Surgery

Question 1

POSSUM score - what is it used for, where to calculate it

Answer 1

estimates morbidity and mortality for patients undergoing general surgery

can be used to help aid decision making

MDCalc can work it out

Question 2

metabolic response to injury - first phase corresponds to what, what if it’s severe, second phase is what; 4 changes in metabolism; how energy production changes in the two phases

Answer 2

ebb phase is short and may correspond to tissue hypoperfusion of shock, with the features an attempt to maintain vascular volume and tissue perfusion, and severity of this phase determines outcome: if severe may develop systemic inflammatory response syndrome which requires intensive life support

flow phase lasts for days to weeks where metabolism is altered to ensure energy is available for vital tissues at expense of muscle/fat

biochemical changes in metabolic response to injury: glycogenolysis up so higher circulating glucose, gluconeogenesis up for same reason, lipolysis up to inc level of FFAs and provide glycerol to make glucose, proteolysis up to provide amino acids which can be catabolised for energy or used for wound healing
ebb as energy production decreases, flow as it increases above normal; initially catabolic, then anabolic

Question 3

acute phase protein response - stimulated by what 3 things, 3 major things that increase and why, 3 more up and 2 more down, interpreting raised CRP post surgery

Answer 3

stimulated by cytokines and raised levels of cortisol + glucagon
C reactive protein and complement increase to combat infection
coagulation factors inc to prevent blood loss
protease inhibitors (alpha antitrypsin, alpha macroglobulin) inc to prevent spread of tissue necrosis when lysosomal enzymes released from damaged cells
misc others with serum amyloid A, haptoglobin, caeruloplasmin up and albumin (redistributed to interstitial fluid), HDL/LDL down

as CRP up post surgery may not be useful to check, but get it POD1 as a baseline and then should fall by POD4 -> if high after this, esp if >100, suggests infection present

Question 4

creatine and creatinine - role of creatine (what catalyses this) and what kind of cell is it for (inc where is most of it), it is synthesised where from what; how much turned into creatinine each day and secreted where, hence 3 things causing higher levels and 4 things making it lower

Answer 4

creatine combines w phosphoryl groups to generate phosphocreatine which is used to regen ATP from ADP (CK catalyses this); for high energy demand cells, 95% of it is in the muscles with the rest in blood, brain, and other tissues

it’s synthesised in the liver and kidneys from glycine and arginine

each day 1-2% of muscle creatine is converted to creatinine in nonenzymatic fashion, and then excreted via the kidneys; higher levels may thus occur if GFR decs, or if dietary creatine or protein intake is increased

levels are decreased if muscle bulk decreased, liver disease, fluid overload, or poor nutrition

Question 5

repair and healing post inflam - what tissue is formed in wound, what two cells are recruited to form scars, what cell coordinates this and what 5 things do they do, how does VEGF work (3 steps)

Answer 5

granulation tissue is new tissue formed in wound during healing process, involving recruitment of new endothelial cells to form blood vessels and fibroblasts to lay down ECM which is remodelled to form strengthened scar tissue;

macrophages pivotal as central control: phagocytose debris (inc RBCs, apoptotic neutrophils, dead organisms etc), produce ROS and NO to kill microbes, recruit fibroblasts via FGF, recruit endothelial cells via VEGF and secrete metalloproteinases to allow remodelling of ECM

VEGF causes existing blood vessels to send out caps into area of damage with endothelial cells breaking off basement membrane of existing vessels and migrating to site of injury before proliferating and differentiating to form a lumen and acquiring supporting pericytes and smooth muscle to form mature vessel

Question 6

unilateral clubbing - normally associated with what, 6 egs of causes

Answer 6

unilateral clubbing: usually associated with local vascular lesions of the arm, axilla, and thoracic outlet

aneurysm, particularly of the subclavian artery; old dislocated shoulder; carcinoma of rul, AV fistula for dialysis, aortic arch problem, or PDA with pulm HTN

Question 7

how does referred pain work? what can shoulder pain tell you about the abdomen (3 problems)

Answer 7

referred pain is due to two first order sensory neurons sharing the same secondary - the brain interprets the pain as coming from the first order that most likely will carry pain signals, invariably this being the somatic one

shoulder pain is C4 ie phrenic nerve ie diaphragm irritation - can be due to subphrenic irritation directly eg gallbladder, or fluid tracking up the paracolic gutter (especially if pt is tilted towards their head), think eg ruptured ectopic or other surgical abdo eg perf ulcer/diverticula etc

Question 8

haematomas (3 types based on size, 5 steps in formation, 4 stages in breakdown, what can breakdown of a large one cause, how are they treated)

Answer 8

haematomas: ecchymoses are 1 centimetres in size or larger, and are therefore larger than petechiae (less than 3 millimetres in diameter) or purpura (3 to 10 millimetres in diameter)

Increased distress to tissue causes capillaries to break under the skin, allowing blood to escape and build up. As time progresses, blood seeps into the surrounding tissues, causing the bruise to darken and spread. Nerve endings within the affected tissue detect the increased
pressure, which, depending on severity and location, may be perceived as pain or pressure or be asymptomatic. The damaged capillary endothelium releases endothelin, a hormone that causes narrowing of the blood vessel to minimize bleeding. As the endothelium is destroyed, the underlying von Willebrand factor is exposed and initiates coagulation, which creates a temporary clot to plug the wound and eventually leads to restoration of normal tissue.

During this time, larger bruises may change colour due to the breakdown of haemoglobin from within escaped red blood cells in the extracellular space. The striking colours of a bruise are caused by the phagocytosis and sequential degradation of haemoglobin to biliverdin
to bilirubin to hemosiderin, with haemoglobin itself producing a red-blue colour, biliverdin producing a green colour, bilirubin producing a yellow colour, and hemosiderin producing a golden-brown colour

breakdown of a large haematoma may cause jaundice

usually even large ones are treated with RICE and get better over time, exception being if it is causing damage (neurovascular structure, organ, skin) or is in a place where it is likely to cause damage (septum, ear, shin)

Question 9

what is mcburneys point and why is it important? where does necrosis start in the appendix and why?

Answer 9

it is the location of the base of the appendix, which is important as the tip is mobile and so can hurt anywhere, but the base tends to be fixed and so very often tender at this point specifically

necrosis begins at the tip as it has the worst vascular supply

Question 10

intestinal obstruction - 2 likely causes if chronic and 2 if acute; proximal 3 features, what accompanying weight loss suggests, 2 features of SBO pain, 3 suggesting strangulation, 2 features of LBO pain, what feature to look for in stool, 4 examination findings, 4ix, 2 things to check in bloods

Answer 10

chronic dev suggests inflam or malignancy as causes whereas acute may be hernia or adhesion
proximal usually pain and vomiting w/o distension, more distal small bowel tends to be more distension and less vomiting; if weight loss accompanies suggests malignancy or chronic inflam eg crohns
pain from SBO generally in central abdo and colicky; severe, localised, unremitting suggests strangulated obstruction
colonic obstruction tends to have pain in umbilical and hypogastric regions; may have difficulty defaecating or a pseudo-diarrhoea if only more liquid parts of stool can pass
tenderness may be generalised in both cases, should check whole abdo for a hernia; high pitched bowel sounds as overactive SB tries to push contents through narrowing or absent if obstruction established; peritonism may accompany is perforation occurs
AXR or CT of small or large bowel; colonoscopy or sigmoidoscopy or barium enema of colon; upper GI endoscopy for oesophagus -> duodenum
check for raised white cell count: strangulation, lactate (necrosis)

Question 11

bilious vomiting in newborns

Answer 11

Bilious vomiting is when there is a significant (more than just a spot or two on the sheets) quantity of green (usually dark green) not yellow vomit

if bilious aspirates/vomiting:
gas/lactate, cultures, start abx, NGT on free drainage, hold feeds, get abdo XR; if acute abdo signs (tenderness, bloating) or obstruction, perf, or NEC shown on XR refer/transfer to paeds surgeons; if abnormal pH/lactate with normal XR but raised inflam markers treat as infection and regularly review, if bilious vomits continue despite treating infection then discuss with surgeons and consider contrast study; if no evidence of infectio, normal exam, normal XR then contrast study and refer/transfer to surgeons

malrotation:
Intestinal malrotation occurs as a consequence of failure of the fixation of bowel inside the abdominal cavity during development of the fetus. Common forms inc intestines all on right side, caecum up in epigastrium, or ladd’s bands causing obstruon

A volvulus is where the intestine twists upon itself and cuts off blood supply to a section of the bowel. This can occur rapidly and is an acute abdominal crisis.

Abnormal adhesions or Ladd’s bands that can partially block the passage of the contents of the intestine which can be more subtle with intermittent bilious vomiting in an apparently well looking infant.

if obstructed malrotation then NGT on free drainage, aspirate 6 hourly and replace gastric losses with IVF containing K and keep accurate fluid balance monitor and keep NBM, proceed to surgery

Question 12

gut ischaemia - 4 causes in order, 6 findings in acute setting, 5 findings in chronic setting

Answer 12

arterial thromboembolism > venous insufficiency > hypoperfusion > vasculitis

acute small bowel: severe abdo pain, reduced bowel sounds; peritonism and rectal bleeding are late, often preterminal signs; leucocytosis and metabolic acidosis
ischaemic colitis: abdo pain unrelated to meals, rectal bleeding, diarrhoea; mucosal oedema (thumb printing) on x ray; biopsy will show haemosiderin laden macros

Question 13

anal sepsis - initial ix and mx, 2 indications for what further ix, 2 associated conditions needing medical management, 3 sx, 2 sx of a common complication + what to investigate for if has this complication, when is seton placed, 2 common age groups

Answer 13

acutely, pus swab and surgical drainage w incision; if complex, or chronic need to define anatomy of abscess to anal sphincters and so MRI (used for most imaging in pelvis due to its bony nature) is first choice
fistulae can form and should be removed surgically

associated crohns or DM needs to be managed medically

tender red swelling near anus, oft very painful, oft fevers and malaise
fistula: rec perianal abscesses, oft pus or blood discharge; symptoms reduce when abscess bursts but often comes back

surgeon opens fistula along its length, it heals and scars; if sphincter involved then place seton (special suture)

Question 14

haemorrhoids - what they are, 4 types, 4 ways to present, 2 mx depending on type

Answer 14

dilatation of anal veins; first degree are internal, 2nd enter anal canal on straining but spont reduce; 3rd need manual reduction; 4th cannot be reduced
most common presentation is feeling lump at anus, 2nd most common is rectal bleeding (usually small amount of fresh blood on toilet paper)
some may thrombose (v painful) or cause faecal incontinence but this is rare; 3rd and 4th degree resected, 1st and 2nd lifestyle changes (if these alone don’t work then eg sclerotherapy, ligation etc)

Question 15

diverticulitis (uncomplicated mx 4 things, 5 mx if severe pain or complications, 5 complications); sigmoid volv how mx

Answer 15

management of uncomplicated diverticulitis in primary care with:

Oral co-amoxiclav (at least 5 days)
Analgesia (avoiding NSAIDs and opiates, if possible)
Only taking clear liquids (avoiding solid food) until symptoms improve (usually 2-3 days)
Follow-up within 2 days to review symptoms

Patients with severe pain or complications require admission to hospital. Hospital treatment involves management as with any patient with
an acute abdomen or sepsis, including:

Nil by mouth or clear fluids only
IV antibiotics
IV fluids
Analgesia
Urgent investigations (e.g., CT scan)
Urgent surgery may be required for complications

Complications of acute diverticulitis are:

Perforation
Peritonitis
Peridiverticular abscess
Large haemorrhage
fistulae or obstruction

Conservative management with endoscopic decompression can be attempted in patients with sigmoid volvulus (without peritonitis).

Question 16

piles management

Answer 16

if local creams, treating constipation, dietary changes dont improve then hospital
may attempt rubber band ligation, infrared coagulation, sclero/electrotherapy
if doesnt work then surgical resection or staple them back in
note heavy lifting, esp long term for job or gym, is a risk factor

Question 17

cholelithiasis - what percent asymptomatic, 2 pigment types, 8 sx, 5 sx in elderly, 2ix, 2mx

Answer 17

gallstones
60-80% dont get symptoms
cholesterol, brown pigment (bacterial infection causing hydrolysis of bilirubin conjugates), black pigment (increased bilirubin or bile pH)
presentation: right hypochondrium or epigastric pain, radiates to upper back or right shoulder, steady and intense pain usually an hour or so after meals (esp fatty food), 75% patients get an urge to walk, each episode 1-24hr; likelihood inc’d if no heartburn and not relieved by defaecation; murphys sign; low grade fever
in elderly only symptoms might be nausea, malaise, weakness, anorexia, vomiting

USS first line ix, then consider eg MRCP

cholecystectomy, UDCA (prophylaxis if thought to be at high risk)

Question 18

rectal foreign bodies (3x when to suspect perf); 5 ix, 3 mx

Answer 18

beware risk of rectal or sigmoid perforation (suspect if PR bleeding, sig pelvis/abdo pain, systemically unwell)

supine AXR (lat pelvis view may also help); abdo signs or PR bleeding then eCXR for perf, G&S in case laparotomy needed, FBC and U&Es

biopsy forceps w/ rigid sigmoidoscopy, local pain relief; GA may be needed
if injury or can’t get it out that way, laparotomy +/- end colostomy

Question 19

stoma (3 types, for first (where, contents consistency, stoma relative to skin, 3 subtypes, how common is hernia and 3 complications), for second (where, contents consistency, stoma relative to skin 3 subtypes), for third (after what procedure, where, bag contents), what if blocked)

Answer 19

colostomy, ileostomy, urostomy

colostomy: generally in LIF, contents of bag generally solid, the stoma is flush to the skin as enzymes less alkaline; permanent ones oft after CRC resection of most of rectum, although anastomosis is preferred; temporary to rest bowel after eg divert or LBO; loop after recent surgery before rejoining; can occur anywhere along colon; parastomal hernia in ~50% cases; dusky in ischaemia, inflamed in infection, prolapse
ileostomy: usually in RIF, contents of bag usually more liquid, enzymes and alkaline nature so spout; permanent usually after panproctocolectomy for UC or familial adenomatous polyposis; temp during emergency resection where not yet safe to anastomose remaining bits eg sepsis or bleeding; loop types may also occur
urostomy: after cystectomy, usually in RIF and bag will contain urine, ureters attached to ileal conduit thence bag

note stomas can get blocked causing obstruction

Question 20

post op complications (what is common in first 24 hrs, 24-72 (4x), day 3-7 (5), after 7 (1); atelectasis (why x2, sx x2, 2mx), LMWH unless when? compression stockings unless when (x3); general source of infection day 1-2; 3-5; 5-7; 4 things to do in postop h+; 4 things giving poor wound healing; 4 steps if wound dehiscence; how late after op can incisional hernia appear; 3 urological problems; 4 sx of postop ileus and 5 mx; 6 sx and 8 mx of suspected anastomotic leak

Answer 20

common post-op complications: fever common in first 24 hours as part of response to surgery; 24-72 may be atelectasis, pneumonia, infected surgery site, reaction to
transfusion or drug; day 3-7 think pneumonia, wound infection, abscess, sepsis, phlebitis, after 7 days DVT or PE

atelectasis due to secretions and light breaths, mild tachyp/tachycard, physio and pos pressure vent if needed or eg incentive spirometer

LMWH unless egfr <30 then UFH; stockings/compression unless periph artery disease, local skin disease, periph oedema

infectious fever generally: Day 1-2 – consider a respiratory source
Day 3-5 – consider a urinary tract source
Day 5-7 – consider a surgical site infection or abscess/collection formation

post op h+ give protamine if heparin used, order cross matched blood, do coag screen and plat count and give FFP etc as needed
poor wound healing due to malnut, steroids/immunosup, excess suture tension, poor blood supply

wound dehiscence usually 7-10 days post op, preceded by serosanguinous discharge: fluid resus, sterile wound dressing, opioid, theatre
incisional hernia: can appear up to 15 years after

urinary retention common and catheter may be needed but conservative if can as may resolve overnight, then soon after TWOC (if fails multiple times exclude source like constipation or infection and plan to bring to TWOC clinic +/- start tamsulosin); also UTI, pt may be at risk of AKI

postop ileus: Failure to pass flatus or faeces
Sensation of bloating and distention
Nausea and vomiting (or high NG output)
absent bowel sounds (unlike tinkling in classical obstruction)
routine blood, CT abdo/pelvis; NBM and daily bloods monitoring for AKI, reduce opioids; warn pt when bowel function returns first stools may be runny
NG tube may be useful
early and late adhesions may occur causing mechanical obstruction

anastomotic leak: abdominal pain and fever. They usually present between 5-7 days post-operatively. Other features* may include delirium or prolonged ileus.

On examination, patients may be pyrexial, tachycardic, and / or with signs of peritonism. It is important to check for any faeculent /
purulent material or bile in any drains.

*Remember, any patient with systemic sepsis or is not improving as expected (“failing to progress”) after a GI resection should be
considered to have an anastomotic leak until proven otherwise
CT scan abdo pelvis with contrast, early resus and senior involvement, urgent bloods inc VBG; NBM, fluids start, catheter, antibiotics
septic or large/multiple collections get laparotomy, single small conservative with antibiotics

Question 21

wound infection (4 levels of wound cleanliness + infection risk, 5 things that inc infection rate, 7 features of wound infection + general mx x2, 5 times when maybe proph abx)

Answer 21

clean: uninfected wound with no viscera opening or inflam eg hernia repair, infection rate <1%
clean contaminated: viscera open but no spillage, rate <10% eg biliary tract
contaminated: visc open with spillage or obvious inflam eg gangrenous appendix, 15-20%
dirty/infected: gross contamination like gunshot wound with devitalised tissue, frank pus, or gross soiling eg perf large bowel, up to 40%

malnutrition, poorly controlled DM, immunosuppression, smoking all inc rate of infection; wounds in poorly vascularised tissue like amputation stump more at risk of infection

wound infection usually days or weeks after initial operation: pain, swelling, heat, malaise, anorexia, vomiting, swinging pyrexia

drain pus, antibiotics for any cellulitis

prophylactic antibiotics for specific cases eg: when implanting a prosthetic, after amputation (due to risk of gas gangrene), penetrating wounds and compound fractures, organ transplant, operation opening GI or biliary tract; metronidazole to cover for anaerobes if GI esp large bowel opened

Question 22

pulmonary collapse (atelectasis inc timeframe, why sats down, 2 reasons why mucous builds up, 9sx, 5 mx)

Answer 22

some degree expected from most thoracic or abdo surgery within first 48hrs

dyspnoea (dec oxygenation as collapsed part acts as a shunt), pulse up, temp poss up; coarse crackles, fruity cough from secretions being retained (anaesthetics inc mucous production but dec cilia activity, though pain preventing expectoration is most important cause); chest movements down, basal dullness and dec air entry, O2 sats down; secondary infection is possible and occasionally may dev into abscess/empyema

smoking and chest infection inc risk so stop both before surgery, post-op cough and breathing exercises (physio may help) +/- incentive spirometry or PEP device, opioids or other analgesia to help suppress pain of coughing, antibiotics if sputum infected

Question 23

thromboembolism (5 things why surg incs risk, 5 other risk factors, 3 ways to reduce risk, how might PE present in elderly, highest risk day + what might provoke, why infarction of lung unlikely from PE and what increases risk of this

Answer 23

blood loss and platelet consumption during op so fibrinogen and platelet synth up, levels peak ~10 days after, inc tendency to thrombose; stasis due to dec mobility during and post op; pressure from mattress, inflam/sepsis, or damage during op all lead to damaged venous endothelium so inc thrombosis risk
pelvic and hip surgery esp risk as veins often damaged

OCP/HRT incs risk; obesity, malignancy, elderly, hypercoaguable state all inc risk

early mobilisation, minimise/treat risk factors, subcut dalteparin (LMWH) start preop and keep going after but cleared by kidney so be careful in CKD as might get over-anticoag’d, consider UH if eGFR low

note in the elderly confusion due to hypoxia may be how PE presents; 10th post-op day is day of highest suspicion but can be before or after too, often occurred when eg straining at stool as raised abdo pressure dislodges pelvic thrombus; lung infarction from PE uncommon as bronchial a’s perfuse the lungs themselves, but can occur esp if preexisting pulm hypertension

Question 24

wound dehiscence (10 things that impair wound healing, 2 things that might weaken wound)

Answer 24

impaired wound healing expected from: obesity, diabetes, on steroids, uraemia, excess wound tension, poor blood supply, being on corner of wound, protein/vit C def, jaundice, distention from eg ascites or ileus obstruction
infection or haematoma of wound weakens it
pink fluid (serous postop fluid tinged with blood) leaks through, often 10th day, and if not spotted then strain may provoke bowel or omentum to protrude; can get massive incisional hernia if deep layers come undone but sup layers hold; prognosis good, simple repair

Question 25

postop pyrexia (8 things to do)

Answer 25

pyrexia of unknown origin often after surgery; check wound site, then for thrombophlebitis at any cannulae; listen to chest and consider CXR or uss, looking for collapse, infection, infarction, subphrenic abscess
check legs for DVT, DRE for pelvic abscess; urine culture, stool culture; consider sensitivity to a drug that was used and any other causes of infection

Question 26

enterocutaneous fistulae - 3 things to test for, what sx suggests SI source, imaging to get, 5 mx inc 3 indications for surgery, 6 reasons to get

Answer 26

effluent, may need to test for eg amylase (SI), bile, stool etc; SI rapid skin excoriation

dye testing or imaging eg CT with oral contrast

protect skin with eg barrier creams, treat sepsis and any abscesses, ensure nutrition, analyse fistula anatomy, plan surgery if needed (usually if proximal, high output, or linked to obstruction); low volume, distal can have conservative management

ECF usually after bowel surgery but can complicate IBD, malig, perf peptic ulcer, abdo trauma like stabbing/gunshot, or from infections

Question 27

CV conditions impact on periops

Answer 27

heart failure inc’s post-op morbidity and mortality substantially, esp if current or recent decompensation (within last 6mo); esp at risk if cant tolerate eg climbing stairs w/o being breathless
hypertension - risk of hypotension on induction, high hypertension on airway stim, arrhythmias, MI, stroke
IHD - risk of periop MI, arrest, or death calculated from lee’s revised cardiac risk index which considers risk of surgery, history of IHD, history of cerebrovasc disease, history of heart failure, DM treatment, preop serum creatinine level

Question 28

preop assessment (ASA grades, mallampati classfication + 4 other oropharynx things they look for)

Answer 28

Anaesthetic exam including airway assessment then give ASA grade on anaesthetic chart (risk of post op complications/mortlity): I is normal healthy pt, II mild systemic disease, III severe systemic disease, IV severe syst disease that is threat to life, V pt prob wont survive w/o the op, E is emergency op

assess airway: look for any obvious facial abnorms, esp retrognathia which could cause difficulties during airway insertion
mallampati classification
check dentition, any loose teeth?’ max extend neck measure thyromental dist (intubation may be difficult if <6.5cm/~3 finger breadths)

mallampati I if full soft palate, II if full uvula just about, III if only base of uvula, IV if cant see uvula/soft palate)

Question 29

general anaesthesia (inhalational use when x2 and 3 egs; how commonly used is propofol and 3 s/e, thiopental 1 perk and 2 drawbacks; 3 other options inc good choice for shocked/elderly

Answer 29

inhalational: only used to induce GA in eg children or rapid onset/offset eg labour but can be used to maintain; fluranes (sevo/des), halothane, NO

iv: used to induce and maintain anaesthesia, sedation in eg ITU; propofol most commonly used, smooth rapid loc and rapid recovery; it depresses myocardium and reduces sys vasc res so marked fall in ABP, also resp depression and relaxes muscles inc in larynx/pharynx; usual emulsion can trigger egg allergic reaction as has egg components (still safe for egg allergy ppl to have); thiopental has less drop in ABP, but can cause periods of myocardial ischaemia if coronary stenosis, has a hangover effect so less good for day cases

more iv: BZDs eg midazolam: anxiolytic, anticonvulsant, amnesic, sedative, hypnotic; CVS stability of this and ketamine and etomidate make them better choices for shocked or elderly patients

Question 30

neuromusc blocking agents - what for rapid induction, 4 egs of non-depol, what reverses them (and what to give with it)

Answer 30

suxameth for rapid induction and short lasting muscle relaxation eg emerg intubation
non depol eg rocuronium, atracurium, pancuronium, vecuronium; the nondepol can be reversed with neostigmine (plus an antimuscarinic like atropine to protect from effects of raised [ACh] at non NMJ sites)

Question 31

misc anaesthetic drugs - analgesics, antiemetics (4 things that mean these needed)

Answer 31

analgesia achieved during operation usually with a strong opioid (fentanyl, oxycodone, morphine) and then postoperatively often with morphine initially or else the WHO pain ladder
antiemetics are also often used post-surgery; opioids and inhalational anaesthetics both inc risk, also time under anaesthesia, and bag and mask ventilation (dilate stomach); dexamethasone may be used at induction as proph; if gastric emptying down then metoclop or domperi unless obstruction suspected; metabolic or biochem imbalance (uraemia etc) or cytotoxic agents trial on metoclop; opioid responds well to ondan or cyclizine; also ensure pain is controlled, pt well hydrated, anxiety treated (as these 3 things might also contribute to feeling sick); consider also any postop comps as might make patient nauseated or sick eg infection, ileus, bleeding etc

Question 32

analgesia during an OP (6 s/e of opioids, ketamine (mechanism, monitoring, given with what to reduce x3),

Answer 32

opioid is standard, but s/e of sedation, nausea, urinary retention, constipation (motility down), vomiting, pruritus

ketamine - NMDAr antag, reduces central sensitization and so opioid requirement; ecg monitoring is required; oft given with benzo to reduce excitability and so hallucinations, delirium, agitation etc

Question 33

opioid tolerant patients (2 problems, who might have this, what to do with them)

Answer 33

need more consideration: pain scores often higher and more difficult to control
risk of withdrawal
may be on opioids long term for cancer pain or chronic non-cancer pain; problem mainly with >120mg/d for >3mo, likely to have been on them for years
so maintain the background opioid equiv theyre on (eg if they take oral morphine convert their normal dose into iv morphine/some other opioid)
then optimise non-opioid management: NSAIDs, paracetamol, local anaesthetics, ketamine, gabapentinoids, maybe iv lidocaine

Question 34

hyperoxia (4 risks)

Answer 34

a risk of oxygen therapy, generally paO2 raised above 11-13kPA, 16kPa as a maximum; may make infarcts in MI or stroke worse, injure lungs, or cause retinopathy, or suppress breathing in chronically hypercapnic pts
so titrate the O2 being received to avoid hyperoxia; reserve 15L/min non-rebreathe mask for emergency situations

Question 35

allergic and fluid loss shocks (what test do twice if suspect anaphylaxis, skin% slough in SJS vs TEN, what test confirms diagnosis and rules out what other condition)

Answer 35

anaphylaxis suspected: serum tryptase at onset, 1-4hrs and 24hrs after

allergic + fluid loss shock: SJS/TEN (macules, erythema, skin sloughing - <10% in SJS, >10% in TEN); mucosa affected giving sore sticky
conjunctiva, red eyes and mouth ulcers, GIT (diarrhoea) and resp tract (coughing); skin biopsy to confirm and exclude eg staph scalded
skin syndrome

Question 36

DIC (11 causes), 2 step process, 4 ix findings, 6 mx

Answer 36

causes inc tumours (solid and blood), pre-eclampsia, amniotic fluid embolism, placental abruption, trauma, burns, rhabdo, sepsis, allergy/venom, transfusion reaction, surgery

TF released after tissue damage or cytokine release, excessively activating clotting cascade; coagulation factors rapidly consumed by tiny

low platelets, high PT, high APTT, d dimer positive

treat underlying condition, if bleeding and plats <50 then give, if PT and aPTT prolonged give FFP, and if hypofibrinogenaemia persists can give cryoprecipitate or fibrinogen concentrate

if thrombosis predominates, such as arterial or venous thromboembolism, severe purpura fulminans associated with acral ischemia or vascular skin infarction, therapeutic doses of heparin should be considered -> monitor for bleeding

In critically ill, non-bleeding patients with DIC, prophylaxis for venous thromboembolism with prophylactic doses of heparin or low molecular weight heparin is recommended.

Question 37

burns (wallace rule of nines and alternative, airway 4 things to assess and 2 mx, breathing 5 things to assess for 1 ix and 1 mx; circulation main threat, how to calculate how much fluid to give and how fast to give

Answer 37

Wallace Rule of 9s: % of total body surface area (TBSA)
Head and neck: 9%
Arms: 9% each
Torso: 18% front and back
Legs: 18% each
Perineum: 1%
(Palm: 1%)

L&B charts more accurate, esp for kids

Airway: examine for respiratory burns, hoarse voice or stridor. Flexible laryngoscopy can
be helpful. Consider early intubation + dexamethasone

Breathing: 100% O2; exclude constricting/circumferential burns; look for signs of CO poisoning: headache, cherry red appearance of skin, confusion, N+V); ABG

Circulation: fluid losses may be huge, 2x large bore cannulae, bloods including G+S, start 2L warmed Hartmann’s immediately
4 x weight (kg) x % TBSA = mL of Hartmann’s in 24h (same in kids)
Replace fluid from time of burn
Give half of this amount in the first 8 hours

Question 38

managing tetanus risk with injuries - 3 options, 3 egs of high risk wound

Answer 38

Patient has had a full course of tetanus vaccines, with the last dose < 10 years ago
no vaccine nor tetanus immunoglobulin is required, regardless of the wound severity

Patient has had a full course of tetanus vaccines, with the last dose > 10 years ago
if tetanus prone wound (most wounds apart from simple clean cuts eg burns, bites, anything with soil, penetrating injuries even eg nail or thorn): reinforcing dose of vaccine
high-risk wounds (e.g. compound fractures, delayed surgical intervention, significant degree of devitalised tissue): reinforcing dose of vaccine + tetanus immunoglobulin

If vaccination history is incomplete or unknown
reinforcing dose of vaccine, regardless of the wound severity
for tetanus prone and high-risk wounds: reinforcing dose of vaccine + tetanus immunoglobulin

Question 39

transplant rejection - type 1 timeframe, cause, what characterises this type, 2 ways to avoid; type 2 timeframe, 2 causes, how common (and why not in transfusions), direct vs indirect, predicted by what (and 3:2 of types of rejection they mediate); type 3 timeframe, possibly related to what and what kind of hypersensitivity

Answer 39

3 types; hyperacute within mins to hours due to preexisiting ab as in ABO (ABO antigen on endothelium), complement damages tissue and aggregation of platelets blocking microvasculature, this type seen in xenotransplants of eg pigs (IgM/G against modified sugars on pig tissue, pig tissue doesnt have proteins to disable complement eg DAF); very fast rejection is characterized by vessels thrombosis leading to graft necrosis. Today, this type of rejection is avoided in most cases by checking for ABO compatibility and by excluding the presence of antidonor human leukocyte antigen (HLA) antibodies by cross-match techniques between donor graft cells and recipient sera

acute: 1 week to several months after; Acute rejection is thought to result from two immunological mechanisms that may act alone or in combination: (1) a T-cell-dependent process that corresponds to acute cellular rejection, and (2) a B-cell-dependent process that generates the acute humoral rejection. With current immunosuppressive treatment, acute rejection occurs in less than 15% of the transplants; part caused by T cells recognising transplanted tissue, no problem in transfusion as RBCs dont have MHC; a type of type IV as involves CTL against HLA class I and CD4 against HLA class II
can have direct recognition (host naive T cell pop has some alloreactive against HLA allotypes not in host, DCs sensitising by presenting from inflamed donor organ, peptides on foreign MHC); indirect when host DCs pick up allogeneic proteins from eg donor DCs that die in secondary lymphoid tissue, with both foreign HLA and minor (H) antigens picked up; indirect slower rejection than direct
predicted by DSA - anti- human leukocyte antigen donor specific antibodies (anti-HLA DSAs). Preformed donor-specific antibodies in sensitized patients can trigger hyperacute rejection, accelerated acute rejection, and early acute antibody-mediated rejection. De novo donor-specific antibodies are associated with late acute antibody-mediated rejection, chronic antibody-mediated rejection.

chronic: rejection years after transplant with no improvement in treating chronic rejection over the last 30 years; mechanism obscure but maybe related to immune response against blood vessels, giving ischaemia and loss of function; may be due to type III hypersensitivity due to IgG against HLA class I on graft, forming immune complexes which deposit in blood vessels

Question 40

minimising risk of transplant rejection - 2 egs of types that have minimal rejection; HLA matching important for which tissues x3, why is precise match uncommon, immunosuppression essential except when x2, in general what 3 meds needed after transplant and for latter 2 give 2 egs each

Answer 40

little rejection with transplant of privileged sites, eg cornea
haematopoietic stem cell transplants: many exhibit no immunological problems as autologous

HLA matching: v important for haematopoietic stem cells, significant in heart/kidney, no effect on liver; precise match uncommon as 6 polymorphic genes

immunosuppression: essential in transplantation unless autologous or immunologically privileged; for kidney transplant do combo of steroids, cytotoxic like azathioprine, immunosuppressive like cyclosporin; in general after a transplant pt will be on 3 drugs: a steroid, an anti-metabolite (azathioprine, mycophenolate), and a calcineurin inhibitor (tacrolimus/ciclosporin)

Question 41

specific chemo drug side effects (doxorubicin mechanism + 4, bleomycin 4, vincristine 4 + mechanism and how you shouldnt give, cyclophos mechanism + avoid when x2 + 5, cisplat 6, methotrex 10 + 2x not to have, thalid 3 + when not to take)

Answer 41

doxorubicin - topoiso inhibitor, pancytopenia, hair loss, sore mouth, dilated cardiomyopathy giving CHF; echo before (maybe during)

bleomycin - flu like symptoms, alopecia, raynauds, pulmonary fibrosis

vincristine - periph neurop (early symptom may be foot drop - avoid if FH of CMT), hyponat, constipation, alopecia; microtubule assembly inhib; dont give intrathec

cyclophos - alkylating agent so avoid in pregnancy, lactating; n&v, pancytopenia, haemorrhagic cystitis (micro or gross haematuria, maybe dysuria), very gonadotoxic; risk of myeloprolif malignancies and bladder/skin cancers inc AML

cisplatin - nephrotoxic so reduce dose if impaired kidney function; neurotoxic; ototoxic; severely emetogenic; hypomag/calc/kal; bone marrow suppression

methotrexate - hepatotoxicity, ulcerative stomatitis, leukopenia, nausea, pneumonitis; teratogenic, dont have if trying for baby and either gender or while pregnant or breast feeding; tender/swollen gums; hair loss, diarrhoea; nephrotoxic

thalidomide - excessive blood clots, teratogenic (dont take if can become pregnant or trying inc if man), periph neuro

Question 42

perioperative medication mx (NBM definition + whether meds can be taken, 9 things to hold)

Answer 42

NBM: No food / particulate fluids for 6 hours pre-operatively
* Clear fluids can freely consumed for up to 2 hours pre-operatively
* Within 2 hours of surgery, medication can be taken with up to 20ml of water
* If medication cannot be tolerated with 20ml of fluid, alternative routes of administration may need to be considered

ACEi/ARB: omit dose on day of procedure if under GA

Antiplatelets: aspirin (prim prevention or spine/eye then stop 7 days prior otherwise continue), ADP (continue, avoiding epidural, unless surgeon doesnt want to and no coronary stents or recent CVA), DAPT (cont aspirin only unless stent in prev 12mo in which case discuss with cardio

Anticoags: warfarin (hold until INR <1.3) hold DOAC for 2 days prior to procedure; IV hep stop 4-6 hrs pre-procedure, VTE proph stop 12hrs pre-op, tx LMWH stop 24hrs pre-op

Bisphos: omit morning dose pre-op

Clozapine: stop 12hrs before surgery

Lithium: hold for 24hrs pre-surgery unless minor op

Galatamine/rivastigmine: hold for 24hrs pre-op

Moclobemide: hold 24hrs pre-op

OCP: minor can continue if immobility risk low, major should ideally stop for 4 weeks prior inc any surgery to legs; POP can continue

HRT: as above, but transdermal can continue

Question 43

periop medications: steroids (2 options), diabetes (insulin rules; which T2DM meds can be continued and why, which held)

Answer 43

steroids: if taking >10mg a day (or have done within previous 3mo) then risk of relative adrenal suppression, or if taking high dose inhaled steroids, then will need steroid cover with 100mg hydrocort at induction and further 200mg hydrocort infusion for 24hrs; if taking <10 then no cover but should continue normal dose

insulin: on the day before surgery, once daily long-acting insulin analogues should be given at 80 % of the usual dose; otherwise the patient’s usual insulin should be given as normal;
on the day of surgery and throughout the intra-operative period, once daily long-acting insulin analogues should be continued at 80 % of the usual dose; twice daily/premixed should be given at 50% dose; all other insulin should be stopped until the patient is eating and drinking again after surgery
once NBM start VRII, give glucose if hypo occurs

Conversion back to a subcutaneous insulin should not begin until the patient can eat and drink without nausea or vomiting

Pioglitazone, dipeptidylpeptidase-4 inhibitors (gliptins) can be taken as normal during the whole peri-operative period - DPP4 glucose dependent mechanism, also means they won’t be too effective while fasted but no risk. GLP1 mimetics held as slow gastric emptying

Sodium glucose co-transporter 2 inhibitors should be omitted on the day of surgery and not restarted until the patient is stable

sulphonylureas should be omitted day of surgery and not restarted until eating and drinking again; If hyperglycaemia occurs, an appropriate dose of subcutaneous rapid-acting insulin may be given. A second dose may be given 2 hours later, and a variable rate intravenous insulin infusion considered if hyperglycaemia persists

metformin stop when pre-op fast begins, start VRII if take >1 dose a day or BM >12 2+ times; restart after 24hrs or when eating

Question 44

warfarin, DOACs, antiplats in hip fractures

Answer 44

stop, send INR, give 2mg vit K IV
check INR after 6 hrs and give further 2mg if INR 2-4, 3mg if 4-6, 4mg if 6-8, and 5mg if >8

restart on first post-op day

if high risk (mechanical heart valve or target 3+ for other reasons) then bridging may be needed if can wait 24 hrs

DOACs/antiplats
don’t delay bc of antiplats
stop DOAC, surgery 24hrs after last dose if eGFR >30 and 48hrs after if <30
dabigatran you need to wait until TT normal

Question 45

6 indications for VRII pre-op; managing pre and post op hyperglyc

Answer 45

Type 1 Diabetes undergoing surgery with long starvation period- missing more than 1
meal.
* Type 1 Diabetes undergoing surgery who has not received background insulin.
* Type 2 Diabetes undergoing surgery with long starvation period-missing more than 1
meal and develops hyperglycaemia (capillary blood glucose > 12mmol/l).
* Patients with poorly controlled Diabetes (HbA1c>69mmol/l) and surgery cannot be
postponed.
* Decompensated Diabetes.
* Most patients with Diabetes requiring emergency surgery

for both pre and post-op hyperglyc if BM >12 check ketones, if not in DKA give sc novorapid and recheck BM and ketones in an hour; if still not DKA but BM not come down start VRII

Question 46

inguinal hernia and hydrocoele in children

Answer 46

Caused by a patent processus vaginalis (PPV). If the PV does not close at all,
intestine may prolapse into the inguinal canal (hernia). If the PV closes partially, there
may be no hernia, but peritoneal fluid can run down into the scrotum (hydrocoele).
 Conditions which result in increased peritoneal fluid being produced (e.g. viral
infections) can result in an apparent “acute onset” of hydrocoele.

hernia found from mid-inguinal point (deep
ring), down inguinal canal+/- into
scrotum or labia, doesn’t transilluminate except in infants, appears when straining or crying, reduced under pressure when lying down (if not reducible then emergency), tender and red when incarcerated; all need routine surgical appt for operation, urgent referral if <12mo as higher risk of incarceration and emergency referral if incarcerated - even if you manage to reduce needs operation on next list; main threat is to the gonads; almost all hernias in children are indirect

how to reduce: give analgesia then use thumb and index finger of one hand to push downwards to create a funnel at the superficial inguinal ring; apply pressure superiorly and laterally with the thumb, index and middle finger of the other hand and direct the hernia towards the internal ring; with a circular motion, apply gradual pressure and guide the hernia into the ring; displacing the scrotum medially may also assist in reduction; if fail then urgent surgical referral

hydrocoele usually found in scrotum, may extend upwards to inguinal canal, or may
be cystic swelling IN canal; can get above it, unlike inguinal hernia; not tender, transilluminates, often appears or gets larger in evenings, not reducible, may close up to 2 years of age so no surgery until after that point, if >2yo then gets routine surgical referral

Question 47

anorectal malformations

Answer 47

if detected whether postnatally or antenatally then attention should be made to the potential presence of cardiac anomalies (VACTERL association)

if concern re: obstruction then don’t feed; place NGT on free drainage with IVF, if tube can’t be placed then CXR with tube as far in as possible for possible atresia; needs surgical referral and mum should express breast milk in the mean time

besides atresia/stenosis may commonly see fistula (to surface, bladder, vagina)

perineal fistula may need anoplasty only, most others need colostomy formation then later repair

Question 48

management of common surgical neonatal problems

Answer 48

congenital diaphragmtic hernia:
link to pulm hypoplasia and pulm HTN
DO NOT use CPAP or bag & mask ventilation unless absolutely necessary as increases volume of stomach, compressing lungs further - thus intubate and ventilate, insert NGT on free drainage and keep NBM, monitor sats

gastroschisis:
Cover lesion with cling film / occlusive wrap. DO NOT cover with moist pack or cotton wool.
Position baby lying right side or supine, support external bowel to prevent injury and
stretch
Observe bowel colour to ensure circulation is not compromised. Reposition if concern.
If bowel condition compromised: record photographically.
NBM/indwelling large bore NGT on free drainage. Aspirate NGT every 20 minutes.
Observe thermoregulation carefully
2 X IV access- peripheral. Assess pain responses and ensure adequate analgesia.
Check circulatory status- perfusion, HR, lactate, acidosis- if concerns consider fluid boluseslikely to require 20-30mls/kg 0.9% Normal Saline (as a minimum – often more).
If respiratory support needed ETT intubation minimises bowel distension-avoid CPAP

exomphalos
Position cord clamp well away from lesion to avoid organ damage.
Not urgent transport as the protective membrane prevents heat and fluid loss, however if this rupture then treat as gastroschisis.
High risk of karyotype abnormalities or associated congenital anomalies.
If isolated – consider Beckwith-Weiderman. Monitor BSL closely (hyperinsulinaemia)

perforation (eg NEC)
Consider paralysis if ventilation difficult.
Occasionally an abdominal drain may be required to improve ventilation
Check circulatory status- if concerns consider fluid boluses, correct acidosis and
consider use of inotropes in sick infant (dopamine first line)
Check coagulation and platelets. Give blood products as appropriate
Triple antibiotics
Care should be taken to provide adequate analgesia
Urgent surgery

obstruction - consider TOF, pyloric stenosis, duodenal atresia, malrotation/volvulus, hirschprungs, meconium ileus (most will have CF), meconium plug, anogenital abnorm
meconium plug syndrome:
appears idiopathic but linked to prematurity, mothers with diabetes or who received Mg for pre-eclampsia and linked to hirschprung disease and small left colon syndrome

In diabetic mothers, the higher occurrence of neonatal hypoglycemia induces the pancreas to secrete glucagon. In turn, glucagon decreases peristalsis in the left colon. Furthermore, neonatal hypoglycemia stimulates the autonomic nervous system. Increased stimulation of the sympathetic nervous system causes a decrease in intestinal movement

abdo XR non-specific: rarely, if there is any air in the rectum, may there be an outline of the meconium mas on an abdominal radiograph. The abdominal film may also demonstrate small bowel gas mixed with colonic meconium producing a granular appearance similar to necrotizing enterocolitis (NEC). When a granular pattern occurs within the first 12 hours, the diagnosis is most likely meconium plug syndrome, as NEC develops after >18 hours. In contrast to meconium ileus, meconium plug syndrome radiographs do not demonstrate microcolon.

Contrast Enema is the investigation of choice and is often diagnostic and therapeutic. serial enemas may be needed. If there is no passage of stools by 48 to 72 hours, surgical options may be a consideration. A suction rectal biopsy should be performed. Additionally, if temporary decompression of the bowel is necessary, a temporary ileostomy is performed.

will want to test for CF and do a rectal biopsy for hirschprungs

Small left colon syndrome(SLCS): Historically considered along with meconium plug syndrome as both are transient functional obstructions of the colon. SLCS characteristically presents a sudden change in the colonic diameter proximal to the splenic flexure. MPS occurs mostly in preterms, whereas SLCS occurs in full-term babies. A majority of both MPS and SLCS patients revert to normal spontaneously within 30 days

Meconium ileus: Here, the inspissated meconium obstructs the small intestine rather than the colon and decreases the diameter of the colon, resulting in a microcolon. In comparison, meconium ileus is a disease of critical nature as it has a higher rate of complications such as perforation, small bowel volvulus, peritonitis, and intestinal atresia and strong association with cystic fibrosis

Question 49

rectal prolapse paeds guidelines

Answer 49

most common in children < 4 years with a peak incidence in 2 – 3 year olds

common causes:
o Idiopathic - usually self limiting
o Chronic Constipation.
o Cystic fibrosis (5 - 20%) – should be considered in Caucasian population. Consider
sweat test if concerns e.g. chronic respiratory symptoms / faltering growth

Usually non tender mucosal mass (red rosette) seen protruding from anus, initially only on straining.
Bleeding occasionally noted as the primary symptom.
May become irreducible

Differential Diagnosis
1. Prolapsing rectal polyp
2. Prolapsing haemorrhoid
3. Intussusception (very rarely prolapses from anus)

If prolapse is present when the child attends hospital, manual reduction with
analgesia. Firm pressure to reduce oedema and then reduction of innermost mucosal
lead point first is usually successful.
 Treat underlying condition (e.g. diarrhoea or constipation) and avoidance of
straining.
 Child should be restricted from spending prolonged periods of time on commode and a
step stool in front of adult commode will assist child in toilet training and may eliminate
straining behaviours

Manual reduction by surgeons under anaesthesia sometimes needed for very large prolapses

all rectal prolapses, even when reduced, should be referred to paediatric surgical outpatients

Question 50

intussusception

Answer 50

the invagination of a proximal segment of bowel into the distal bowel lumen. The commonest occurrence is a segment of ileum moving into the colon through the ileo-caecal valve.
It may occur at any age but commonly occurs in the 2 month to 2 year age group with a
peak incidence at 5 to 9 months.
It is a surgical emergency

Intermittent pain which is colicky, severe and may be associated with the child
drawing up the legs.
o Episodes typically occur 2-3 times/hour and may increase over the next 12-24 hours
o During these episodes the child may have pallor and lethargy which may be the
predominant presenting signs
o Vomiting is usually a prominent feature (but bile stained vomiting is a late sign)
o Bowel motions
 blood and/or mucus
 classic “ red currant” jelly stool is a late sign
o Diarrhoea is quite common and can lead to a misdiagnosis of gastroenteritis
o There may be a preceding respiratory or diarrhoeal illness, or recent immunisation

may see:
Pallor, lethargy - may be intermittent, and the child may look well in between episodes
o Abdominal mass - sausage shaped abdominal mass palpable in about two thirds of children (most often in RUQ).
o Distended abdomen
o Hypovolaemic shock

get FBC, U&Es, gas, glucose, G&S

USS is ix of choice
Target or doughnut sign- round mass with alternating hypo- and hyper-echoic areas
2. Pseudokidney- longitudinal or oblique image that simulates a kidney due to inner
hyperechogenicity
o Large volume of free fluid suggests perforation (consider AXR if not already performed)
o Ultrasound can also exclude a pathological lead point
o Colour doppler may suggest bowel necrosis (air enema reduction less likely to be
successful)

place IVs, resus with 20mls/kg fluid bolus of 0.9% sodium chloride, place NGT on free drainage, refer to surgeons, start cef + metro, consent for air enema inc risk of perf and laparotomy needed

if reduced keep NBM and admit, if not reduced discussed with paeds consultant surgeon and consider 2nd air enema or going to theatre; if perforates may develop tension pneumoperitoneum so decompress with wide bore cannula into LLQ and put out priority call, then to theatres when stable

Question 51

vitellointestinal duct remnant and urachus

Answer 51

an embryonic structure, which connects the yolk sac to the midgut and failure of its resorption results in various anomalies including Meckel’s diverticulum, patent vitelline duct, fibrous band, sinus tract, umbilical polyp and cyst, enteric fistula with ileal intussusception prolapsing over the umbilicus or hemorrhagic umbilical mass

Generally, the duct fully obliterates during the 9th week of gestation

connection in patent VID is usually to the ileum, but less commonly to the appendix or colon

may be asymptomatic; however, common presentations include abdominal pain, rectal bleeding, intestinal obstruction, umbilical drainage and umbilical hernia

treatment of a patent VID is wedge or segmental resection

urachus meanwhile is a fibrous remnant of the allantois, a canal that drains the urinary bladder of the fetus that joins and runs within the umbilical cord; failure of its obliteration allows cyst or fistula formation, with potential for urine to drain from the bladder out of the umbilical cord

Question 52

meckels diverticulum

Answer 52

common congenital abnormality of the small intestine caused by incomplete obliteration of the vitelline (omphalomesenteric) duct. Most of the patients with Meckel diverticulum are asymptomatic, with the abnormality discovered only incidentally on imaging studies.

if the duct fails to partially or entirely separate and involute, it can result in an omphalomesenteric cyst, omphalomesenteric fistula that drains through the umbilicus, or a fibrous band from the diverticulum to the umbilicus, which can cause an obstruction; If there is no additional attachment, it forms into a Meckel diverticulum

may contain ectopic gastric mucosa without pancreas to neutralise, so secretes an acid that is not neutralized resulting in ulceration of the adjacent mucosa leading to painless rectal bleeding distal to the diverticulum; may cause obstruction by acting as a lead point for volvulus or else via a fibrous band attached to the diverticulum; may become inflamed giving diverticulitis +/- perforation

counts for approximately 50% of all lower GI bleeding in children younger than 2 years of age; XR and contrast studies detect rarely; most sensitive test is meckels scan where nuclear study is done by injecting technetium-99m which is absorbed by the ectopic gastric mucosa allowing for visualization of the Meckel diverticulum; tagged red blood cell scan an option if bleeding; if results of this negative then consider angiogram; if still inconclusive or pt is haemodynamically unstable then laparotomy/scopy is needed

volume resus +/- translation, and surgical referral for theatre

ddx for rectal bleeding:
Stool may be mistaken for hematochezia if children ingest bismuth, iron, or spinach. A hemoccult test will show that the stool will be negative. In infants, swallowed maternal blood from bleeding nipples, milk protein allergy, intussusception, and anal fissures can commonly cause rectal bleeding. Necrotizing enterocolitis should be on the differential in neonates and premature infants. Other common causes of rectal bleeding in older children include colitis, gastroenteritis, HSP, HUS, intussusception, inflammatory bowel disease, and vascular malformation

Question 53

mesenteric adenitis

Answer 53

Primary mesenteric adenitis is most commonly lymphadenopathy in the mesentery near the terminal ileum without a discoverable underlying cause for the inflammation

so presents secondary to bacterial or viral gastroenteritis, with 2 common gram-negative bacteria that are known to cause mesenteric adenitis include Yersinia pseudotuberculosis and Yersinia enterocolitica but also salmonella, E coli, and streptococci among others

child under ten years of age who presents with acute onset right lower quadrant abdominal pain is more likely to have mesenteric adenitis rather than acute appendicitis. Mesenteric adenitis commonly follows recent gastroenteritis or upper respiratory infection. Common symptoms include fever, vomiting, change in bowel habits, periumbilical, and/or right lower quadrant abdominal pain

CRP/WCC may be raised, get urine dip to exclude UTI; USS needed to tell from appendicitis: will show enlarged nodes

home with good fluid intake, regular simple analgesia, and explanation may take up to 4 weeks to resolve

Question 54

Mittelschmerz pain

Answer 54

now more commonly called ovulation pain

occurs midcycle (between days 7 and 24) in women

Mittelschmerz most often presents as an acute lower quadrant (usually right-sided) pain ranging from a mild ache to intense pain. Along with several other gynecologic pathologies, mittelschmerz may present similarly to acute appendicitis, leading to misdiagnosis

pain is felt on the side of ovulation, and because ovulation occurs on a random ovary each cycle, the pain may switch sides or stay on the same side from one cycle to another.

may resolve in an hour or up to 2-3 days

underlying mechanism is unclear but may involve irritation due to release of blood and fluid from the follicle or high blood levels of luteinizing hormone causing contraction of smooth muscle

Diagnosis involves ruling out other potential causes such as appendicitis, endometriosis, ovarian cysts, ectopic pregnancy, and sexually transmitted infections

Diagnosis of mittelschmerz is generally made if a woman is mid-cycle and a pelvic examination shows no abnormalities. If the pain is prolonged and/or severe, other diagnostic procedures such as an abdominal ultrasound may be performed

ibuprofen to relieve pain, contraceptives might help to prevent

Question 55

acute abdo pain algorithm

Answer 55

first identify if in shock and if yes treat that first

next bilious vomiting -> if present get AXR, refer to surgeons if problem identified
if not then is there inguinal/genital swelling? if yes try to reduce and refer to surgeons

if severe lower quadrant pain and post menarche female get pregnancy test + USS abdo, refer findings to surgeons/O&G

if severe pain that is episodic (and not constipated) consider intussusception and get abdo USS, refer to surgeons + perform air enema in this case

red urine? check for haematuria (then consider eg renal USS), and if not then consider testing for porphyria

get a urine dip ?UTI, rx if identified

any cough or focal signs get CXR, rx pneumonia if confirmed

if RUQ/epigastric pain consider cholecystitis and get USS

then apply alvorado scroe for appendicitis (if 3 criteria or RLQ pain >8 hours then take bloods so you can fully calculate it; if >6 refer to surgeons, if 4-6 with maintained oral intake and response to analgesia get USS within 48 hours

if diarrhoea consider if gastroent or IBD flare explains

if systemically unwell or WCC >20 or CRP >20 get senior review; if systemically well and tolerating oral intake admit for 2-4 hours and if continues on same trajectory then for discharge with GP f/up

Question 56

potty training

Answer 56

Most children are ready to master potty independence and lead in many parts of the process from around 18 months. The majority of children will be capable of doing most things including wiping by themselves when they start school.

Research shows it is better for your child’s bladder and bowel health to stop using nappies between 18 and 30 months

From the time a child can safely sit up by themselves, they can start sitting on a potty with your help.

Good times to try a potty sit include:
Shortly after they wake up
After mealtimes
Anytime you know they need to go

trouble shooting:
doesn’t want to use potty - Leave the potty training for a month or so, then try again, slowly and calmly. A reward chart with stickers may help your child stay motivated.
won’t stay on potty - make potty training interesting eg keep certain books or toys in the bathroom especially for potty times and don’t keep them on it for too long if they’re not going
keeps wetting themself - could go back to nappies for a while and try again in a few weeks, or you can keep leaving the nappies off, but be prepared to change and wash clothes a lot; If you do stop, leave it for a few weeks before you start again.
was dry, now wetting again - may mean they have a bladder infection, constipation, or type 1 diabetes or else an emotional reason (change of routine or another disruption, such as moving house or a new baby arriving, can often have an effect)

rectal prolapse is most common to occur when child is potty training

Question 57

undescended testes

Answer 57

Inspect the external genitalia to assess for any abnormalities:
An undescended testis with hypospadias (penile abnormality) or bifid or unfused scrotum may suggest a disorder of sexual development.
Bilateral impalpable undescended testes with ambiguous genitalia may suggest an endocrine abnormality, such as congenital adrenal hyperplasia.

If the testis is not located in the scrotal sac and there is a suspected undescended testis, use the fingers to ‘milk’ from the external ring to the scrotum along the inguinal canal to try to palpate the testis.
A possible inguinal testis may ‘bounce’ under the fingers. Once located, assess whether the testis can be moved to the scrotum.
If it cannot be palpated or manipulated into the base of the scrotum, this suggests an undescended testis.
If it can be manipulated into the base of the scrotum, but retracts back to an inguinal position after a variable time following manipulation, this suggests a retractile testis.

compensatory hypertrophy is likely if the scrotal testis is larger than the glans penis and this suggests testicular absence or atrophy on contralat side

If a disorder of sexual development is excluded and the testes are not present in the scrotum by 4–5 months of age, ensure the child has been referred to paediatric surgery or urology, to be seen by 6 months of age
If disorder of sexual dev is suspected then urgent referral to a paediatrician within 24 hours has been arranged (ideally within a tertiary children’s unit with a specialist disorders of sexual development service), as the child may need urgent endocrine or genetic investigation

orchidopexy will generally be performed before 12mo to minimise risk of fertility problems and cancer

retractile testes can be monitored and should fully descend on their own by puberty - refer if not