre diet and stool softners e.g. Glycerol Supps
