Surgery Review Flashcards
why might a dermatofasciotomy be required following a femoral angioplasty for a patient with critical limb ischaemia?
on revascularisation, there is a rapid increase in blood flow to the patient’s limb, causing a rise in pressure within a limb compartment which may lead to compartment syndrome which is treated with a dermatofasciotomy.
an odd pattern of ischaemic damage is noted in the foot, what is the most likely cause?
embolisation
oesophageal surgery procedure name?
Ivor Lewis procedure
A Hartmann’s procedure is performed when disease affects which part of the bowels?
Sigmoid colon
How is severity of pancreatitis assessed?
CT scan-look for low density changes
CRP monitoring
Modified Glasgow criteria/Imrie scoring: 3 or more positive factors within 48hr of symptom onset suggest severe pancreatitis requiring prompt transfer to ITU/HDU:
PANCREAS: PaO2 less than 8.0 kPa
age over 55yrs
neutrophilia more than 15X10^9 cells per L
calcium less than 2mmol/L
urea more than 16mmol/L
LDH more than 600iu/L, AST more than 200iu/L
albumin less than 32g/L (serum)
blood glucose more than 10mmol/L
cause of pigment GSs?
haemodialysis
when does serum amylase start to fall in acute pancreatitis?
within 24-48hr of onset
if presentation after this time, urinary amylase may still be raised
continuing care required post acute pancreatitis attack?
must advise to stop drinking alcohol even if attack not result of alcoholic ‘binge’
cholecystectomy if GSs were demonstrated once pt fully recovered
acute pancreatitis prognosis?
mortality less than 1% if single episode of mild pancreatitis
mortality of 10% if severe, rising to 30% if severe necrosis and nearly 40% if pancreatic necrosectomy required.
complications that may follow a perforated peptic ulcer?
re-perforation-ensure H pylori eradication therapy given abscess wound infection lung atelectasis PE gastric outlet obstruction-occurs with fibrotic stenosis of dudodenum or gastric antrum, and may follow long standing chronic peptic ulceration, presents with massive and effortless vomiting often containing undigested food. sub-phrenic abscess multi-organ failure
if vomitus contains bile, what causative conditions can we rule out?
anything pathology proximal to the ampulla of Vater
why is melaena usually associated with gastric haemorrhage?
gastric acid turns the Hb to haematin, responsible for the black, tarry and unpleasant smelling stools.
why is the term ‘biliary colic’ not really an appropriate use of the word colic?
despite the intermittent nature of the pain, it does not remit entirely between each spasm, and the bile duct has a very weak muscle layer, in contrast the the small of large bowel.
when is a pt said to have an acute abdomen?
if moderate to severe pain lasting between a few hrs and a few days
a very high WCC in the context of acute abdominal pain supports the diagnosis of which conditions?
severe acute pancreatitis
mesenteric ischaemia
conditions to be met for referral under the 2 week wait for suspected colorectal Ca?
rectal bleeding and change in bowel habit for more than 6 weeks
persistent rectal bleeding without anal symptoms in those aged over 45, with no obvious external evidence of benign anal disease
Fe deficiency anaemia (microcytic, hypochromic), without an obvious cause and Hb less than 10g/dL
palpable abdo or rectal mass
recent onset of looser stools and/or increase frequency of defecation, persisting for more than 6 weeks
most common organisms implicated in ascending cholangitis?
klebsiella spp. E.coli enterobacter spp. enterococci streptococci
what additional features might a pt with ascending cholangitis present with other than charcot’s triad?
hypotension due to septic shock
mental confusion
=Reynold’s pentad
How should the management of a pt proceed if they are suspected of having a non-disabling stroke or TIA, identified as candidate for carotid endarterectomy on specialist assessment, but carotid imaging within 1wk of symptom onset shows non-significant stenosis?
should have best medical management: lifestyle advice-increase exercise, lipid lowering diet and drugs, BP control, antiplatelet agents.
this is carried out rather than carotid endarterectomy if carotid imaging (duplex USS) within 1wk of symptom onset shows stenosis of less than 50% with NASCET criteria, or less than 70% with ECST criteria, in pt with stable neurological symptoms and symptomatic stenosis.
How should the management of a pt proceed if they are suspected of having a non-disabling stroke or TIA, identified as candidate for carotid endarterectomy on specialist assessment, and carotid imaging within 1wk of symptom onset shows significant stenosis?
require best medical management and assess and refer for cartoid endarterectomy within 1wk of symptom onset. Carotid endarterectomy should be performed within 2wks of symptom onset.
this is carried out if carotid imaging within 1 wk of symptom onset shows stenosis of 50-99% according to NASCET criteria or 70-99% according to ECST criteria, and pt has stable neurological symptoms and symptomatic stenosis.
in a pt with sudden onset neurological symptoms, what blood test is important to rule in/out particular differential?
blood glucose-exclude hypoglycaemia
how is TIA defined and how are these patients assessed in hospital?
sudden onset focal neurological defecit with neurological symptoms lasting for no more than 24 hours.
assessment for subsequent stroke risk using ABCD2 scoring tool-score 0-3 mild risk, 4-5 moderate risk and 6-7 high risk.
imaging in suspected TIA or non disabling stroke?
urgent brain scanning required if symptoms of acute stroke
if TIA, pt should have specialist assessment within 1wk of symptom onset before decision on brain imaging made
if TIA and high risk of stroke (ABCD2 score 4 or more) and vascular territory or pathology uncertain, do urgent brain imaging with diffusion-weighted MRI
same if low risk of stroke
if after specialist assessment deemed suitable for carotid endarterectomy, should have carotid imaging within 1 wk of symptom onset.
define buerger’s angle?
the angle to which the leg has to be raised before it becomes white
vascular angle less than 20 degrees indicates severe ischaemia.
how do veins appear in an ischaemic foot?
‘guttering of the veins’: appear as pale blue gutters as veins collapse and sink below the skin surface
components to inspection of lower limb for assessing arterial circulation?
colour
buerger’s angle (vascular angle)-raise both legs to determine vascular angle and compare, then pt should sit up and dangle feet over edge of bed, ischaemic leg will slowly turn from white to pink to purple-red-deoxygen bld filling dilated capillaries.
venous filling
pressure areas
what is palpated on arterial assessment of lower limb?
skin temperature
CRT
pulses-femoral, popliteal, dorsalis pedis, posterior tibial
causes of skin ulceration?
arterial-gangrene-atherosclerosis and AV malformations
venous-DVT-post thrombotic deep vein damage, and varicose vein association, 80-85% of leg ulcers
neuropathic ulceration-DM, tabes dorsalis-tertiary syphilis, syringomyelia, spina bifida, nerve injuries
lymphatic insufficiency
osteomyelitis
vasculitis-RA, SLE, scleroderma, polyarteritis nodosa, wegener’s granulomatosis
squamous or basal cell carcinoma, melanoma
marjolin’s ulcer-malignant change of an ulcer
bowen’s disease-slow growing red/brown scaly plaque e.g. lower legs, carcinoma in situ
sarcoidosis
pyoderma gangrenosum e.g. assoc. with IBD, wegener’s
traumatic e.g. radiation, cold injury, burns, pressure sore
haematological e.g. sickle cell anaemia, polycythaemia rubra vera-somatic mutation in single haemopoietic stem cell causing erythroid hyperplasia, thrombocytosis and myeloid leukocytosis, and splenomegaly, plus risk of transformation to acute myeloid leukaemia, only tested in females as polymorphism on X chromosome taking advantage of its inactivation.
if a pt complains of aching calves, this may be the result of intermittent claudication- should clarify walking distance (claudication distance), however how could a CXR be useful in ruling out an important differential for aching calves?
CXR to look for lung Ca-small cell lung Ca assoc. with the paraneoplastic syndrome of lambert-eaton myasthenic syndrome, for which 1 of the presenting symptoms is aching muscles, in addition to weakness-usually proximal lower limb muscles affecting gait, and autonomic symptoms e.g. dry mouth and postural hypotension.
what are the components of the EWS and which would you be monitoring most closely and why after a pt returns to the ward from theatre when assessing for complications?
BP, HR, RR, SpO2, temperature, conscious level
RR- 1st to change in pt becoming acutely unwell e.g. when assessing hypovolaemia from blood loss, class I with a blood loss of less than 750ml would be unlikely to alter HR, BP or urine output, but RR may be between 14 and 20/min, which might be notable increase if pt normally 12/min.
what important investigation should be carried out on all afro-caribbean patients preoperatively?
sickle cell testing:
importance as heterozygotes (HbAS) have sickle-cell trait, which causes no disability and protects against falciparum malaria, EXCEPT IN HYPOXIA- e.g. in anaesthesia, where vaso-occlusive events may occur e.g. stroke, mesenteric ischaemia, avascular necrosis e.g. of femoral head, and leg ulcers.
gas in the biliary tree on AXR is consistent with what diagnosis?
GS ileus
how can barium enema be used to distinguish between true large bowel obstruction and pseudoobstruction?
barium will pass through proximal dilated bowel in pseudo-obstruction
why should laparoscopy be avoided when bowel obstruction?
dilated bowel loops obscure view and can be perforated during cannulae insertion, espec. if bowel adherent to abdo wall.
caution with IV fluid resuscitation in suspected ruptured aneurysm?
hypotension in this case is homeostatic reducing risk of rebleed
PUD diagnostic confirmation?
upper GI endoscopy (oesophago-gastro duodenoscopy)
how are biopsies taken from gastric ulcers to exclude early malignant change?
from all 4 quadrants
Calot’s triangle components?
cystic artery-from the R hepatic artery (or superior border of triangle formed by inferior liver in term cystohepatic triangle*)
cystic duct
common hepatic duct
*significance in cholecystectomy- cystic artery and duct dissected out and then clipped, or ligated by endosuture and divided. GB dissected off undersurface of liver.
lap cholecystectomy complications?*
residual stones
bile duct damage
cystic duct bile leakage
haemorrhage from cystic artery
acute cholecystitis complications?
obstructive jaundice acute pancreatitis GB empyema mucocele of GB mirizi's syndrome-CBD obstructed by GS in hartman's pouch acute cholangitis cholecysto-enteric fistula and GS ileus
2 presentations of perforated diverticular disease?
purulent peritonitis: diverticulitis has proceeded to form a pericolic abscess that has burst into the peritoneal cavity but does not communicate with the bowel (Hinchey stage 3 classification of acute diverticulitis).
faecal peritonitis: true connection between bowel and peritoneal cavity as orifice of diverticulum patent. Mortality of at least 50%, characterised by septic SHOCK: severe sepsis plus hypotension unresponsive to adequate fluid resuscitation.
why do diverticula NOT form in the rectum?
at rectosigmoid junction, the taeniae join to form a complete outer longitudinal muscle layer.
presentation of acute sigmoid diverticulitis?
LIF pain, colicky if large bowel obstruction from inflammation or stricture predominates
pain may spread across whole abdomen if pericolic abscess or diverticulum ruptures causing generalised peritonitis
usually constipated, a few develop diarrhoea
often accompanying nausea
abdo tenderness
fever
urinary symptoms if inflamed colon lies against bladder
RIF pain if sigmoid loop flops over to R
bleeding PR unlikely as inflammation-oedema*?
3 criteria defining the PAIN in intermittent claudication?
pain in a muscle, usually calf
pain only when muscle is exercised
pain disappears when exercise stops
if restenosis follows therapeutic interventions for chronic leg ischaemia, what is the likely cause?
intimal hyperplasia
NICE recommendations on IC management?
CVS RF reduction: smoking cessation-CVS risk halved within 1 yr of stopping, also improve walking distance and amputation rates.
of managing all RFs, stopping smoking along with exercise training provides most notable improvement in walking distance.
lipid modification with statin-reduce CVS events and stabilise atherosclerotic plaques.
exercise-CVS benefit, improve walking distance. offer supervised or unsupervised if not available exercise programme
HTN-manage to reduce risk of stroke and CVS events
DM-good glycaemic control benefit on CVS disease progression in general
AP treatment-Clopidogrel 75 mg daily is the preferred antiplatelet in PVD. If contraindicated or not tolerated, give low dose aspirin alone. If both contraindicated or not tolerated, give modified-release dipyridamole alone.
Naftidrofuryl oxalate- a peripheral vasodilator via 5-HT antagonism, can be given if exercise unsuccessful, managing RFs has been enforced, and pt does not want consideration for angioplasty or bypass.
complications of surgical treatment for intermittent claudication?
failed angioplasty vessel thrombosis arterial wall dissection restenosis bypass occlusion
causes of visceral pain?
ischaemia-e.g. acute mesenteric ischaemia- may present with periumbilic pain
stretching/distensions e.g. large bowel distension with large bowel obstruction due to a colorectal Ca, presenting with suprapubic pain
tension
hindgut derivatives which are responsible for visceral referred pain to the suprapubic region?
from distal 1/3 of transverse colon to the anal verge
referrred biliary tract pain?
R inferior scapular area
how does pain duration help to determine differentials for the acute abdomen?
sudden onset: rupture or perforation e.g. splenic rupture, AAA rupture, PUD perforation, diverticulum perforation
in onset, ? how long to reach maximal pan?
also ensure rule out cardio/resp pathologies e.g. aortic dissection, PE and pneumothorax
rapidly accelerating: colic-ureteric, biliary, SBO- e.g. adhesions, hernia or strictures e.g. Crohn’s disease
gradual onset (over a few hrs): inflammatory, obstructive processes, mechanical causes
if movement aggravates pain so pt remains as still as possible, what does this indicate in acute abdomen?
generalised peritonitis
features suggestive of malignancy in acute abdomen presentation?
intermittent pain for more than 48 hrs change in bowel habit, may be absolute constipation with LBO abdominal distension mass weight loss
features suggesting perforated viscus in acute abdomen presentation?
sudden onset pain constant severe pain aggravated by movement and coughing diffuse tenderness silent rigid abdomen
important components to abdomen inspection in presentation of acute abdomen?
scars-indicative of previous surgery e.g. Lanz incision-appendicitis, Kocher-gallbladder, maybe prev surgery causes adhesions now presenting as SBO
distension-in flanks and epigastrium suggestive of LBO
bulge, mass-? diverticular abscess, CR Ca
movement-board like rigidity if peritonitis
bruising-periumbilical cullen’s sign and flank grey turner’s sign in acute pancreatitis
the most common cause of SHOCK in a surgical pt is hypovolaemia, how is hypovolaemia resulting from blood loss assessed?
look at patients pulse, BP, pulse pressure, RR, urine output and mental state
Class I: with less than 750mL blood loss (less than 15%), pulse less than 100, BP normal, pulse pressure normal or raised, RR 14-20/min, urine more than 30mL/hr, pt may be slightly anxious, ONLY REAL ABNORMALITY=RR
Class II: 750-1500 mL blood loss (15-30%), PR more than 100, BP normal, pulse pressure decreased, RR 20-30, urine output 20-30, mildy anxious.
Class III: 1500-2000 blood loss (30-40%), pulse more than 120, BP decrease, pulse pressure decrease, RR 30-40, 5-15 mL urine ouput, confused pt.
NOTE BP ONLY DROPS AFTER 30-40% OF BLOOD VOLUME LOSS
Class IV: more than 2000mL (40%) bld loss, pulse more than 140, BP and PP decrease, RR more than 35, negligible UO and pt lethargic- needs blood aswell as crystalloid.
what score is used to risk-score upper GI bleeds?
Rockall score
what is meant by a positive Rovsing’s sign?
palpation of LLQ increases pain felt in RLQ
this is indicative of acute appendicitis
what is ascending cholangitis?
infection of the CBD superimposed on an obstruction e.g. due to a gallstone, or stricture
what is the purpose of bile duct sphincterotomy?
help improve bile drainage*
causes of adhesions other than previous operation?
trauma e.g. RTA, blunt spleen injury
intra-abdominal infection e.g. salpingitis
indications for surgery in small bowel obstruction?
unresolving
fever
marked tenderness indicating peritonitis
evidence of perforation on imaging
what imaging is used to identify gallstone ileus, and what triad is this associated with?
plain AXR- shows pneumobilia, small bowel obstruction and radiolucent gallstone=rigler’s triad
complications of small bowel obstruction?
perforation, producing peritonitis and sepsis*
ischaemia
why is checking for anaemia by performing an FBC as part of the pre-operative assessment so important?
in order to correct the anaemia prior to surgery so as to reduce the risk of cardiovascular events
importance of LFTs as part of the pre-operative assessment?
assess for any coagulopathy that can be corrected
help in determining drug choices and dosages bearing in mind their metabolism by the liver
low albumin or protein level indicative of poor nutritional state that may affect post-operative recovery
what must be done prior to a X match of bloods?
a group and save!
name of syndrome for oesophageal rupture?
Boerhaave’s syndrome
differentials for sudden onset severe abdo pain that rapidly progresses to become generalised and constant?
hollow viscus perforation
ruptured AAA
acute mesenteric ischaemia
pain fibres carrying visceral pain in GI tract?
sympathetic splanchnic nerves
somatic pain from parietal peritoneum and abdominal wall carried by intercostal (spinal) nerves
why might acute cholecystitis present with R scapula pain?
irritation of the diaphragm, referred pain to shoulder.
why might a patient with a PMH of COPD be delayed in waking up post GA?
if patient is a retainer of CO2, they will have compensated for this through HCO3- release by the choroid plexus cells to normalise pH so CO2 conc no longer driving their urge to breathe, hypoxia is, BUT it is hypercarbia which is the stimulus to waking following a GA.
aim of pre-op assessment?
is the patient fit for surgery?
can we optimise the pt prior to surgery, paying close attention to management of pt co-morbidities? ability to postpone or cancel the surgery if necessary.
can we identify and reduce the risk of any complications that might occur?
establish rapport with pt
take hx, examine and investigate
in terms of r/ving the CVS and Resp functioning of a pt pre-op, what specifically should be asked about?
patient’s functional capacity (exercise tolerance)
e.g. are they able to manage a flight of stairs in one attempt?
why is it important to ask a pt pre-op whether they, or anyone in their family, has suffered from a rapid rise in temperature after being given an anaesthetic?
to assess for malignant hyperthermia-potentially lethal condition usually triggered by an anaesthetic and result of genetic defect of the ryanodine receptor causing massive intramyoplasmic increase in Ca2+ from SR, causing muscle rigidity and rhabdomyolysis.
?muscle disorders in the family (assoc. with Duchenne’s and becker’s muscular dystrophy), pt myalgia and muscle cramps. bloods may show persistent raised CK.
in diagnosed patient, can avoid the causative anaesthetics e.g. halothane and suxamethonium. non-depolarising NM blockers e.g. pancuronium are safe, as is NO and barbiturates includ thiopental. check CK before and after surgery, and put pt 1st on the list and flush apparatus through with O2 for 10mins before using.
management of malignant hyperthermia?
switch from volatile anaesthetics to alternatives
give 100% O2 and adjust ventilation according to blood gas and end-expiratory CO2
deepen anesthesia with BZDs, opioids, propofol
monitor blood gas, electrolytes, lactate, myoglobin, CK
stop surgery if elective and signs of masseter spasm or a fulminant crisis
continue surgery if no hyperkalaemia, no acidosis and no triggers
IV DANTROLENE-muscle relaxant
If a fulminant malignant hyperpyrexia crisis occurs:
Sodium bicarbonate may be given according to blood gas analysis.
Arrhythmia may be treated with a beta-blocker or lidocaine.
Stop surgery as soon as possible.
Cool the patient - eg, iced water through a nasogastric tube.
Intensive monitoring including arterial catheter, central venous catheter, Swan-Ganz catheter, urinary catheter. Monitor renal function, check myoglobinuria, coagulation screen, temperature, electrolytes and CK.
Forced diuresis to help protect the kidneys
components to hx of PC and PMH in pre-op assessment?
hx of condition and procedure to be done
confirm site of operation and side
PMH: CVD, including prev. MIs, HTN, and current exercise tolerance-risk of acute cardiac event increased during anaesthesia.
Resp disease e.g. COPD, asthma-control, triggers, med.s e.g. steroids-dose and duration, prev hosp admissions espec. ITU. In peri-op period, adequate oxygenation vital to reduce risk of acute ischaemic events.
Renal disease: surgical complications risk increased with anaemia, coagulopathy and BC disturbance. Signif. disturbance of renal funtion can occur with IV contrast and blood loss.
DM-type, medication, related co-morbidities. thyroid disease.
MSK illness e.g. cervical spondylosis which can make intubation difficult necessitating specific equipment.
also want to check if pt could be pregnant, and if could have undiagnosed sickle cell disease if of african or AC origin.
post-op complications in patients with sickle cell disease?**
acute chest syndrome infection hyperhaemolytic crisis relative aplastic crisis alloimmunisation with delayed transfusion reactions
additions to PMH in a surgical patient?
past surgical history-operations and why
anaesthetic hx-prev anaeasthetic? any complications? PONV? rapid rise in temp-malignant hyperthermia.
how is the airway assessed prior to surgery?
look for facial abnormalities e.g. receding mandible-can cause difficulties in airway insertion
look in the mouth-teeth-present?dentition?loose teeth?crowns? degree of mouth opening-favourable if inter-incisor distance more than 3cm
oropharnyx-Mallampati classification-correlates with difficulty of intubation, classed as I-IV, ask pt to maximally protrude tongue.
neck-flex, extend and lateral flexion, then max extend and measure distance between thyroid cartilage and chin-thyromental distance-less than 7cm suggests difficult intubation.
definition of ASA 3?
severe systemic illness, leading to functional limitation of their activity
importance of Us and Es before surgery?
baseline function of kidneys assessment to indicate susceptibility to AKI
general pre-op investigations?
FBC-anaemia?-correct before surgery to reduce risk of acute cardiac events
Us and Es-baseline
LFTs-correct coagulopathy, determine met of part drugs-appropriate and doses, low albumin-poor nutrition-poor post-op recovery.
clotting-identify abnormalities and correct
G+S- determine pt’s blood group (ABO and RhD) and screen for atypical Abs. recommended if blood loss not anticipated but bld may be required in surgery if greater blood loss than expected.
X match- mix patient’s bld with donor’s bld to see if immune reaction occurs. do if bld loss anticipated. must G and S 1st.
ABG if pt has condition that may cause pulmonary impairment.
ECG-if hx of CVD, undergoing major surgery. indicate underlying pathology and provide baseline if post op signs of cardiac ischaemia.
CXR-indicated if respiratory illness and not had a CXR within 12 months, new cardiorespiratory symptoms, recent travel from areas with endemic tuberculosis or significant smoking history.
spirometry if chronic lung condition-may predict post-op pulm. complications.
preg test
sickle cell testing-HbS
MRSA swabs-nasopharyngeal, perineal, throat. if colonisation isolated, give antiseptic hair and body wash, and topical ointment.
urinalysis-ongoing glycosuria or UTI? undiagnosed diabetes mellitus?-increase complications peri-operatively.
2 potential complications of gastric contents aspiration in pts perioperatively?
aspiration pneumonitis- inflammation causing desquamation
aspiration pneumonia-secondary infection following pneumonitis or direct aspiration of infected material.
presentation of biliary colic?
sudden severe pain across the upper abdomen, may not be able to indicate which side is more affected
constant pain with excruciating exacerbations, pain does not remit in between these
severe pain usually lasts no longer than a few hours unless acute cholecystitis develops
usually N+V
pain relieved only by strong analgesia
jaundice may be present, in this case may be dark urine and pale stools
hx of flatulent dyspepsia-upper abdo pain accompanied by feeling of fullness, with nausea and frequent belching of air
mild tachycardia often present but temp usually normal
abdomen extremely tender, with intense guarding in upper abdomen
acute cholecystitis management (and that of biliary colic)?
pain relief with opioids
admit for bed rest and USS confirmation of dignosis
restrict oral fluids if nauseated or vomiting
commence IV fluids
Abx e.g. cephalosporin such as cefuroxime 1.5g/8h if pt pyrexial or marked leucocytosis
SC LMWH
Cx management if attack lasted several days or pt jaundiced, re-admit for elective lap chole 6-8wk later
early chole if pt fit, US confirmed diagnosis and attack less than 24-48hrs duration.
medication which must be STOPPED before sugery?
clopidogrel-stopped at least 1 week before to reduce risk of profuse bleeding. aspirin can be continued as cardio and cerebroprotective benefits outweigh risks + long t1/2 and minimal effects on surgical bleeding.
warfarin-stopped 5 days before. ensure INR checked day before surgery, may convert to heparin for elective but must stop 6hrs prior to surgery and monitor APTT peri-op. if prev DVT/PE, admit day before surgery and may give high dose prophylactic LMWH. if prosthetic heart valve, admit 2-3days post op, check INR, allow decrease to 2, start IV unfractionated heparin and stop 4hrs pre-op.
OCP and HRT-stopped 4 wks before, advise alternative contraception e.g. barrier, at this time.
don’t give oral hypoglycaemics and most antihypertensives on morning of surgery
antihypertensive drug considerations peri-op?
stop ACEIs, AngII receptor blockers and diuretics on day of surgery, as BP reduction that occurs anyway during surgery with vasodilating effects of anaesthetics will be difficult for the body to cope with as used to a high BP.
a patient presents with large bowel obstruction requiring emergency surgery. they have a PMH of AF and are currently treated with warfarin, with a CHADS-VASC score of 2. how will the warfarin be managed peri-op?
if immediate reversal of warfarin required as surgery cannot wait, give beriplex (prothrombin complex concentrate) which contains clotting factors II, VII, IX and X, and protein C.
if can wait 3hrs or more, give |V Vit K SLOWLY 1-5mg over 30mins, and then recheck INR.
general guidelines for management of diabetic patients for surgery?
all patients undergoing surgery should ideally have urinalysis pre-op (and lab blood glucose if indicated as undiagnosed DM is common)
if possible, place 1st on morning list
if known diabetic undergoing major surgery, admit 24-48hrs prior for assessment and prep.
avoid hartmann’s solution
establish IV access
type 1 DM peri-op management if undergoing major surgery?
if major surgery:
admit at least the day before
check CBGT pre-meal and before bed (4-6hrly)
check Us and Es and lab blood glucose day before, make necess. adjustments to improve control
avoid LA insulin, ensure LA analogues reduced by 1/3-1/2 day before
if morning surgery: reduce SC basal insulin (intermediate acting) by 1/3-1/2 night before, and omit normal morning SC insulin.
insert IV cannula with Y extension, start infusion at least 1hr before, a 1 way valve must be used in the limb through which the glucose is running.
start 500 ml of 5% glucose, with 1 gram (13 mmol) K+
in each bag, at 100 ml/hr via a volumetric pump, with insulin infusion by variable rate.
start IV variable rate insulin infusion 50 Units of human actrapid (SA) in 50ml 0.9% sodium chloride-rate dependent on CBGT (fingerprick glucose/BM)
Check CBGT post-op and then every 2 hours
Check U&Es and lab blood sugar daily while on this regime
Continue infusion until pt able to eat and drink
Continue the infusion until the next meal, give S/C actrapid or short-acting analogue (about ⅓ of
previous daily dose) 20 minutes before the meal
Stop IV insulin and glucose 30 – 60 minutes after S/C injection
Check the insulin infusion if there is any doubt (e.g. has the IV tissued, etc)
type 1 DM peri-op managment if undergoing minor surgery?
if morning: ensure 1st on list
reduce previous evening intermediate insulin by 1/3, LA e.g. glargine day before may have to be reduced by 1/3-1/2.
omit morning insulin
check CBGT, if 4-13 proceed, if less than 4 start 5% glucose infusion, if more than 13 start IV variable rate insulin infusion with glucose as for major.
monitor CBGT 2hrly
pt should be E and D by lunchtime, give 1/2 morning insulin dose 20mins before lunch, then normal evening insulin.
if later in day, give 1/2 normal insulin dose with a light breakfast (finishing 6hrs before)
check CBGT before and proceed as above
monitor CBGT 2hrly
normal insulin at evening meal
type 2 DM diet controlled management peri-op?
minor surgery: avoid glucose-containing solutions, do CBGT pre and post-op, and 6 hrs later
major: if well controlled, as above
if poorly controlled, treat with variable rate insulin infusion, ensuring no insulin if CBGT less than 4, and rate may have to be increased if CBGT remains high in type 2 DM obese pts who are insulin resistant.
type 2 DM tablet controlled management peri-op?
aim to stop metformin and LA sulfonylureas 48hrs before if possible
omit all oral hypoglycaemics on day
do CBGT pre and post-op, and 4hrly until recovery
if fasting bld glucose more than 10, or random more than 15, treat as for type 1
if major surgery and well controlled, treat with variable rate IV insulin infusion and 5% glucose at least 1hr pre-op.
if poorly controlled, convert to SC actrapid or novorapid QDS, adjust dose to achieve CBGT 4-11, then manage as for type 1 peri-op.
why is prothrombin time prolonged in patients with liver disease and how can this be corrected pre-operatively?
reduced synthesis of clotting factors by the liver
and
reduced bile production by the liver so reduced bile salts necessary for fat absorption and subsequent Vit K absorption from the small bowel as fat soluble vitamin
vitamin K supplementation (?IV), and fresh frozen plasma
when would we NOT operate in bowel obstruction?
if SBO due to adhesions and NO evidence of peritonitis
if LBO due to volvulus and NO signs of peritonitis
abdo USS appearance of an AAA?
*calcification of aorta (calcified outline)
differentials for sudden onset severe back and epigastric pain?
ruptured AAA acute pancreatitis perforated peptic ulcer aortic dissection MI ureteric colic
define an aneurysm?
a localised permanent dilatation of an artery of more than 50% of its normal diameter.
true aneurysms occur with pathological degeneration of all or part of the arterial wall
what is a false aneurysm and how is this different from an arterial dissection?
false aneurysm=these are associated with penetrating trauma e.g. a gunshot wound or knife injury, and refer to blood collection outside the artery, but with the extravasated blood still maintaining continuity with the main bloodstream. a fibrotic wall grows around the blood but it lacks the normal 3 arterial layers of a true aneurysm.
in dissection, blood collects within the wall of an artery as tear in tunica intima and media, and so blood flows through the wall in parallel with the main bloodstream.
causes of aneurysms other than atherosclerosis and its RFs-smoking, HTN, hyperlipidaemia?
berry aneurysms in the circle of Willis*-congenital, sometimes present in patients with adult PKD
infective (mycotic)-endocarditis, syphilis
CT disease-Marfans syndrome, Ehlers-Danlos syndrome
what degenerative changes take place within the arterial wall to cause an aneurysm?
inflammation drives loss of elastin and smooth muscle from the tunica media
most aneurysms are asymptomatic until rupture, but what symptoms might a patient with an inflammatory aneurysm experince?
abdo pain
general malaise
weight loss
US surveillence of patients with aneurysms found to be less than 5.5cm in size?
annually if diameter between 3.5 and 3.9cm
and 6mnthly if between 4.0 and 5.5cm
those which are more than 5.5cm or expanding at a rate of more than 1cm per year should be operated on electively.
what can found o/e of a patient with an aneurysm*?
pulsatile and expansile mass
minimum requirement for EVAR in AAAs?
1.5cm length of normal aorta below the renal arteries to enable implantation and a good seal with the stent-graft
this is assessed with a CT angiogram- can define anatomy of the aneurysm, including neck and iliac arteries, and determine size of required graft.
who is screened for AAA in England?
all men aged 65 years of age ONCE using US screening
why was AAA screening introduced?
to reduce mortality in men from ruptured AAAs
initial management in suspected AAA rupture?
A to E patient assessment
give O2 15L/min
insert large bore IV cannula antecubital fossa
bloods-FBC, Us and Es, clotting screen, glucose, serum amylase, G and S and X match 6-8 units of blood
insert urinary catheter, central venous catheter and arterial line
contact vascular surgeon urgently and involve them, decision as to whether image e.g. CT abdo, made by them. if pt unstable, need transfer to theatre ASAP.
features o/e of patient with ruptured AAA?
pale, cold and clammy extremities
hypotension, weak and thready pulse, rapid
tender expansile pulsatile central abdo mass mass few cm above umbilicus, or abdo distension
features of acute abdomen as bleeding causes peritoneal irritation-rigid abdomen, guarding, percussion tenderness
features of lower limb acute ischaemia e.g. pale, cold, pain, pulseless, paraesthesia and paralysis, as peripheral shutdown, limb may appear ischamic
benefits and complication of open aneurysm repair vs. EVAR?
EVAR: reduced early mortality smaller incisions less pain reduced hospital stay need life long follow up imaging-scan stent at 3mnths by CT then yrly with US or CT higher re-intervention rate risk of stent movement/migration risk of stent thrombosis endoleaks-persistent flow into aneurysm sac
open: higher early mortality lower re-intervention rate higher CVS mortality risk e.g. MI -hypotension link with reperfusion late complications-graft infection, false aneurysm formation, aorto-enteric fistula-can present as upper GI bleed-haematemesis/malaena, dizziness, syncope
complications of open surgery for ruptured AAA?
immediate (within 24hrs): haemorrhage, MI, death
early: ischaemic lower limbs from thromboembolism, acute mesenteric ischameia, renal failure, multi-organ failure, ileus, wound infection
late: graft infection (can be years later), aorto-enteric fistula, incisional hernia
adverse effects of pain post-operatively?
patient doesn’t want to move-increase DVT/PE risk
urinary retention
CVS-increase HR and BP- increase workload of heart and myocardial O2 demand-increase MI risk
Resp- basal atelectasis, chest infections, reduce TV, VC and FRC
GI-N and V-dehydration and worsen hypovolaemia, ileus
respiratory complications post-operatively?
upper airway obstruction-reduced consciousness, muscle relaxation-soft tissues can cause obstruction
upper airway secretions-risk reduced with antimuscarinic drugs e.g. glycopyrrolate/glycopyrronium
foreign body
hypoxia-inadequate o2 supply-basal atelectasis-pain, too much o2, hypoventilation, V/Q mismatch-PE, pneumonia, HF, inadequate delivery-shock, severe anemia
hypoventialtion. or increased consumption-fever, shivering, hypermetabolic state
contraindications to use of anti-embolic stockings in DVT prevention?
peripheral arterial disease
RFs for PONV and complications of PONV?
patient: young patient or child, non-smoker, pre-op anxiety, previous PONV, prone to travle sickness
surgery: ENT, gynaecological, abdominal
aneasthetic: inhalational, opioids, pain, dehydration
complications: dehydration can't take normal PO medication delayed discharge distress aspiration poor surgical outcome
management: keep pt well hydrated
reduce pain
give anti-emetic
prevention of post-operative atelectasis?
early ambulation
spirometry use
encourage patient to cough and breathe deeply
nebulised bronchodilators-help liquefy secretions and promote their easy removal
if occurs, give vigorous chest physio which frequently helps re-expand the collapsed lung, if unsuccessful within 24hrs, consider flexible fiberoptic bronchoscopy
management of a shocked patient with an upper GI bleed?
A to E assessment of patient
protect airway and keep NBM
insert 2 large bore cannulae (14-16G)
draw bloods-FBC, Us and Es, clotting screen, LFTs, glucose, G and S and X match 6 units of blood
give high flow O2
rapid IV crystalloid infusion up to 1L
if remains shocked, give blood-group specific or O Rh-ve until X match done
otherwise slow 0.9% sodium chloride infusion, to keep lines open
transfuse as dictated by haemodynamics
correct clotting abnormalities-Vit K, FFP, PLT concentrate
set up CVP line to guide fluid replacement, but may mislead if CCF or ascites, a swan-ganz catheter may help
urinary catheter, monitor output aiming for more than 30mL/hr
monitor vital signs every 15min until stable, then hrly
notify surgeons of all severe bleeds
urgent endoscopy for diagnosis with/without control of bleeding
what is the Rockall scoring system?
used for prognosis in acute GI bleeding
score of 0-3 points for each variable:
age-0 if under 60, 1 if 60-80, 2 if over 80
shocked?-SBP less than 100 and pulse more than 100 scores 2, and more than 100 and pulse more than 100 scores 1
any major co-morbidity scores 2, renal/liver failure or malignancy scores 3
diagnosis-MW or normal=0, malignancy is 2 and all other diagnoses 1
visible blood/clot, spurting vessel-2
score less than 3=excellent prognosis
more than 8= high death risk
causes of GI perforation?
peptic ulcer disease small bowel Ca small bowel obstruction small bowel trauma foreign bodies large bowel Ca large bowel obstruction diverticular disease IBD iatrogenic e.g. colonoscopy
initial radiological investigation in GI perforation?
erect CXR-look for air underneath the diaphragm
* be wary this can also occur post laparoscopy, with gas forming infections e.g. clostridium perfringens
investigations in lower GI perforation?*
FBC Us and Es clotting profile G and S, and X match ABG-lactate-metabolic acidosis ECG erect CXR-air under diaphragm AXR-rigler's sign-seen bowel wall as air both inside bowel and outside the bowel CT
management of GI perforation?
A to E assessment of patient large bore cannulae, IV fluids urinary catheter oxygen therapy IV Abx analgesia
non operative (medical)-ONLY if no generalised sepsis/peritonitis, treat with Abx, bowel rest, PPI (UGI), and radiological drainage where required bowel perforations usually require resection, often with stoma formation-emergency Hartmann's procedure where bowel removed and rectum oversewn/stapled foring LIF end colostomy. upper GI perforations can often be oversewn surgically.
what blood product could be given to correct anaemia?
red cells
1U increase Hb by 1-1.5g/dL
what can fresh frozen plasma (FFP) be used to correct?
clotting defects:
DIC-disseminated intravascular coagulation e.g. in sepsis, acute pancreatitis, burns, trauma, malignancy
liver disease
warfarin overdosage where Vit K would be too slow (but now often use of prothrombin concentrate complex-beriplex e.g. for emergency surgery in pts on warfarin)
thrombotic thrombocytopenic purpura- this is a haematological emergency where a deficiency in a protease which cleaves vWf multimers means large vWf multimers form, causing PLT aggregation and fibrin deposition in small vessels, causing microthrombi. Px with fever, fluctuating CNS signs, microangiopathic haemolytic anaemia-often severe with jaundice-raised bilirubin, raised urobilinogen, decreased haptoglobin, reticulocytosis, normocytic or macrocytic anemia, reduced PLT-with/without mucosal bleeding, renal failure and haematuria/proteinuria.
early complications (within 24hr) of blood transfusions?
acute haemolytic rections e.g. ABO or rhesus Rh incompatibility
anaphylaxis
bacterial contamination
febrile reactions (e.g. from HLA Abs)
allergic reactions-itch, urticaria, mild fever
fluid overload
transfusion related acute lung injury (TRALI)-acute resp distress syndrome due to anti-leucocyte Abs in donor plasma.
delayed complications (after 24hr) of blood transfusions?
infections e.g. Hep B/C, HIV, bacteria, protozoa, prions-creutzfeldt-jacob disease (CJD)
iron overload
graft versus host disease
post-transfusion purpura-potentially lethal fall in PLT count 5-7 days post transfusion requiring specialist tment with IV immunoglobulin and PLT transfusions.
define massive blood transfusion?
replacement of individuals’s entire blood volume (more than 10U) within 24hr.
complications: reduced PLTs, reduced Ca2+, reduced clotting factors, increase K+ and hypothermia.
whole blood is rarely used for transfusion, but may be used for exchange transfusion or in gross exsanguination. what is exchange transfusion?
blood is removed at the same time as blood is being transfused.
how are acute haemolytic reactions and anaphylaxis post blood transfusion treated?
acute haemolytic reaction: pt may present agitated with raised temp (rapid onset), flushing, decrease BP, abdo/chest pain, oozing venepuncture sites, DIC. should STOP transfusion. check identity and name on unit, tell haematologist and send unit and FBC, UandE, clotting, cultures and urine (haemoglobinuria) to lav. keep IV line open with 0.9% sodium chloride. treat DIC-can give FFP.
anaphylaxis: bronchospasm, cyanosis, soft tissue swelling, hypotension. STOP transfusion. maintain airway and give O2. contact anaesthetist.
presentation and treatment of TRALI-transfusion related acute lung injury?
dyspnoea, cough, CXR-white out
STOP transfusion
give 100% oxygen
treat as ARDS- admit to ITU, give supportive therapy and treat underlying cause. may use CPAP with 40-60% oxygen, but often require mechanical ventilation. haemodynamic monitoring with arterial line or swan-ganz catheter. conservative fluid management approach and inotropes to maintain CO and )2 delivery, plus vasodilator. nutritional support best enteral.
treatment of non-haemolytic febrile transfusion reaction and allergic reactions?
NHFT reaction: stop or slow transfusion, give anti-pyretic e.g. paracetamol 1g. monitor closely and if recurrent, use leucocyte depleted blood or WBC filter.
allergic reaction: slow or stop transfusion. give chlorphenamine 10mg slow IV/IM and monitor closely.
name given to malignant change in a chronic venous ulcer?
Marjolin’s ulcer
how can the venous circulation be assessed?
ask pt to stand up: inspection: site, tortuosity and size of visible veins effect of elevation and dependency ankle oedema skin colour, espec. above medial ankle
palpation: trunks of long and short saphenous veins, sapheno-popliteal junction, and feel texture of skin and SC tissues
percussion: percussion wave conduction upwards or downwards
auscultation: bruits over prominent varices
tourniquet tests
doppler US
causes of leg ulcers?
venous disease (80-85%)
peripheral arterial disease
neuropathic
vasculitis-RA, SLE, scleroderma, wegener’s, polyarteritis nodosa
lymphatic insufficiency
haematological-polycythaemia rubra vera, sickle cell anaemia
traumatic-burns, pressure sore, radiation
neoplastic-basal cell carcinoma, squamous cell, marjolin’s ulcer
sarcoidosis
pyoderma gangrenosum e.g. in IBD
describe the presentation of Boerhaave’s syndrome
due to full-thickness tear at OGJ, poss. as consequence of attempting to suppress a vomit
sudden onset severe pain upper abdo or lower chest, after a bout of vomiting
tenderness, guarding and rigidity in upper abdomen, and supraclavicular subcutaneous emphysema-clinically felt as crepitus and may cause soft tissue swelling and discomfort
triad of pain, vomiting and SC emphysema=Mackler’s triad
define critical limb ischaemia
arterial insufficiency which without intervention is likely to lead to limb loss, characterised by rest pain, gangrene-visible necrosis and putrefaction, or tissue loss, which have been present for more than 2 wks. and an ABPI of less than 0.5, with 0.3 or less implying impending gangrene.
NICE recommended management of critical limb ischaemia?
assess by vascular MDT, duplex USS can be used as initial assessment, but more detailed imaging e.g. contrast enhanced magnetic resonance angiography will be required, or CT angiogram if MR contraindicated or not tolerated. formal angio often needed to define distal run off vessels for bypass.
disease almost always secondary to occlusive or stenotic disease at multiple levels, each level must be treated.
in those requiring revascularisation, angioplasty or bypass should be offered taking into account patient comorbidities, preference, disease pattern and vein availability, consider primary stent placement if aorto-iliac complete occlusion, and use bare metal stent. use an autologous vein wherever possible for bypass. bypass often more favourable for long lesions e.g. SFA occlusions, can use axillofemoral, iliofemoral, aortofemoral, femor-femoral, femoropopliteal and femorodistal bypass. vein bypass best for LT patency and resistance to infection.
for PAIN, offer paracetamol, and weak or strong opioids, plus laxatives and anti-emetics to tackle ADRs of opioids
r/f to specialist pain management service if pain persists after revascularisation, if unsuitable for revascularisation e.g. extensive distal disease, sugery impossible and pain persists, or on persistent high dose opioids
note it is not possible to dilate very calcified or fibrotic stenoses e.g. in DM
do not offer major amputation unless all other options for revascularisation have been considered by the vascular MDT.
post op care of patient after revascularisation surgery for critical limb ischaemia?
monitor for post op bleeding or infection-EWS-RR increasing 1st, then increase in HR and decrease BP
observe circulation of limb to detect early graft occlusion
AP agents, dual AP following stent insertion e.g. clopidogrel and aspirin
complications: restenosis-result of vessel recoil soon after angioplasty, and later intimal hyperplasia and recurrent atheroma, graft occlusion from poor inflow, late restenosis can be treated with angioplasty and stenting, or bypass graft, graft infection can occur soon after surgery or later from haematogenous spread.
regular duplex US surveillence of vein bypass to detect restenosis
thrombolysis for graft occlusion, angioplasty if occlusion due to stenosis
what is a SALT assessment?
speech and language therapist assessment e.g. when querying TIA/stroke? used if speech impairment
patients also likely to have swallowing difficulty so should do swallowing assessment aswell to identify aspiration risk.
investigations for vascular disease if pt presents with likely chronic venous insufficiency, but also has an ABPI of 0.7 on that side?
so features of both venous disease and arterial insufficiency-ABPI of 0.5-0.9 indicative of claudication
bloods: FBC-anaemia, polycythaemia, infection CRP-vasculitic cause, Us and Es-baseline before use of IV contrast in imaging-angiogram, and assess for renovascular disease, ECG-AF, prev MI, lipids, HbA1c, blood glucose.
duplex ultrasound scan-arterial duplex and venous
if considering revascularisation in arterial disease, would also want a magnetic resonance angiography with contrast.
where does the junction between the superficial femoral artery and the popliteal artery occur?
in the region of the adductor canal-space between adductor magnus muscle-comprising hamstrings part innervated by tibila nerve, and adductor part innervated by obturator nerve, and the femur
in patients with post-op ileus, complaining of nausea and abdo distension, how can symptomatic relief be provided?
insert NGT
classic locations for renal stone deposition after formation in kidney collecting ducts?
regions of narrowing: pelvic-ureteric junction
at the pelvic brim where there is bifurcation of the common iliac artery*
at the vesico-ureteric junction
majority of renal stones are what type?
calcium oxalate
different ways other than renal colic-excruciating spasms loin to groin often with N+V, that a pt with renal stones might present?
asymptomatic
renal obstruction-felt in loin between 12th rib and lateral edge of lumbar muscles
obstruction of mid-ureter-may mimic appendicitis or diverticulitis
obstruction of lower ureter-may cause bladder irritability, pain in scrotum, penile tip or labia majora
obstruction in bladder or urethra-pelvic pain, dysuria, strangury-desire but inability to void, +/- interrupted flow
UTI, pyelonephritis-fever, loin pain, rigors, N+V
haematuria
proteinuria
sterile pyuria-raised WCC but sterile culture
anuria
considerations in hx when confronted by a renal stone?
diet-chocolate, tea, strawberries, nuts-increase oxalate
summer-increase Ca2+ and oxalate with increase vit d synthesis
job-are they dehydrated?
precipitating drugs e.g. thiazides, loop diuretics, antacids, corticosteroids, theophylline, aspirin, allopurinol
predisposing factors: recurrent UTIs-in magnesium ammonium phosphate stones
metabolic abnormalities: hypercalciuria/hypercalcaemia-hyperparathyroidism, neoplasia, sarcoidosis-1-alpha hydroxylase enzyme in granulomas, hyperthyroidism-increase bone turnover?, addison’s, cushing’s, lithium
hyperuricosuria/increase plasma urate-on its own or with gout
hyperoxaluria-primary, or secondary to high tea intake, or increased intestinal reabsorption due to ileal disease e.g. crohn’s, low Ca2+ intake
cystinuria
renal tubular acidosis-normal anion gap
UT abnormalitis: pelviureteric junction obstruction, hydronephrosis, horseshoe kidney
FH?
infection above stone? e.g. fever, loin pain, pyuria? this needs urgent intervention
tests for renal calculi?
FBC-infection? Us and Es Ca2+ PO43- urate HCO3- glucose urine dip-usually +ve for blood MSU-microscopy, culture and sensitivity 24 hr urine for calcium, oxalate, urate, citrate, sodium, creatinine, stone biochemistry X-ray KUM-kidneys, ureters, bladder, 80% of stones visible IV pyelogram USS-look for hydronephrosis or hydroureter spiral non-contrast CT
tment of renal stones?
analgesia e.g. diclofenac 75mg IV/IM, or 100mg suppository, opioids if CI, and IV fluids if can’t tolerate oral e.g. vomiting
antibiotics e.g. cefuroxime 1.5g/8h IV if infection
stones less than 5mm in lower ureter most pass spontaneously, increase fluid intake and sieve urine for analysis
stones more than 5mm/pain not resolving-medical expulsive therapy e.g. tamsulosin alpah blocker, or nifedipine ca2+ blocker, with or without prednisolone
can use ureteroscopy
shockwave lithotripsy using US, but may cause increase BP and DM
percutaneous nephrolithiotomy
indications for urgent intervention in renal stones?
infection and urinary tract obstruction-percutaneous nephrostomy may be needed to relieve obstruction
urosepsis
intractable pain and vomiting
impending ARF-urine ouput less than 0.5ml/kg/hr for more than 6hr in adults, creatinine increase by 26micromol/L or more within 48hr, 50% or greater increase from baseline creatinine within past 7 days or 25% or greater drop in eGFR in children in young people within past 7 days
obstruction in a solitary kidney
bilateral obstructing stones
how can renal stones be prevented?
drink plenty
normal calcium intake in diet
thiazide diuretic can be used in hypercalciuria
reduce oxalate intake e.g. drink less tea, take pyridoxine (vit B6)
allopurinol for urate
d-penicillamine to chelate cystine (also used in chelating copper in wilson’s disease)
how is GS diagnosis confirmed?
ultrasound scan of abdomen
what is a gallbladder mucocele?
occurs with failure to relieve cystic duct obstruction, the contents of an obstructed gallbladder, which are not infected
if infected, pus collects in gallbladder=empyema
what is Boas’ sign?
hyperaesthesia detected by drawing a pin lightly down the back of a patient’s chest with acute cholecysitis due to GB pain radiating through to tip of scapula (because of diaphragmatic irritation?)
what happens to the bowel which is left behind in a Hartmann’s operation?
proximal end of bowel is brought out as an end-colostomy
rectal stump is oversewn or stapled and left in peritoneal cavity
contents of inguinal canal in males?
spermatic cord: vas deferens artery to vas deferens cremasteric artery testicular artery pampiniform venous plexus genital branch of genitofemoral nerve sympathetic nerves lymphatics obliterated processus vaginalis
ilioinguinal nerve
external spermatic fascia from external oblique
cremasteric fascia from internal oblique and transversus abdominus
internal spermatic fascia from transversalis fascia
tests to perform when skin ulcers, and how are skin ulcers managed?
skin and ulcer BIOPSY may be necessary e.g. vasculitis assessment-need immunohistopathology, or malignant change in an established ulcer-marjolin’s ulcer
management: treat cause, focus on prevention
optimise nutrition
treat adverse RFs e.g. smoking and HTN in those with arteriopathy
expert nursing care, consider r/f to communtiy nurse, varciose leg ulcer clinic
4-layer compression bandaging may help in venous ulcers-only if ABPI acceptable-more than 0.8
can sometimes use topical agents e.g silver sulfadiazine and gentamicin
gangrene management?
cultures-look out for group A beta-haemolytic streptococci-cause of fournier’s (male genitalia) or meleney’s gangrene (post-op ulceration), both form of rapidly progressive necrotising fasciitis or myositis
get prompt surgical help in an atypical cellulitis
radical debridement with or without amputation needed, always covered by Abx including 5 days of benzylpenicillin IV starting 1hr pre-op, to prevent gas gangrene
get help of plastic surgeon
remember to consider mycobacteria in any necrotizing infection
gas gangrene-C.perfringens, oedema, creptius and bubbly brown pus, usually amputation, plus Abx and hyperbaric O2.
causes of anal fissures?
primary-low fibre diet-constipation, recurrence rate of 50%
secondary-crohn’s disease, Ca-may be suspected in elderly person presenting for the 1st time with an anal fissure
treatment of an anal fissure in presentation to primary care?
offer diet advice-need to increase fibre in diet to avoid constipation, 20-30g of fibre/day, and ensure adequate fluid intake
can give topical GTN-relaxes anal muscle and cause vasodilation to increase b.flow and hence improve fissure healing, should heal within 6-8 wks, if so may then use a 2nd course, patients may complain of headaches
can also consider topical diltiazem-Ca2+ blocker
may consider a stool softener e.g. docusate-a laxative which lowers surface tension and allows water and salts to penetrate accumulated hard dry faeces, can prevent hard dry stools and reduce straining.
if non healing, consider r/f to secondary care- may inject botulinum toxin-last about 6 weeks, or if recurrent consider lateral sphincterotomy.
treatment of haemorrhoids in primary care?
diet advice-increase fibre-aiming for 25-30g insoluble fibre per day-raw fruit and veg, cereals, fibre supplements, drink plenty, avoid excessive caffeine intake
laxative-bulk forming e.g. fybogel (isphagula husk)
analgesia e.g. paracetamol
corticosteroid cream, or suppository
diverticular disease risk factors?
being over 50 years of age and poor dietary intake of fibre- causing less distension of colon which permits high intramural pressures to develop that causes muscular hypertrophy and subsequent mucosal herniation at sites of potential weakness corresponding to points of b.vessel entry
obesity in young people
complicated diverticular disease seen more commonly in those who smoke, take NSAIDs and paracetamol, and in those who are obese and have low dietary fibre.
presentation of acute diverticulitis?
LLQ PAIN, typically acute onset (minimal time to max pain) low central abdo pain which shifts to LIF, but Asian pts commonly R sided diverticula so RIF pain, pain intermittent or constant, and may be assoc with change in bowel habit
accompanying fever, vomiting, anorexia
may be vague mass in LIF and on DRE, espec. if low-lying pelvic abscess
o/e:
fever, tachycardia
local tenderness, guarding (voluntary-due to pain, involuntary-due to parietal peritoneum irritation), with perforation of pericolic abscess-tender mass accompanied by swinging pyrexia and leucocytosis, or bowel-faecal peritonitis, will be board like rigidity, generalised tenderness, guarding
may also be presentation with colonic partial obstruction or pseudo-obstruction, and recurrent diverticulitis episodes can cause fibrosis and structuring that may present as complete obstruction
why are sigmoid diverticula examples of false diverticula?
they lack the normal muscle coats, so do not comprise all layers of bowel wall in contrast to meckel’s diverticulum
complications of diverticular disease?
haemorrhage-usually abrupt painless bleeding that may follow urge to defecate or mild lower abdo cramps, passage of large amounts of red or maroon blood or clots
abscesses
faecal peritonitis following bowel perforation in acute diverticulitis
fistulae e.g. colovesical-presenting with pneumaturia and faecaluria, and colovaginal-occur following abscess rupture
bowel obstruction due to diverticular structuring following recurrent diverticulitis episodes with subsequent fibrosis
chronic pain
how can acute diverticulitis and ischaemic colitis be differentiated between in an elderly patient?
can present quite similarly with LIF pain and vomiting
however, passage of bright red blood with bowel movements, and a barium enema showing thumb-printing-due to thickened mucosa with inflammation, suggest ischaemic colitis
ischaemic colitis=compromise of blood supply to colon, commonly as result of atheroma of mesenteric vessels: transverse and descending colon supplied by middle colic branch of SMA and L colic branch of IMA, L branch of middle colic anastomoses with ascending branch of L colic artery, anastomoses combine to form marginal artery.
why might ischaemic colitis occur in younger patients?
assoc with drugs: OCP cocaine abuse methamphetamine abuse and sickle cell disease
investigation results in acute diverticulitis?
FBC: raised WCC
CRP/ESR rasied
Us and Es-risk of pre-renal AKI if sepsis develops with peritonitis from ruptured pericolic abscess of bowel perforation
erect CXR-look for pneumoperitoneum due to perforation
AXR-bowel obstruction, soft tissue densities suggesting abscesses, bowel dilation
contrast enemas-extravasated contrast material outlining abscess cavity
CT with contrast-best for diagnosing and following course of an abscess
if urinary symptoms e.g. as inflamed colon lies against bladder, should test urine for blood, protein and bacteria, and MSU sent for culture
management of acute diverticulitis if patient is managed at home?
Broad-spectrum antibiotics should be prescribed to cover anaerobes and Gram-negative rods - eg, co-amoxiclav or a combination of ciprofloxacin and metronidazole (if allergic to penicillin). Antibiotic treatment should last for at least 7 days if used; however, recent evidence suggests that this should be reserved for the treatment of complicated rather than simple diverticulitis.
Paracetamol should be used for pain. opioids and NSAIDs assoc with increased risk of perforation.
Recommend clear liquids only; gradually reintroduce solid food as symptoms improve over 2-3 days.
Review within 48 hours, or sooner if symptoms deteriorate. Hospital admission should be arranged if symptoms persist or deteriorate.
Mesalazine (5-ASA) has been shown to be more effective in improving the severity of symptoms, bowel habit, and in preventing symptomatic recurrence of diverticulitis, than antibiotics alone.
indications for surgery in acute diverticulitis?
purulent or faecal peritonitis obstruction fistula uncontrolled sepsis inability to exclude carcinoma
surgery=hartmann’s procedure-sigmoid colectomy with formation of an end LIF colostomy, and oversewing/stapling of rectum, but has been found that forming a primary anastomosis reduced rates of post-operative peritonitis and emergency re-operation.
in hospital management of acute diverticulitis?
IV fluids and Abx-cephalosporin and metronidazole for 5-7 days
urinary catheter
DVT prophylaxis
radiological drainage for abscess-CT guided percutaneous drainage
BS and anti-anaerobe Abx e.g. co-amoxiclav and metronidazole, or ciprofloxacin and metronidazole for perforated disease
hartmanns’s-less risk of anastamotic leak
continue Abx post op, nurse on ITU if severe sepsis
may need careful fluid management, inotropic support, ventilation and haemofiltration to prevent or treat multi-organ failure
rpt US/CT may show intra-abdo collection requiring radio drainage
complications of tments for complicated diverticular disease:
peritonitis
anastamotic leak
paralytic ileus
multi-organ failure
left ureter and bladder damage during dissection
direct inguinal hernias travel through what?
hesselbach’s triangle:
base=inguinal ligament
lateral border=inferior epigastric artery
medial border= lateral border of rectus abdominis muscle
predisposing factors to inguinal hernias?
males chronic cough constipation urinary obstruction heavy lifting ascites past abdominal surgery e.g. iliohypogastric nerve damage during appendicectomy
location of superficial inguinal ring?
split in external oblique aponeurosis, just superior and medial to pubic tubercle
surgery for an inguinal hernia?
mesh repair-lichtenstein repair
polypropylene mesh used to reinforce posterior wall, and repair defect weakness to stop further omentum/bowel from herniating
warn about recurrence-less than 2%
lap repair can be done with less post-op pain, quicker recovery, and identification of undiagnosed contralateral hernias
advice to patients regarding return to work following inguinal hernia repair?
if open, may need 4 weeks’ rest and convalescence over 10 wks
new mesh or lap repairs, if comfortable, can return to manual work and driving in 2 weeks or less.
investigations to perform in suspected TIA/stroke?
FBC coagulation screen Us and Es glucose-hypoglycaemia cause of acute neurological impairment? cholesterol CXR-?infection cause of delirium ECG-AF? CT head/MRI carotid duplex scan vasculitis screen echo if cardiac cause suspected
drug treatment for secondary prevention of CVD post stroke?
ensure optimal management of HTN, DM and AF
ensure antiplatelet offered-aspirin 300mg daily for 2 wks following ischaemic stroke, then clopidogrel 75mg daily long term and consider PPI, modified release dipyridamole plus aspirin can be given if clopidogrel CI or not tolerated.
statin normally started 48hrs after an acute stroke, and cholesterol re-checked 1-3mnths after starting tment, and statin increased if total cholesterol more than 4mmol/L or LDL more than 2mmol/L.
no aspirin intially?, but LT clopidogrel treatment and statin if TIA
radiological assessment in suspected ruptured AAA?
AXR-75% of cases AAA shown as often calcified
CT abdominal aortogram- confirms diagnosis-gold standard
chronic pancreatitis causes?
chronic alcohol ingestion-most common
familial
trauma
AI chronic pancreatitis-ANA and RF assoc. steroid responsive and reversible, IgG and serum gammaglobulins raised
tropical-assoc. with insulin dependent DM development
metabolic-hypercalcaemia and hyperlipidaemia
ERCP
drugs e.g. azathioprine
chronic pancreatitis presentation?
severe epigastric pain with radiation through to the back
nausea and vomiting
malabsorption features e.g. steatorrhoea, diarrhoea, weight loss and protein deficiency
diabetes mellitus
chronic pancreatitis investigations?
FBC Us and Es and creatinine CRP LFTs-?biliary tract obstruction serum amylase (us normal) glucose and HbA1c Ca2+ secretin stimulation test low nutritional markers e.g. albumin, Hb, Mg2+ faecal elastase-malabsorption abdominal US-classically pancreatic calcification CT abdomen ERCP MRCP endoscopic US
chronic pancreatitis complications?
diabetes mellitus
malabsorption, require enzyme replacement
pericardial, pleural or peritoneal effusions
GI haemorrhage with pseudocyst erosion into artery
pseudocyst
vit B12 deficiency
pancreatic Ca-chronic inflammation may lead to changes predisposing to adenocarcinoma
if a severely ill pt has a GB empyema after acute cholecystitis but not yet fit enough for cholecystectomy, what tment can be done?
cholecystostomy-catheter placed through abdo wall to drain contents of a blocked GB
indications for surgery in IBD?**
refractory to medical tment
life threatening bleeding, massive haemorrhage
toxic megacolon
bowel obstruction, perforation with peritonitis
abscess, fistulae, strictures
investigations in PVD?
FBC-anaemia=correctable may be improve pain?, polycythaemia e.g. COPD pt due to renal hypoxia, hypercoagulable blood-prone to clots
Us and Es-reduced with renal artery stenosis, check function before IV contrast use in CT angiogram
ESR-check for vasculitis e.g. SLE, scleroderma
glucose/HbA1c-DM increased PVD risk
LFTs-check before drug tment e.g. statin
lipid profile
ECG
CXR
ABPI
arterial duplex USS
indications for hospital r/f in ulcerative colitis presentation?
more than 6 stools a day, plus at least 1 of: temp more than 37.6 degrees C HR more than 90 Hb less than 10.5 g/dL ESR more than 30
step 1 tment recommended by NICE for acute severe UC admitted to hospital?
IV corticosteroids and consider features prompting need for surgery
results of investigations in acute appendicitis?
if diagnosis not in doubt, no further investigation required
FBC: leucocytosis, but even in severe cases may be normal
urine dipstick-blood and protein, ?blood pyelonephritis and renal stone
pregnancy test-ruptured ectopic pregnancy
abdo USS
laparoscopy
management on acute appendicitis?
pt to be put NBM
opioid analgesics if severe pain
may benefit from IV crystalloids if been vomiting repeatedly, will need maintenance IV fluids as being put NBM
metronidazole 500mg/8h and cefuroxime 1.5g/8h, 1-3 doses starting 1hr pre-op IV, reduces rate of wound infections, give longer course if perforated
DVT prophylaxis to adults, espec. elderly
appendicectomy
complications of appendicectomy?
wound sepsis
pelvic abscess-swinging pyrexia, raised WCC, mass PR, needs drainage
common ABG result in patients following open surgery for ruptured AAA and why?
metabolic acidosis, PaO2 likely high if receiving 100% oxygen (intubated)
metabolic acidosis common due to aortic clamping, vasopressor use, massive blood loss/transfusion and hypothermia during prolonged anaesthesia.
this will worsen with complications of anastamosis bleeding, or acute lower limb or mesenteric ischaemia occurring in 1st 24-48hrs
patients at high risk of multi organ failure
how can severe HTN in emergency surgery be managed?
pt needs invasive BP monitoring-with an arterial line-catheter inserted into an artery.
risks: myocardial ischaemia, arrhythmias and intracranial haemorrhage
importance of encouraging smoking cessation prior to surgery?
improves airways, airway irritability and carboxyHb levels.
CO reduces O2 carrying capacity of Hb and inhibits release to tissues, increases risk of myocardial compromise
nictoine stimulates SNS-increases HR, BP and causes CA narrowing-again increasing risk of acute myocardial event
impaired ciliary function increases post op risk of chest infections.
increased risk with smoking of laryngospasm
how can bronchospasm be treated in surgery?
ephedrine hydrochloride-adrenoceptor agonist-act on beta 2 adrenoreceptors in bronchi to stimulate bronchodilation
why must adrenaline given with LA NOT be given into the digits or body appendages?
risk of ischaemic necrosis
risks with inhalational anaesthesia e.g. isoflurane?
increased risk of laryngospasm
more likely to cause PONV
more likely to get excitement phase-Guedel’s signs 2
principles of spinal anaesthesia?
LA e.g. lignocaine, or bupivacaine-slower onset of action but longer duration, injected directly into CSF within SA space
spinal needle inserted below L2 vertebra and above S1 vertebra, as termination of SC to form cauda equina at IV disc between L1 and L2, and sacral vertebra fused so access virtually impossible.
small opioid doses injected with SA extends duration of analgesia for up to 12-24hr post op.
post op hypotension is common due to vasodilatation, ensure O2 always given
contraindications to epidural and spinal anaesthesia?
coagulopathy e.g. haemophilia, or therapeutic anticoag. risk of epidural haematoma.
local skin sepsis-risk of introd. infection
hypovolaemia-will be signif. falls in cardiac output as compensatory vasoconstriction lost
low fixed cardiac output e.g. severe aortic stenosis-reduced venous return will further reduce cardiac output
raised IC pressure-risk of precipitating coning
what can be used to guide IV fluid resuscitation in a patient with a severe upper GI bleed where a CVP line may not be useful due to CCF or ascites?
a swan-ganz catheter (a catheter inserted into the pulmonary artery through the R side of the heart)
why should hartmann’s solution be avoided peri-op in diabetic patients?
contains lactate 29g, which can increase blood glucose
why is aortic cross clamping required in open AAA surgery?
to prevent retrograde bleeding
ensure for elective open repair that IV heparin given before clamps applied
*unclamping can lead to massive decrease in BP due to release of vasodilatory cytokines and metabolites from ischaemic tissues decreasing peripheral resistance, and central hypovolaemia due to blood sequestration by reperfused organs.
EVAR doesn’t require aortic cross clamping
recovery room discharge criteria?
patient fully conscious without excessive stimulation, able to maintain clear airway and exhibits protective airway reflexes
satisfactory respiration and oxygenation
CVS stable, no unexplained cardiac irregularity or persistent bleeding, pulse and BP close to pre op values, and peripheral perfusion adequate
pain and emesis controlled, appropriate analgesic and anti-emetic regimens prescibed
temp within acceptable limits, do not return to ward if significant hypothermia-at risk of significant cardiac arrhythmias
oxygen and IV therapy if appropriate should be prescribed
side effects of dexamethasone IV given as anti-emetic?
hyperglycaemia
dyspepsia
perineal burning if patient is awake
what is an epidural?
LA and opioid injected into the epidural space=potential space outside of the dura, bounded anteriorly by the posterior longitudinal ligament, posteriorly by the ligamentum flavum and vertebral lamina surface, and laterally by vertebral pedicles and intravertebral foramen.
needle must pass through skin, superficial fascia, deep fascia, supraspinous ligament, interspinous ligament then ligamentum flavum.
complications= hypotension
resp depression
urinary retention
motor block (leg weakness)
epidural haematoma or abscess
what is a cholangiocarcinoma, what are the RFs?
a cancer arising in any part of the biliary tree from the small intrahepatic bile ducts to the ampulla of vater
most common site= peri-hilar at bifurcation of the R and L hepatic ducts (klatskin’s tumour)
usually a ductal adenocarcinoma
at risk:
UC patients who develop primary sclerosing cholangitis
primary sclerosing cholangitis-10-20% lifetime risk of Ca
some crohn’s disease patients
parasitic infection-liver flukes
intra-hepatic cancer at risk-HIV, Hep C, cirrhosis and diabetes
cholangiocarcinoma presentation and investigations?
RUQ pain jaundice, dark urine and pale stools weight loss, anorexia pruritus hepatomegaly splenomegaly courvoisier's sign-palpable GB in presence of jaundice, possible with tumours distal to cystic duct
markedly raised ALP, GGT, conjugated bilirubin
prolonged PT and INR
raised CA-19-9, CEA
contrast MRI best for diagnosis, abdominal US may reveal intra-hepatic duct dilatation, ERCP can be used to show site of obstruction and take a biopsy
cholangiocarcinoma management?
surgical resection with adjuvant chemo
radiotherapy improves survival if inoperable or unresectable tumours
stents can be used for symptom relief
hiatus hernia presentation, investigations and management?
sliding type- usually reflux oesophagitis symptoms-burning retrosternal discomfort, acid taste in mouth, excess saliva, chronic cough.
rolling type-SOB, palpitations, arrhythmias, hiccupping and vomiting
CXR-poss widened mediastinum, with large fluid level sitting behind heart
barium swallow-confirms presence
endoscopy-hernia and reflux oesophagitis-erythema, benign stricturing, ulceration
24hr pH monitoring to confirm low pH in oesophagus
medical tment as for reflux oesophagitis-smoking cessation, low alcohol, lose weight, raise head of bed, large gap between evening meal and going to bed, avoid spicy foods, antacids e.g. gaviscon, H2 antagonists e.g. cimetidine, PPIs e.g. omeprazole
surgery-fundoplication as for reflux oesophagitis, if sliding
if rolling, stomach needs to be repositioned in abdomen before diaphragm repaired either directly or with a mesh.
prognosis good unless gastric volvulus occurs.
management of boerhaaves’ syndrome?
this refers to oesophageal perforation following a suppressed vomit, causing severe epigastric pain and cervical subcutaneous empysema due to air tracking along cervical muscles in the neck.
must give analgesia, Abx, IV fluids and restrict oral intake
can do simple surgical closure through high mid-line abdominal incision, and cover repaired area with fundoplication, flap of IC muscle or adjacent diaphragm.
if delayed diagnosis or small leak, pleural drain and conservative approach.
in hospital setting with severe diarrhoea, what is the 1st and essential step in investigation?
stool culture to exclude infective cause
if a panproctocolectomy (removal of all colon, rectum and anus) is performed to cure ulcerative colitis, what stoma is formed and how is skin irritation and digestion prevented?
an end ileostomy-1 lumen
terminal ileum is fashioned into a spout that protrudes above the level of the skin=the brooke ileostomy
how can risk of pelvic sepsis due to anastamotic leakage from ileo-anal pouch following surgery for UC be reduced?
fashion a temporary proximal loop ileostomy
after pouch surgery, bowel function is abnormal with 3-6 actions per day, and patients likely to suffer small bowel obstruction from adhesions.
how can the need for a blood transfusion for surgery be avoided?
correction of anaemia before surgery e.g. Fe and vit B12 supplementation
can give drugs to reduce bleeding e.g. tranexamic acid in cases of knee replacement, this is an anti-fibrinolytic drug-inhibits plasminogen activation so clot stabilised
stop anticoagulants before surgery-warfarin stopped at least 5 days before, if cover with LMWH stop 6 hrs prior to surgery
use of minimally invasive surgery e.g. laparoscopic
intraoperative cell salvage
features of an obstructed airway?
paradoxical chest and abdo movements-see-saw respirations
no sounds of air movement or abnormal associated noises e.g. gurgling, snoring, crowing, stridor, wheeze, rattling-secretions
absence of airflow on feeling for expired air
manoeuvres to relieve obstructed airway?
chin lift
jaw thrust
why are Hb levels less useful in actively bleeding patients?
delayed drop in Hb
signs to look for in suspected testicular torsion?
- very tender testicle o/e
- scrotal erythema
- absent cremasteric reflex-this is not specific, but if present, then strongly suggestive of another pathology
- prehn’s sign-helps distinguish between epididymitis and testicular torsion-elevating affected scrotum relieves pain in epididymitis (+ve sign) but won’t in torsion.
