Surgery conditions Flashcards

1
Q

Causes of peritonitis

A

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)

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2
Q

Management of peritonitis

A

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

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3
Q

Causes of a right hypochondriac acute abdomen

A
• Right lower lobe
pneumonia/
embolism
• Cholecystitis
• Biliary colic
• Hepatitis
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4
Q

Causes of an epigastric acute abdomen

A
• Pancreatitis
• Gastritis
• Peptic ulcer
• Myocardial
infarction
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5
Q

Causes of left hypochondriac acute abdomen

A
• Left lower lobe
pneumonia/
embolism
• Large bowel
obstruction
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6
Q

Causes of right flank acute abdomen

A
  • Renal colic

* Appendicitis

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7
Q

Causes of umbilical acute abdomen

A
• Intestinal
obstruction
• Intestinal ischaemia
• Aortic aneurysm
• Gastroenteritis
• Crohn’s disease
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8
Q

Causes of left flank acute abdomen

A

• Renal colic
• Large bowel
obstruction

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9
Q

Causes of right iliac fossa pain

A

• Appendicitis
• Crohn’s disease
• Right tubo-ovarian
pathology (abcess, PID, ectopic)

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10
Q

Hypogastric/ suprapubic pain causes

A
  • Cystitis
  • Urinary retention
  • Dysmenorrhoea
  • Endometriosis
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11
Q

Causes of left iliac fossa pain

A

• Sigmoid
diverticulitis
• Left tubo-ovarian
pathology

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12
Q

Severe pain out of proportion to clinical findings

A

Ischaemic pain

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13
Q

Abdo injuries from blunt trauma

A

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.

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14
Q

Abdo injuries from penetrating trauma

A

stab wounds commonly involve the liver
(40%), small bowel (30%), diaphragm (20%), colon (15%).

small bowel (50%), colon (40%), liver (30%),
and vessels (25%).
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15
Q

Initial management of abdo trauma primary survey

A

• 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.

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16
Q

Pertinant history questions abdo trauma - secondary survery

A

• 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.

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17
Q

Investigations in acute abdominal trauma

A

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.

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18
Q

Indications for resuscitative laparotomy (trauma)

A

Blunt abdominal trauma.
Unresponsive hypotension despite adequate resuscitation and no other
cause for bleeding found.

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19
Q

Indication for urgent laparotomy (trauma)

A

• 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.

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20
Q

Gastric outlet obstruction Causes

A

PUD (scarring)
TB
Pyloric steonosis
Pancreatic pseudocyst

Gastric cancer any

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21
Q

Treatment gastric outlet obstruction

A

Medical
-PUD - oedema will settle with conserv so nasogastric suction, PPI, fluid and Es

Endoscopic baloon dilation
Pyloroplasty (+/-vagotomy (vagus nerve)) or partial gastrectomy

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22
Q

Signs and symptoms gastric outlet obstruction

A
Vomiting devoid of bile
History of peptic ulcers or weigt loss
Wasting and dehydration
Visible peristalsis
Succussion splash in LUQ
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23
Q

Causes of small bowel obstruction

A

Adhesions
Hernia
Large bowel cancer
CD

Rarer
Volvulus
Intersussception
Mesenteric infarction
Gallstone ileus
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24
Q

Symptoms of small bowel obstruction

A

Absolute constipation
Abdominal distension
Abdominal pain
+/- vomiting (faeculent)

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25
Signs of small bowel obstruction
``` Visible peristalsis Visible hernias Tinkling dehydration Tachycardia Hypotension Fever Tenderness Scars Think cause ```
26
Investigations into small bowel obstruction
CT Barium meal Colonoscopy
27
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
28
How is presentation of large bowel obstruction different from small bowel?
Rarely vomiting unless ileocaecal valve dysfunction | Interval between pain is longer
29
Causes of large bowel obstruction
Cancer Diverticulitis Sigmoid vulvulus - constipation, hypothyroidism, congential abnormality Caecal volvulus - development failure with adhesion or mass
30
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) ```
31
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.
32
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.
33
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 ```
34
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. ```
35
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).
36
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).
37
Acute lower limb ischaemia definition
Any sudden decrease in limb perfusion that causes a \ | potential threat to viability.
38
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.
39
Symptoms of acute limb ischaemia and complications
Six Ps: • Pain, pallor, pulselessness, paraesthesia, paralysis, perishingly cold. death (20) Loss of limb
40
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.
41
Cause of carotid artery disease
Colour duplex scan (all patients with stroke) | If it fails then MRA or CTA
42
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
43
Diagnosis
Colour duplex scan | If it fails then MRA or CTA
44
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.
45
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.
46
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. ```
47
Predisposing features to mesenteric ischaemia
``` Age CVS factors Cocaine AF Emboli ```
48
Features mesenteric Ischaemia
Sudden pain (often at splenic fecture) - with eating and N/V Rectal bleeding Vomiting Diarrhoea
49
Investigation mesenteric ischaemia
CT angio MR angio Transfermoral digital subtraction angio/aortogram Assessment renal function, coronary circ, aneurysmal disease
50
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.
51
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.
52
AAA epidemiology
Male Associated with hypertension, tobacco smoking, and family history (all associated with atherosclerosis).
53
AAA symptoms
asympto
54
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).
55
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.
56
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 ```
57
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.
58
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.
59
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%
60
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.
61
Complications of AAA rupture
* Death (overall up to 50% of operated cases). * MI. * Renal failure. * Lower limb embolism. * Gut ischaemia/infarction. * Abdominal compartment syndrome.
62
Haemorrhoids pathophys/ epi
Low fibre, constipation, pregancy, develop in young adult, long time on toilet, exercise
63
What are haemorrhoids?
Normal cushions that help contain stool
64
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
65
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)
66
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.
67
Complications from an ileostomy
Volume depletion Lactic acdosis Electrolyte imbalance Social
68
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).
69
Which bowel cancer can get radiation therapy and why?
Rectal - extraperitoneal
70
Palliative options for cancer causing blockage?
Stent or defunction with a proximal loop stoma
71
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
72
Treatment fissure
Topical diliazem or GTN Injection of botulinum toxin into anal sphincter High fibre diet and stool softners e.g. Glycerol Supps
73
Symptoms fissure
Acute severe, localized, ‘knife-like’ pain in the anus during defecation. Often associated with deep throbbing pain for minutes or hours afterwards due to pelvic fl oor spasm. Blood on the paper when wiping (small volume, red-pink streaks or spots).
74
Diagnosis of fissure
DRE painful often clinical
75
Fistula in ano location and epidemiology
A fi stula is an abnormal connection of two epithelial surfaces and the two surfaces joined in fi stula in ano are the anorectal lining and the perineal or vaginal skin. Very common, especially in otherwise fi t young adults. May occur in the presence of Crohn’s disease; minor association with obesity and diabetes mellitus, very rarely due to trauma or ulceration of anorectal tumours.
76
Fistula in ano pathology
Commonest cause is sepsis arising in an anal gland that forces its way out through the anal tissues to appear in the perianal or in women, vaginal skin (cryptoglandular theory of fi stula in ano). Often presents initially as an acute perianal abscess.
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Clinical features of fistula in ano
• Acute perianal abscess. Rapid onset of severe perianal or perineal pain. Swelling and erythema of the perianal skin with fever and tachycardia. • Recurrent perianal sepsis. Recurrent intermittent sepsis typifi ed by gradual build-up of ‘pressure’ sensation and swelling in the perianal skin and eventual discharge of bloodstained purulent fl uid. • Chronic perianal discharge. Persistent low grade sepsis of the track with chronic discharge of seropurulent fl uid via a punctum that is usually clearly identifi ed by the patient. Puritis Odor
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Diagnosis and investigation of fistula in ano
Diagnosis and investigation should aim to confi rm the presence of a fi stula and identify the course of the track to determine the type of fi stula: • Examination of the perineum and rectal examination may reveal a palpable fi brous track. • EUA with probing of any external opening to aid identifi cation of the course of the track. • Endoanal ultrasound (sometimes with hydrogen peroxide injected into the track) identifi es the course of the track. • MRI scanning is probably the most sensitive method of determining the course of the track and identifying any occult perianal or pelvic sepsis. • Flexible sigmoidoscopy if associated colorectal disease, e.g. Crohn’s disease, is suspected.
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Treatment of fistula in ano
Medical treatment • Antibiotics may reduce symptoms from recurrent sepsis, but cannot treat the underlying fi stula. • Medical treatment of infl ammatory bowel disease may dramatically reduce symptoms from associated fi stulas. Principles of surgical treatment are as follows: • Drainage of any acute sepsis if present. • Prevention of recurrent sepsis. Usually by insertion of a loose seton suture (allows drainage), e.g. silastic sling. • Low fi stula in ano. Lay open track, remove all chronic granulation tissue, and allow to heal spontaneously (fi stulotomy); little risk of impairment of continence due to minimal division of sphincter tissues. • High fi stula in ano: • Remove fi stula track and close the internal opening (core fi stulectomy and endorectal fl ap advancement). • Slowly divide the sphincter tissue between the fi stula and the perianal skin (cutting seton); low risk of incontinence. • Fill the fi stula with fi brin glue.
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Post op causes of pyrexia
Early causes of post-op pyrexia (0-5 days) include: Blood transfusion Cellulitis Urinary tract infection Physiological systemic inflammatory reaction (usually within a day following the operation) Pulmonary atelectasis - this if often listed but the evidence base to support this link is limited ``` Late causes (>5 days) include: Venous thromboembolism Pneumonia Wound infection Anastomotic leak ``` When considering causes of post-op pyrexia, it is helpful to consider the memory aid of 'the 4 W's' (wind, water, wound, what did we do? (iatrogenic).
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Which one of the following may be used to monitor patients with colorectal cancer?
Carcinoembryonic antigen may be used to monitor for recurrence in patients post-operatively or to assess response to treatment in patients with metastatic disease Discuss (2) Improve
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A 17-year-old man undergoes an elective right hemicolectomy. Post operatively he receives a total of 6 litres of 0.9% sodium chloride solution, over 24 hours. Which of the following complications may ensue?
Excessive infusions of any intravenous fluid carry the risk of development of tissue oedema and potentially cardiac failure. Excessive administration of sodium chloride is a recognised cause of hyperchloraemic acidosis and therefore Hartmans solution may be preferred where large volumes of fluid are to be administered.
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Risk of transfusion with plasma components in lung
Transfusion lung injury may occur after infusion of plasma components. Microvascular damage occurs in the lungs leading to diffuse infiltrates on imaging. Mortality is high.
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Complication of TPN
Although it may be infused peripherally, this may result in thrombophlebitis. Longer term infusions should be administered into a central vein (preferably via a PICC line). Complications are related to sepsis, re-feeding syndromes and hepatic dysfunction.
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INvestigation to see if anastomosis is goood
Gastrografin enema (barium more toxic)
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Wound dehiscence management
Wound dehiscence is a post-operative complication in which a wound ruptures along the surgical incision site. In this case, deep dehiscence has occurred as bowel can be seen protruding. This is an emergency and senior help should be called for immediately. Non-urgent senior review should be considered for superficial dehiscence. Applying pressure with dry gauze is inappropriate immediate management for this patient. However, a large sterile swab soaked in 0.9% saline can be used while waiting for senior help to arrived. Packing the wound can be considered for superficial dehiscence but is an inappropriate immediate management for this patient. Sepsis six protocol is a possibility and the patient's vital signs should be recorded after senior help has been called for.
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What is dumping syndrome?
Dumping syndrome, which can be divided into early and late, may occur following gastric surgery. It occurs as a result of a hyperosmolar load rapidly entering the proximal jejunum. Osmosis drags water into the lumen, this results in lumen distension (pain) and then diarrhoea. Excessive insulin release also occurs and results in hypoglycaemic symptoms.
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3 Features of an obstructed airway
See - Sternal recession, tracheal tug (thyroid cart moves down with each insp), see saw- A pattern of breathing seen in complete (or almost) complete) airway obstruction. As the patient attempts to breathe, the diaphragm descends, causing the abdomen to lift and the chest to sink. The reverse happens as the diaphragm relaxes. It is almost always associated with use of the accessory muscles of respiration and drawing in (recession) of the intercostal muscles of the chest wall. Feel - Breath movement in chest Listen - stridor/ stertor
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What is a massive blood transfusion?
Replacing 100% in 24hrs or 50% in 4 hrs
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FFP vs cryoprecipiatie?
Certain clotting factors vs all FFP can be used prophylactically if blood disorder as wll as major haemorrhage Cryo only in major blled and if fibroinogen <1.5g/litre (Prothrombin complex concentrate) if warfarin and sever bleed.
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Blood transfusion adverse efects
Acute Anaphylaxis Fluid overload Transfusion Related acute lung injury - O2 to ventilator support BBV Varied CJD Acute haemolytic transfusion reaction (mistmatch RBC) - fever, bleeding, hypotension - give blood components for bleeding, dopamine. Delayed (24h) Delayed haemolytic transfusion reaction Transfusion associated immunomodulation - (to leukocytes or proteins) - risk of infection, cancer recurrence or organ dysfunction. need Transfusion associated graft vs host disease Posttransfuion purpure - give steroids, plasmaphosesis Iron overload
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How much water in human
Male 60 | Female 50
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Who is eligable to give blood
``` >50 17-66 years Immunixations <4 weeks Complicated dental work Infectious disease BBV risk Anal sex ```
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Blood transfusion targets
 When using a restrictive red blood cell transfusion threshold, consider a threshold of 70 g/litre and a haemoglobin concentration target of 70-90 g/litre after transfusion.  Consider a red blood cell transfusion threshold of 80 g/ litre and a haemoglobin concentration target of 80-100 g/litre after transfusion for patients with acute coronary syndrome.
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NICE guidance on waterm K, Na, Cl and glucose maintainance
25-30 ml/kg/day of water and approximately 1 mmol/kg/day of potassium, sodium and chloride and approximately 50-100 g/day of glucose to limit starvation ketosis
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What are third space losses?
Interstitial space. Sequestration proportional to extent of tissue injury
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Maximum O2 flow through nasal specs
4L (35%)
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Potential order of O2 therapy
Nasal specs Venturi Non re breath (90%)
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What is in well's score?
``` Active cancer Treatment or palliation within 6 months No0 Yes+1 Bedridden recently >3 days or major surgery within four weeks No0 Yes+1 Calf swelling >3 cm compared to the other leg Measured 10cm below tibial tuberosity No0 Yes+1 Collateral (nonvaricose) superficial veins present No0 Yes+1 Entire leg swollen No0 Yes+1 Localized tenderness along the deep venous system No0 Yes+1 Pitting edema, confined to symptomatic leg No0 Yes+1 Paralysis, paresis, or recent plaster immobilization of the lower extremity No0 Yes+1 Previously documented DVT No0 Yes+1 Alternative diagnosis to DVT as likely or more likely ```
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Anxiety premed
Benzo (anterograde amnesia) Opiods Oral antihistamine in children
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Amnesia premed
Lorazepam or midazolam Especially useful in the young or those having repeated general anaesthetics. May allow a lighter depth of anaesthesia by reducing risk of awareness during surgery.
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Analgesia premed
Opioids, paracetamol and non-steroidal anti-inflammatory drugs reduce the required dose of anaesthetic agent and improve patient comfort in the immediate postoperative period. Caution must be taken when considering the use of cyclo-oxygenase-2 (COX2) inhibitors, because of their association with increased risk of myocardial infarction and stroke.[2] Opioids are the drugs of choice in the presence of acute pain. In the absence of pain, some people may experience intense dysphoria. Opioids also cause variable sedation and cardiorespiratory depression. All opioids cause nausea and vomiting and this may outweigh any beneficial effects. Opioids may also precipitate bronchospasm or anaphylaxis.
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Antivagal premed
TIVA with ketamine or awake fibre optic intubation E.g. hyoscine - anti sialogogues Amnisia and sedation also but can cause dry mouth and periop confusion
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Antiemetic premed
Are used either to reduce the emetic effects of anaesthetic agents (antihistamines, butyrophenones, hyoscine) or to enhance gastric emptying (metoclopramide). Those with a risk of regurgitation of gastric contents or undergoing procedures with a high incidence of nausea and vomiting (eg, laparoscopy) should receive agents to reduce gastric acidity. Can use H2-receptor antagonist or proton pump inhibitors several hours pre-operatively and oral sodium citrate 15-30 minutes before induction.
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List inducations for premed
Reduction of anxiety and pain. Promotion of amnesia. Reduction of secretions. Reduction of volume and pH of gastric contents (to avoid Mendelson's syndrome). Reduction of postoperative nausea and vomiting. Enhancing the hypnotic effects of general anaesthesia. Reduction of vagal reflexes to intubation. Specific indications - eg, prevention of infective endocarditis.
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Diagnosis of appendicitis
Over 65 do a CT abdo US in women of child baring age
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Blood supply of appendix
End artery (appendicular artery) off the ileocaecal
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Pathology and behaviour of herniae
• Reducible. Contents can be fully restored to the abdominal cavity, spontaneously or with manipulation. • Incarcerated. Part or all of the contents cannot be reduced due to a narrow neck and/or adhesions; there is a risk of strangulation. • Obstructed. Contains an obstructed bowel loop due to kinking; usually goes on to strangulation. Groin hernias rank third, after adhesive obstruction and cancer, as the most common cause of bowel obstruction in the west. In tropical Africa, strangulated external hernia is the commonest cause of intestinal obstruction. • Strangulated. Blood supply to the contents of the sac is cut off; the tight neck of the peritoneal sac is the usual site of strangulation. Pathological sequence Venous and lymphatic occlusion l oedema and i venous pressure l impeding arterial fl ow l bowel necrosis and perforation.
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Diagnosis of hernia
US | MRI/ CT (not for femoral)
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Management of inguinal hernia
YOung and symptomatic (dull ache or dragging especially end of day - linked to specific activity at onset) or irreducible then remove Elderly and immobile can leave Groin truss potential but not great
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Compare indirect and direct hernias
``` Indirect Direct Age Any age, but usually young Uncommon in children and young adult Aetiology Congenital (patent processus vaginalis) Acquired weakness in abdominal wall Relationship to inferior epigastric artery Lateral Medial Descending to scrotum Often Rarely Occluding the internal ring Controls it Does not control it Neck Narrow Wide Strangulation More likely Rare Treatment Infant—herniotomy (ligation and excision of the sac) Adult—open mesh repair, laparoscopic repair ```
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Contents of the inguinal canal
- Three vessels (testicular artery, cremasteric artery, artery to the vas). - Three nerves (genital branch of genitofemoral, autonomic supply to the testicle, ilioinguinal nerve). - Three structures (vas, pampiniform venous plexus, testicular lymphatics). - Three coverings (external spermatic fascia, cremasteric fascia, internal spermatic fascia).
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Anatomy of the deep and superficial rings
The deep ring is formed through the transversalis fascia and lies 1–2cm above the inguinal ligament, midway between the symphysis pubis and the anterior superior iliac spine. - The superfi cial ring is a V-shaped defect in the aponeurosis of external oblique, above and medial to the pubic tubercle.
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What is Hessebach's triagle
Direct inguinal hernias pass through a weakness in the transversalis fascia in the Hesselbach’s triangle area (bounded by inguinal ligament inferiorly, inferior epigastric artery laterally, and lateral border of the rectus muscle medially).
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Mid inguinal point vs midpoint of inguinal line?
Mid-inguinal point – halfway between the pubic symphysis and the anterior superior iliac spine. The femoral pulse can be palpated here. Midpoint of the inguinal ligament – halfway between the pubic tubercle and the anterior superior iliac spine (the two attachments of the inguinal ligament). The opening to the inguinal canal is located just above this point.
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Boarders of the inguinal canal
Anterior wall – aponeurosis of the external oblique, reinforced by the internal oblique muscle laterally. Posterior wall – transversalis fascia. Roof – transversalis fascia, internal oblique, and transversus abdominis. Floor – inguinal ligament (a ‘rolled up’ portion of the external oblique aponeurosis), thickened medially by the lacunar ligament.
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Treatment femoral hernias
All treated due to high rate of strangulation (bony/ ligaentous structures around entry)
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Anatomy of the femoral canal - boundariex
- Lies medial to femoral vein within femoral sheath. - Contains loose areolar tissue and a lymph node known as the lymph node of Cloquet. - The femoral ring is the abdominal opening of the femoral canal. The increased diameter of the true pelvis in females proportionally widens the femoral canal. - Boundaries to the femoral ring are: - Anteriorly, inguinal ligament. - Medially, lacunar ligament. - Posteriorly, pectineal ligament. - Laterally, femoral vein. - An aberrant obturator artery branch of inferior epigastric may cross the lacunar ligament and can cause haemorrhage during surgical repair.
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treatment of acute limb ischaemia
Heparin (after surgery) Thrombolyse or surgical embolectomy Risk of reperfusion injury
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The Fontaine classification of lower limb ischaemia
The Fontaine classifi cation of lower limb ischaemia • I. Asymptomatic. • II. Intermittent claudication. • III. Rest pain. • IV. Ulcers/gangrene. Grades III and IV = critical limb ischaemia.
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Describe rest pain in critical limb ischaemia
Buening relieved by hanging foot e.g. night
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What is Buerger's disease
x
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Diagnosis of intermittent claudication
Drop in ABPI after exercise Clinical diag Imaging only if intervention planned e.g. angiography with digital subtraction (DSA), CT angiogram or MRA Abdo US if anyeursm suspected
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Treatmetn IC
Lifestle Superfised exercise program to improve collarerals Endovasc angioplasty adn stent (best aorto iliac) (percutaneous transluminal angiopolasty) Graft e.g. aortobifemoral, femorofemoral , Endarterectorys Femoral distal etc..
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Sugns of PAD
``` Buerger's angle <20deg Delay cap refil Absent pilses COld white Atrophic Pinched out ulsers ```
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ABPI diagnosis of PAD vs CLI
0.5-0.9 vs 0.5
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Diagnopsis CLI
CLI also <50mmHg or rest pain 2 weeks or arterial ulceration or gangrene
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Cause of false normal result of ABPI
DM - calified vessels
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Imaging in PAD
Colour duplex US - | MR/ CT angio for planning oif opeation
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VV pathophysiology
Veins in leg between superficial and deep = perforator veins Valves become incompetant - blood from deep to superficial causing distention and increase in VBP.
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VV cause/ RFs
Primary mech failure (most): Standing, preggers, obesity, FH, OCP Secondary: Cycling (muscle action), obstruction e.g. DVT/ tumour, Av malformaiton
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VV symptoms/ comp
``` Cosmesis Pain Cramps Tingling Heaviness REstless legs (only slightly commoner with VV ```
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VV signs
``` Bleeding Ulceration Atrophy blanche (healed ulcers Lipodermatosclerosis - subcut sclerosis and lipid necrosis Tap test - felt at Saphenofemoral junction Eczema Oedema Haemosiderin Phlebitis ```
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What can mimic femoral hernia
Saphena varix | Increase with cough but blue tinge - dilation o fsaph vein
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Treatmetn of VVs
Refer if bleeding, phelbitis, ulceration, , impact on QoL Education - avoid standing, elevation, walks, weight loss Endovasc - radiofrequency, laser ablation, sclerotherapy Surgery - sa[henofemoral ligation
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Investigationsof ulcers?
Biopsy if vasculitis or malignant?
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Management of ulcers
Treat cause Prevention Lifestyle (drugs, smoking, DM) Specialist nursing Compression bandage if ABPO >0.8 Neg presure wound therapy for DM Surgery - debride Only use abx if ulceration
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Where venous
Above MM - gaiter - VHYT e.g. damage to deep valves e.g DVT
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What is Boerhaave syndrome
Rupture of oesophagus due to vomiting causing oesophageal perforation (mallory-weiss is only a mucosal tear) Can cause subcut emphasema, chest pain
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Ascites on AXR
Ascites is also seen, with mottled gas densities over bilateral paracolic gutters
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Pneumoperitoneum on AXR
Rigler's sign (double wall sign) may be seen on an abdominal film.
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Symptoms of bowel cancer
Change in stool habits (particularly left as its thinner) normally diarrhoea. ->6 weeks, >40years, no infection PR Bleeding (particularly right/ caecum as its longer until symptoms) Anaemia Constitutional symptoms e.g. anorexia, weight loss, malaise
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Describe the location of colorectal cancers
Most in rectum then sigmoid then caecum
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Explain genetic risk factors for bowel cancer
FAP - familial adenomatous polyposis. 100% of people have cancer by 40yrs so propylactic colonectomy AD (second commonest) HNPCC - Hereditary non-polypoposis colorectal cancer/ Lynch syndrome - other cancers too AD (suspect if cancer (commonest) Gardener's syndrome/ familial colorectal polyposis - AD, (variant of FAP with osteomas of skull and thyroid ca)
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Describe the pathogenesis of colorectal cancer
Adenoma - carcinoma change/ sequence | Stepwise pattern of activation of oncogenes and inactivation of TSG (p53).
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Describe how screened polyps are followed up
Removal during colonoscopy | >1cm or 2-3 polyps then 1yr follow up if not then 3yrs (depends on other factors too e.g. histology).
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Investiations into colorectal cancer
Routine bloods: FBC (anaemia), U&Es, Colonoscopy - if patient can't tolerate then do CT colonogram with contrast or a barium enema CT chest, abdo and pelvis/ Xray for mets/ staging (chest, abdominal, pelvic) Clotting, group and save If rectal then MRI to look for stage CEA - not diagnostic but to track progress/ success of operation
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Spread of colorectal cancer
Direct - normally through wall, may affect other structures such as other bowel, bladder, uterus Lymph - mesentary, paracolic, para aortic, pre aortic Vascular - liver and then lung
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Describe staging of colorectal cancer
``` Dukes A - Mucosa, submucosa, MP B - Serosa C 1- Lymph - paracolic 2 - Lymph terminal ``` ``` TNM T1-mucosa 2- submucosa 3- MP 4- Serosa N1 - 3 nodes M1 - mets ```
150
Management of colorectal cancer
Right/ transverse up to splenic = extended right hemicolectomy Sigmoid = high anterior resection Rectum = anterior resection Lower rectum/ anus= abdominoperineal resection APER Neo/adjuvant chemo if mets or rectall Hepatic or lung resection possible If not fit for surgery then - chemo-radio - Defunctioning colostomy if obstructive and palliative - stenting
151
Risk of bowel cancer surgery
``` Bleed Leak Stoma prolapse Ureter damage Bowel damage ```
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Treatment of CBD cancers
``` Hilar then liver resenction Middle third then resection of duct Periampullary then peri-pancreatoduodenectomy Palliative - ERCP/ stent Percutaeous drainage ```
153
Types of oesophageal cancer, risk factors and presentation
Clinically the same. SCC- anywhere, age, alcohol, smoking ACC- GORD, dietary nitrosamines - (acid, frying, beer), Barretts, lower 1/3
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Tx oesophageal cancer
Rarely resectable surgically | Palliative chemo 5FU of neoadjuvant
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Pharyngeal pouch pathophys
``` weakeness - killian's dihiscence Uncoordinated contraction of the cricopharyngeus. Occurs posteriorly Not a true diverticulum (Zenker's diverticulum) Older patients ```
156
Symptoms of pharyngeal pouch
Dysphagia - point to pharynx Palpable lump - right or left due to vertebrae Regurg Hallotosis Nocturnal aspiration - waking up coughing
157
Tx pharyneal pouch
Surgical criocpharyngotomy
158
90% of colon cancer is what type?
ACC
159
Pancreatic cancer gold standard diagnosis
CT
160
Treatment gastric cancer
Often palliative Pre and post chemo radical gastrectomy local ablation for symptom control if palliative
161
Types of gastric tumours
Adenocarcinoma CT - GIST (stromal) Neuroendocrine - carcinoid Lymph - lymphomas
162
What is leriche syndrome
Blockage of AA at bifurcation Erectile disfunction Claudication of buttocks, thigh and calf Absent fem pulses
163
Signs of adenoarcinoma stomach
Weight loss epigastric ass palpable supraclavicular nodes (Troisier's sign) if diseminated disease
164
Liver cancers
mets = 95% Primary mostly cholangiocarcinoma and HCC (HCC=75%)
165
Diagnosis of liver tumours HCC
CT/ MRI (usually both) are the imaging modalities of choice a-fetoprotein is elevated in almost all cases Biopsy should be avoided as it seeds tumours cells through a resection plane. In cases of diagnostic doubt serial CT and αFP measurements are the preferred strategy. Patients should be staged with liver MRI and chest, abdomen and pelvic CT scan. The testis should be examined in males (testicular tumours may cause raised AFP). PET CT may be used to identify occult nodal disease.
166
Main RF for cholangiocarcinoma
PSC, thyphoid and flukes 20% actually in liver
167
Diagnosis of cholangiocarcinoma
Patients will typically have an obstructive picture on liver function tests. CA 19-9, CEA and CA 125 are often elevated CT/ MRI and MRCP are the imaging methods of choice.
168
How do you tell the difference between an ileostomy and a colonostomy?
Sprouted on iliostomy to prevent acid
169
Osteosarcoma
* Affects younger population (20s) mainly but elderly as well. * Distal femur and proximaln tibia * Assoc with Pagets disease
170
Chondrosarcoma
Axial skeleton in older patients e.g. vertebrae, pelvis, ribs Lymphoma
171
Ewing sarcoma
10-20 years Onion/ lamellated periosteal reaction to the lytic lesion Most present with mets high mort
172
Giant cell tumour
x-ray soap bubble Pain or pathological fracture presentation Common mets to lung
173
Myeloma
``` alcohol, obesity, fx, cause kidney probs from abs spine and ribs localised pain = fracture Treatable but incurable ```
174
What is tracheostomy and why is it useful?
Reduces the work of breathing (and dead space) May be useful in slow weaning Percutaneous tracheostomy widely used in ITU Dries secretions, humidified air usually required
175
What is a laryngeal mask and why is it useful?
Widely used Very easy to insert Device sits in pharynx and aligns to cover the airway Poor control against reflux of gastric contents Paralysis not usually required Commonly used for wide range of anaesthetic uses, especially in day surgery e.g. inguinal as no suxa Not suitable for high pressure ventilation (small amount of PEEP often possible)
176
What is an oropharyngeal airway and why
Easy to insert and use No paralysis required Ideal for very short procedures Most often used as bridge to more definitive airway
177
Surgical and trauma VTE RFs
if total anaesthetic + surgical time > 90 minutes or if surgery involves pelvis or lower limb and total anaesthetic + surgical time > 60 minutes or if acute surgical admission with inflammatory or intra-abdominal condition or if expected to have significant reduction in mobility or if any VTE risk factor present (see below)
178
Early causes (0-5days) of post op pyrexia
Blood transfusion Cellulitis Urinary tract infection Physiological systemic inflammatory reaction (usually within a day following the operation) Pulmonary atelectasis - this if often listed but the evidence base to support this link is limited
179
Late causes (>5 days) of post op pyrexia
Venous thromboembolism Pneumonia Wound infection Anastomotic leak
180
RFs for urinary retention
removal of urinary catheter, constipation, immobility, opiate analgesia, infection, haematuria and benign prostatic hyperplasia (in males