1 - The Acute Abdomen and Surgically Unwell Patient Flashcards

Question

Which triad is said to be classic of oesophageal perforation?

Answer 1

Mackler's triad - Vomiting - Chest pain - Subcutaneous emphysema

Answer 2

This pic - contrast has leaked out from lower oesophagus and into the chest.

Answer 3

Small ones - may not need repair - sometimes just draining the leak and NBM will allow it to heal.

Answer 4

Peptic ulceration

Answer 5

Duodenal - 90-95% Gastric - 70-85%

Answer 6

Rarely - very large holes may require a distal gastrectomy

Answer 7

Ischaemia Inflammatory Erosion Trauma

Answer 8

Iatrogenic

Answer 9

Diverticular disease NSAID use (30% of cases) Smoking

Answer 10

Caecal perforation Relief of pain can occur initially when perforation occurs.

Answer 11

CT = gold standard

Answer 12

Trauma - foreign body, penetrating trauma or iatrogenic

Answer 13

Pelvic or back pain May be systemically unwell (unless contained in the pelvis) PR bleeding

Answer 14

Extrinsic (external) compression Bowel wall problem Luminal

Answer 15

Bowels may still be functional despite obstruction - so be cautious. These Ps will have early vomiting as a symptom.

Answer 16

50-80% = gastric malignancy

Answer 17

D2 If obstruction is before CBD - will not have bilious vomiting. If the obstruction is after D2 you will have bilious vomiting (green colour).

Answer 18

Hypokalaemia Hypochloraemia

Answer 19

Adhesions cause 80-90%

Answer 20

Crohns Previous abdominal surgery Age

Answer 21

Small bowel

Answer 22

CT = gold standard Contrast can confirm obstruction

Answer 23

When a segment of bowel is incarcerated at two different points.

Answer 24

A mechanical obstruction in which a large gallstone gets stuck onto nearby bowel - inflammation - over time, stone gradually erodes through the walls, goes into the bowel (fistula) and sometimes it can obstruct the bowel towards terminal ileum. .

Answer 25

Features of SBO May have Hx of RUQ pain / cholecystitis

Answer 26

Small bowel obstruction - gallstone may be seen Aerobilia (air in the biliary tree)

Answer 27

Surgery usually needed - small bowel is opened and stone removed. Gallbladder fistula means they are unlikely to form more stones

Answer 28

Paralytic ileus

Answer 29

Surgery (10-30% of Ps after colorectal surgery) Can also occur from - Critical illness - Uraemia or renal failure - Peritonitis - Abdominal trauma

Answer 30

1-14 days after surgery

Answer 31

Often can be done clinically due to Hx of previous surgery. If doubt - CT = gold standard

Answer 32

Supportive Tx - IV fluids NG tube Reduced oral intake IV nutrition if prolonged (v rare)

Answer 33

Ileal Crohn's Age <40 at diagnosis Smoking Perianal disease

Answer 34

CT & MRI Absence of inflammation = surgery is more likely to be needed.

Answer 35

If fibrotic stricture = surgery If inflammation = medical therapy can be tried

Answer 36

>75% Wider and thinner bowel more distally and more solid luminal contents. Also - cancer and diverticular disease are more common in the distal colon

Answer 37

Cancer (60%) Diverticular disease (20%) Volvulus Intussusception Acute colonic pseudo-obstruction

Answer 38

Ogilvie syndrome, also known as acute colonic pseudo-obstruction (ACPO), is a sudden and unexplained paralysis of your colon. Your colon acts like it's blocked or obstructed by something (pseudo-obstruction) but nothing is physically obstructing it. The problem is in your colon's motor system.

Answer 39

AXR - may show dilated bowel CT = gold standard

Answer 40

Surgical emergency Urgent decompression of obstruction needed to prevent upstream caecal perforation

Answer 41

Laplace's law

Answer 42

Acute obstruction - surgery - resection +/- anastomosis or +/- stoma. If resection not possible - defunction upstream.

Answer 43

Intussusception

Answer 44

Cancer (2/3rds) Also - IBD, Meckel's diverticulum, large colonic polyps

Answer 45

AF HF Kidney failure Prothrombotic conditions Older Ps Smoking

Answer 46

Embolus Thrombus Volvulus

Answer 47

Abdo pain - out of proportion with clinical findings Nausea, vomiting, diarrhoea PR bleeding if colonic Academia

Answer 48

Can also get raised IRP

Answer 49

If it is due to a venous occlusion = the lactate can't return into the bloodstream - so serum lactate appears normal.

Answer 50

HF Atherosclerotic disease AF Acute thrombosis Medications - chemo, NSAIDs, vasopressors Previous AAA repair (causing interruption of IMA)

Answer 51

Splenic flexure Rectosigmoid junction These are watershed areas

Answer 52

CT Endoscopy can differentiate between causes of colitis

Answer 53

Mesenteric angina Usually caused by chronic arterial stenosis / occlusion due to atherosclerosis.

Answer 54

Abdominal pain 15-30 mins after eating a meal - leading to chronic weight loss and a fear of eating. Caused by arterial stenosis - not enough blood can enter into the bowel to deal with increased demands.

Answer 55

An acute circulatory failure that compromises tissue perfusion

Answer 56

Carcinoid syndrome - sign of neuroendocrine tumour

Answer 57

Increased oestrogen levels due to chronic liver disease

Answer 58

Fat Fluid Faeces Foetus Flatus

Answer 59

Always the RHS

Answer 60

Alcohol Excess

Answer 61

Resonant = gas - bowel / lungs Dull = solid organs

Answer 62

Start at 5th IC space and percuss downwards. An abnormal liver will extend > 2 finger breaths below the costal margin

Answer 63

Always pathological

Answer 64

MUST Screening Tool

Answer 65

Valvulae conniventes

Answer 66

Extends from oesophagus to D2 Supplied by coeliac artery Nerve = vagus nerve

Answer 67

Parietal cells produce H+ via H+/K+ ATPase These can be stimulated by - PSS vagus nerve directly - by Histamine release (from ECL cells) - by gastrin release (from G cells) - produced in response to peptides in bowel lumen

Answer 68

Gastritis Dyspepsia Peptic ulceration Gastric cancer

Answer 69

Diarrhoea Inc risk of GI infection (e.g. C Diff)

Answer 70

Sliding & Rolling

Answer 71

Are reversible inhibitors of COX enzymes COX1 = produces prostaglandins which are protective in the GI tract COX2 = produces PGs which mediate pain and inflammation Lose these PGs - get reduced gastric mucous and bicarb production, reduced gastric BF --> reduced protection of gastric mucosa and a reduced ability to repair.

Answer 72

H Pylori NSAIDs Rarer: - Stress - Malignancy - Zollinger-Ellinson syndrome - Medications

Answer 73

Rare neuroendocrine tumour of G cells - most often of the pancreas --> uncontrolled and excessive gastrin = multiple GI ulcers due to excessive acid production.

Answer 74

Duodenal ulcers Gastric ulcers Duodenal x 4 more likely than gastric

Answer 75

Lesser curve of the stomach

Answer 76

Hx and Ex OGD

Answer 77

Variceal (11%) and non-variceal bleeds (89%)

Answer 78

Increased portal venous pressure (e.g. cirrhotic liver disease)

Answer 79

Stop the bleeding Reduce portal pressure Medication (β blockers reduce portal pressure) Radiological intervention Endoscopic tx

Answer 80

Behind D1 Can be eroded into by a posterior ulcer

Answer 81

Metaplasia = change from one cell type to another Dysplasia = disordered cell development

Answer 82

Replacement of squamous epithelium with columnar epithelium in the oesophagus

Answer 83

Based on level of dysplasia High grade - needs Tx inc ablation, endoscopic removal or surgery Low grade - mostly surveillance Metaplasia without dysplasia - surveillance only

Answer 84

Hypovolaemic Cardiogenic Distributive (severe peripheral dilation - sceptic or anaphylactic) Obstructive

Answer 85

Hypotension Hyperventilation Rapid weak pulse Cold, clammy, cyanotic skin Oliguria Poss confusion, combativeness or anxiety Clinically - metabolic acidosis, low O2, low central venous pressure.

Answer 86

Stage 1 - attempt at compensation = vasoconstriction Stage 2 - decompensation - body mechanisms are unable to sustain perfusion Stage 3 - irreversible changes - major damage to organs

Answer 87

Hypovolaemic

Answer 88

Preload insufficiency = reduces diastolic filling = low cardiac output. Causes = haemorrhagic or non-hemorrhagic (e.g. volume loss from burns, V&D)

Answer 89

Inappropriate expansion of circulatory capacity compared to volume. Caused by failure of peripheral resistance or vasodilation of large veins

Answer 90

Maintains cardiac after load - is controlled by the tone of arteriolar and capillary sphincters.

Answer 91

Septic shock

Answer 92

IgE Type 1 hypersensitivity - mast cells release histamine -> dilation of venous compartment and rapid movement of fluid into tissues.

Answer 93

Abx Radiological contrast

Answer 94

Failure of the pump = drastic reduction in cardiac output.

Answer 95

Caused by extracardiac causes - e.g. pulmonary problems (causing RHF) or mechanical disruption = reduced preload. E.g. PE, pul HT, valvular stenosis, tension pneumo etc.W

Answer 96

Is a fall in arterial BP SS activated. HR inc and tries to inc CO. Intense vasoconstriction (except sepsis) to restore vol by inc peripheral resistance. Hypoxic tissues use anaerobic respiration - causes metabolic acidosis - then tachypnoea tries to compensate. P = cold, pale, clammy, hypotensive, thready pulse and increased RR. Septic shock - peripheries are vasodilator - unresponsive to SS. Skin is flushed, hot and CO is increased to fill dilated periphery. Pulse = bounding.

Answer 97

Identify cause of fluid loss - stop loss and give fluid replacement.

Answer 98

Respiratory support Correct electrolyte and acid-base Drugs to maintain BP and CO Treat underlying cause.

Answer 99

DIC (disseminated intravascular coagulation) Sepsis - activation of clotting cascade exhausts supply of platelets and clotting factors and fibrinogen. Get high D-Dimer (as this is a fibrin degradation product). DIC - causes spontaneous bruising or bleeding and uncontrollable haemorrhage

Answer 100

Manage initial cause IV heparin Transfusion of clotting factors (FFP and cryoprecipitate)

Answer 101

Remove cause Secure airway and give O2 Lie flat and raise feet Start IV fluids 500mcgs IM adrenaline - 5m intervals if necessary. Antihistamine by IV Hydrocortisone by IV - blocks histamine receptors (takes several hours)

Answer 102

Ps stabilise but relapse later on

Answer 103

Small bowel obstruction - get symptoms within hours Large bowel obstruction - more insidious onset - presentation can be delayed by up to a week

Answer 104

(1). Gastric outlet obstruction (2). Small bowel obstruction (3) Large bowel obstruction - distal.

Answer 105

Bowel can become trapped and the lumen obstructed. Venous return is occluded - causes bowel wall oedema and further obstruction. Closed loop of bowl dilates with gas fermentation - this and venous back pressure inhibits arterial inflow - this causing ischaemia and infarction.

Answer 106

Inguinal Femoral Umbilical Incisional

Answer 107

Rigid and tender abdomen Bowel sounds are absent (no peristalsis)

Answer 108

Causes irritation and peritonitis like symptoms, but more muted.

Answer 109

Worsening continuous abdominal pain Diarrhoea High swinging temperature

Answer 110

Blood lost beyond the duodenum should pass rectally.

Answer 111

FBCs U&Es Prothrombin ratio LFTs Blood group & antibody test Order blood for transfusion

Answer 112

Determining the patient's ABO and Rh D group. Performing an antibody screen, and identifying any atypical antibodies which may be present. Checking the results against any historical data that might be available for the patient. The process takes around 40 minutes and no blood is issued. If patient blood have atypical red cell antibodies, the laboratory will do additional tests to identify them. If they have been pregnant or transfused in the last 3 months the sample is valid for 72 hours. If not, sample is valid for 7 days.

Answer 113

A crossmatch is the final step of pretransfusion compatibility testing, to request blood from the laboratory. Crossmatching involves physically mixing of patient’s blood with the donor’s blood, in order to see if any immune reaction occurs After ensuring that donnor blood is compatible, the donor blood is issued and can be transfused to the patient. This process takes around 40 minutes, in addition to the 40 minutes required to G&S the blood. It is not possible for the laboratory to provide crossmatched blood without having processed a G&S sample first. When is Crossmatch required? Crossmatch is performed if blood loss is anticipated – the surgeon will usually inform about this.

Answer 114

Vomiting and diarrhoea, dehydration, reduced urine output, diuretic therapy, urinary tract disease, renal failure, pancreatitis and sepsis

Answer 115

Acute pancreatitis and septicaemia (DIC), severe bleeding (consumption coagulopathy) or those with Hx of bleeding disorders

Answer 116

Can affect the clotting of the blood and make it hypercoaguable

Answer 117

(2) Give high flow oxygen (15L via non re-breathe mask) This question is about understanding the ABCDE priorities as discussed in the lecture for this week. As the patient is talking coherently, one can assume that his airway is patent which means that breathing should be the next priority. There are 2 oxygen options here – high flow or 28%. In the lecture, we discuss that an acutely unwell surgical patient is by default given high flow oxygen. The COPD here actually is clearly not too significant as he is generally fairly asymptomatic. In reality there are actually very few COPD patients who are genuinely dependent on their hypoxic drive to breathe, and therefore giving high flow oxygen is the correct answer for a clearly unwell surgical patient as he is more likely to die from hypoperfusion and hypoxia of the tissues than from hypoventilation from retention of CO2. Regardless, the latter will take time to develop (if at all), and clearly if concerned about the risk then you should monitor for signs of hypoventilation which can then be corrected/managed should the need arise, but the priority is to get the patient high flow O2 as he is clearly critically unwell. Sepsis 6 comes later after initial resuscitation (or during for some of the elements), fluids come as part of circulation (the next priority) and a CT and emergency theatre are clearly likely going to be needed at some point but are not the next priority.

Answer 118

The classic triad for appendicitis is migratory abdominal pain moving from the central area to the right iliac fossa (McBurney’s point), GI upset (vomiting and/or diarrhoea) and anorexia (>70% of cases). Despite this, appendicitis remains a challenge to diagnose clinically as many patients do not have some or even all of these. Three of the options are signs not symptoms, although they are strong indicators of appendicitis when present with the symptoms (RIF mass, raised temperature Rovsing’s sign). Dysuria is sometimes seen with appendicitis due to irritation of the bladder, but is not a classic feature and non-migratory RIF pain alone is not a classic symptom, although clearly some patients do present in this way. Answer b has the migratory pain moving in the wrong direction.

Answer 119

The correct answer here is c) the Hinchey classification helps to guide treatment for diverticular perforation. Complications of diverticular disease only occur in around 10% of patient with diverticula in the bowel with diverticulitis being the most common. The diverticula protrude between the teniae coli muscles which run along the length of the colon but which fuse together in the rectum so therefore diverticula are not seen there. Many diverticular perforations can be managed without surgery if localised, often with antibiotics and sometimes requiring interventional radiology drainage of an abscess. Most cases of diverticulitis are isolated with <1/3 patients experiencing a further episode so hence elective surgery is not indicated for those with a first episode. Even a second episode is unlikely to be repeated further.

Answer 120

he correct answers here are c), d), f) and h). There are so many factors that can impact this decision and the list below is not exhaustive. This is simply to identify some of the considerations as has been eluded to in the lecture to say why patients may or may not be suitable for an anastomosis. The age of the patient per se is not a factor in deciding on an anastomosis but comorbidities are more likely in this group. Bowel obstruction can lead to relative size discrepancy between the proximal and distal bowel making an end to end join impossible, however a side to side or end to side join are alternatives and bowel obstruction per se does not mean an anastomosis is not possible – clearly this is a factor in the decision making that will need to be considered. Disease factors Malignant v non malignant (and if malignant then evidence of residual or metastatic disease?) Crohns disease – possibly more likely to fail Degree of contamination (faecal peritonitis v local contamination) Abnormality of bowel ends (inflammation, ischaemia, diverticular disease) Cause of perforation (gangrene from vascular problem high risk of worsening; isolated pathology less likely to propagate (e.g. strangulated hernia, iatrogenic injury)) Patient factors Comorbidity (diabetes, heart/vascular disease) Medications (steroids, immunosuppressants) Cardiovascular instability in surgery (need for inotropic support) Anatomical variants (narrow pelvis for male, short bowel segments or mesentery, hostile splenic flexure etc) Previous surgery (adhesions, vascular compromise from previous bowel resection) Body habitus (stoma complications higher from obese patients) Surgeon factors Senior v junior surgeon Specialty experience (colorectal surgeon more likely to join a diverticular resection than a non specialist) Personality (degree of risk acceptance/aversion) Outcomes (surgeon level morbidity and mortality data in public domain) Recent experience (similar cases with complications or not) Environmental factors Time available Assistance available (colorectal anastomosis often requires an additional assistant) Equipment availability (staplers etc)

Answer 121

The correct answer here is “c) developing peritonitis and rising blood lactate levels.” This is because if the patient develops peritonitis then it is an indicator of possible perforation and the rising lactate levels suggest worsening shock and possibly can indicate bowel ischaemia which can happen with obstruction if it is not relieved. This is a clear indication for surgery. Vomiting and constipation are hugely variable with SBO because it will depend on the level of obstruction and the longevity of symptoms but in itself does not help with prognosis. Similarly, obstruction of the proximal small bowel does not predict a higher chance of surgery as long as one is confident it is adhesional. Answer d) is potentially confusing but is representative of the mixed clinical picture that we so often see with SBO. The fact that the water soluble contrast has reached the colon means that, by definition, it has managed to traverse the entire small bowel suggesting the obstruction has relieved, and it may well be that the NG drainage has just yet to settle. Clearly if this persists then one would need to consider if the obstruction is still present or has re-occurred, however again this on its own in the initial period after the contrast passes would not predict surgical intervention. If adhesional SBO has not relieved by 72 hours (not 48 as is the option) then this is predictive of a higher chance of failure of conservative management and therefore surgery is more likely to be needed.

Answer 122

The correct answer here is “d) She likely has a closed loop obstruction with competent ileocaecal valve and her caecum is at risk of perforation.” A competent ileocaecal valve (in about 50% of the population) means that passage of faecal material can only go into the colon and cannot reflux back into the small bowel. If the colon is obstructed then this is important because the pressure will build much faster than if faeces can reflux back into the small bowel. The caecum has the widest diameter and the thinnest wall within the colon and therefore the wall tension will be highest (Laplace’s law) and hence the caecum is most likely to perforate if there is an obstruction – indicative by the RIF pain in this case. As mentioned in the lecture, a sudden relief of the RIF pain in this context can suggest that the caecum has ruptured, but regardless intervention is needed urgently. Answer b) is incorrect because this suggests the obstruction is not a closed loop and there is therefore more time to deal with the situation. If one diagnosis explains everything then it is not normally necessary to look for a second pathology and whilst statistically possible, acute appendicitis (answer a)) would not be likely here. Pains from the site of obstruction itself would not be likely as mentioned above (answer c)) and although colorectal cancers can cause ureteric obstruction (e)) this would not likely to present with this clinical picture.

Answer 123

The answer is “b) Small bowel ischaemia.” He has a number of risk factors for vascular disease (smoker; new onset AF) which raises the possibility of a vascular issue. He also seems to have pain which is out of proportion with the clinical findings (that his abdomen is soft but he is requiring significant doses of pain relief). This is a diagnosis which is very hard to make clinically and therefore a high index of suspicion is needed. Adhesional bowel obstruction does not usually cause such significant pain unless there are complications, and he has had no previous surgery which makes this much less likely. A closed loop LBO would likely result in significant abdominal distension but vomiting is not invariable and a perforated peptic ulcer would likely have more abdominal signs such as peritonitis and tenderness and acute diverticulitis would likely be more localised, but again more tenderness would be expected and lactate levels would not necessarily be high unless the patient is dehydrated.

Answer 124

It is important to note that all of these are potential diagnoses for this patient and the questions is what is most likely. With that in mind, the correct answer is “a) paralytic ileus” as the patient is in the early days after an open colorectal procedure. Looking at the rest of the possible diagnoses, they are less likely, but if the ileus seems to be persisting longer than expected (most are resolved within 14 days and most sooner than that), then a review of the other differentials is needed. Early adhesional SBO is very unusual but sometimes is seen. This is seen on a CT as a focal area of obstruction rather than a more widespread small bowel distention without specific site of hold up seen with ileus. If the muscle incision through which the stoma is pulled (and even more unusually the skin) are too tight then the stoma may not work and sometimes a stoma will need revision to increase the size of the aperture – there may also be oedema in the SB in the stoma which worsens the problem, but a CT will show dilatation to the stoma and then collapsed bowel beyond. Getting the stoma the wrong way round in this type of surgery would be unusual but in other situations, such as performing a trephine to pull out a defunctioning stoma without being able to check the orientation of the bowel within the abdomen, they can be twisted which can result in obstruction. Again, a CT will show the issue to be at the stoma rather than elsewhere, and sometimes this is not fully appreciated until the patient is in theatre for a revision. Once again, early hernias are unusual but need consideration if an apparent ileus is prolonged. It is thought that larger (10-12mm) laparoscopic port sites are more at risk of this than smaller (5mm) ones, but some surgeons do not close these defects. It is also possible for small bowel to be caught up in a wound closure stitch or to slide up into the wound between stitches, but this is unusual and CT will confirm any potential site of herniation with obstruction.