General Surgery Flashcards
1
Q
What is pancreatitis?
A
Definition – inflammation of the pancreas, usually due to autodigestion which results in necrosis. Most commonly caused by alcohol or gallstones in western countries.
2
Q
What are the causes of pancreatitis?
A
I GET SMASHED • Idiopathic • Gall Stones • Ethanol • Trauma • Steroids • Mumps/Malignancy • Autoimmune • Scorpion sting/Spider bite • Hyperlipidaemia/hypercalcaemia/hyperparathyroidism • ERCP • Drugs (azathioprine, meslazine, Bendroflumethiazide, didanosine (HIV med) furosemide, pentamidine, steroids, sodium valproate and ACEi)
3
Q
What are the clinical features and diagnostic criteria for pancreatitis?
A
2/3 criteria needed for clinical diagnosis
- Amylase greater than 3 times normal limit (if less that this but still raised – SBO and perforated duodenal ulcer are differentials)
- Pattern of pain starting epigastric and radiating to the back
- Diagnostic CT
Cullen’s bruising – oedema and bruising in umbilical region
Grey-turners sign – bruising up the flanks
Vomiting
Ileus
Fever
Ischaemic retinopathy (Purtscher retinopathy) – rare
4
Q
How should suspected pancreatitis be investigated?
A
Serum amylase may give false positive and negative results i.e. also raised in pancreatic pseudocyst, mesenteric infarct, perforated viscus, acute cholecystitis, and diabetic ketoacidosis. Note the amylase level is not of prognostic value.
Serum lipase is more sensitive and specific and has a longer half life
Blood gas
FBC, U&Es and calcium, LFTs, LDH, albumin and blood sugar
Early USS to check for gall stones or other aetiology
CT to rule out perforated ulcer/cancer
MRCP (magnetic resonance cholangiopancreatography)
5
Q
How do we assess the severity of pancreatitis?
A
There are multiple scoring systems used to quantify severe cases of pancreatitis which include Ranson score, APACHE II and Glasgow score.
Modified Glasgow scoring system If 3 or more let ITU know no matter how well the patient looks (PANCREAS) • PaO2 < 8kPa • Age > 55 • Neutrophilia > 15 • Calcium < 2 • Renal Function – Urea > 16 • Enzymes – LDH > 600 and AST > 200 • Albumin < 32 • Sugar > 10
6
Q
How is acute pancreatitis managed?
A
ABCDE
Maintain enteral feeding to prevent bacterial translocation from the gut and to prevent malnutrition which patients are susceptible to
Analgesics with IV opioids (fluids also help with pain by reducing lactic acidosis)
Very aggressive fluid resuscitation with crystalloids, aim for urine output of > 0.5ml/kg/hr
Nutrition – NBM if clear reason, enteral nutrition if moderate or severe within 72 hours, parenteral nutrition only if enteral fails or is contraindicated
NO antibiotics unless clear indication e.g. infected pancreatic necrosis
Surgery
Aspiration and debridement if necrotic or cyst formation
Gall bladder removal if pancreatitis caused by gallstones.
ERCP early if stone is stuck.
7
Q
What are the two main complications to be wary of when treating pancreatitis?
A
AKI due to large fluid movements
ARDS due to fluid build-up in lungs and enzyme damage from serum pancreatic enzymes
8
Q
What are peripancreatic fluid collections and how are they managed?
A
Peripancreatic fluid collections – can develop into pseudocyst or abscess. Most resolve on their own but aspiration and drainage may be required.
9
Q
What are pancreatic pseudocysts and how are they managed?
A
Pseudocysts – peripancreatic fluid that communicates with the ductal system and typically occurs 4 weeks post pancreatitis attack. Most resolve on their own but symptomatic cases may be observed for 12 weeks and if treatment is required then endoscopic or surgical cystogastrosomy or aspiration.
10
Q
What is pancreatic necrosis and how is it managed?
A
Pancreatic necrosis – early surgical intervention should be avoided due to high mortality rate. Sterile necrosis should be managed conservatively. If infection is suspected fine needle
aspiration can be done.
11
Q
What are pancreatic abscess and how are they managed?
A
Pancreatic abscess – collection of pus associated with the pancreas in the absence of necrosis. Typically, as a result of infected pseudocyst. Managed with trans gastric drainage or endoscopic drainage.
12
Q
What are the common causes of chronic pancreatitis?
A
Alcohol most common Idiopathic Cystic fibrosis Hemochromatosis Ductal obstruction
13
Q
What are the clinical features of chronic pancreatitis?
A
Epigastric pain typically 15-30mins after eating
Steatorrhea – usually 5-25yrs after symptoms
Diabetes mellitus – usually 20yrs after symptoms
14
Q
What investigations should patients suspected of having chronic pancreatitis have?
A
Abdominal X-ray – speckled calcification in 30%
CT more sensitive
USS
Faecal elastase
15
Q
How is chronic pancreatitis managed?
A
Pancreatic enzyme supplements Analgesia Antioxidants Insulin if required Diet – no alcohol and low fat
16
Q
What are the 3 types of bowel ischaemia?
A
There are 3 main ischaemic bowel conditions
• Acute mesenteric ischaemia
• Chronic mesenteric ischaemia
• Ischaemic colitis
17
Q
What are the risk factors of bowel ischaemia?
A
Increasing age
Atrial fibrillation (particularly for mesenteric)
Other causes of emboli – endocarditis or malignancy
Cardiovascular risk factors – smoking, hypertension, diabetes etc.
Cocaine – ischaemic colitis in young patients following cocaine use
18
Q
How does bowel ischaemia present generally?
A
Abdominal pain Rectal bleeding Diarrhoea Fever Bloods typically show elevated WCC and lactic acidosis
19
Q
What investigations should be done for bowel ischaemia?
A
AXR – thumbprinting sign seen in ischaemic colitis
CT scan is investigation of choice
20
Q
What is acute mesenteric ischaemia and what are its specific features?
A
Typically, small bowel but can occur to lower GI tract due to an embolism blocking one of the arteries supplying the bowel. Sudden onset and severe symptoms, out of keeping with clinical findings.
21
Q
How is acute mesenteric ischaemia managed?
A
Urgent surgery required
High mortality especially if surgery is delayed
22
Q
What is chronic mesenteric ischaemia?
A
This is effectively intestinal angina, presents with nonspecific features of intermittent colicky pain, weight loss and an abdominal bruit.
23
Q
What is ischaemic colitis and what are its specific features?
A
Typically, large bowel, due to multifactorial causes resulting in transient compromise of blood flow to the large bowel. This leads to inflammation, ulceration, and haemorrhage. Most commonly occurs in ‘watershed’ areas such as the splenic flexure (borders of territory supplied by both the SMA and IMA). Presentation is with transient, less severe symptoms including bloody diarrhoea.
24
Q
What is seen on AXR in ischaemic colitis and why?
A
Thumbprinting seen on AXR due to mucosal oedema/haemorrhage
25
How is ischaemic colitis managed?
Conservative management required with supportive therapy
Surgery may be required in minority of cases if above measures fail
Indications include generalised peritonitis, perforation or ongoing haemorrhage
26
What can cause perforation of the bowel?
Peptic ulcers – Epigastric pain or back pain
Obstruction
Appendicitis
Crohn’s
Diverticulitis – most commonly perforates in the sigmoid
Trauma and foreign body
Colonoscopy
27
What are the clinical features of a perforated bowel?
Severe constant abdominal or epigastric pain
If in gut then gradual onset of pain if in stomach then sudden
Septic symptoms
Pain intensified by movement (rigid abdomen)
Nausea and vomiting and haematemesis
Rebound tenderness
Ceased bowl movements and flatus
28
How does location of pain change depending on where a perforation has taken place?
Intraperitoneal perforation – generalised abdominal pain
Retroperitoneal perforation – shoulder tip pain, back pain normal examination
Thoracic – chest pain, neck pain, pain radiating to the back and pain on inspiration
29
How should suspected perforation be investigated?
Erect chest x-ray
Abdominal x-ray showing Rigler’s sign (both sides of the bowl wall visible)
CT scan
30
How is perforated bowel managed?
IV fluids and antibiotics – ciprofloxacin and metronidazole
Emergency investigative laparotomy
If upper GI perforation, then closure may be an option using stent (oesophageal) or conservatively (peptic) with bowl rest and PPI
If lower GI perforation, then likely a resection will be needed
31
What is necrotising fasciitis?
Definition – infection of the deep fascia resulting in necrosis of the tissue. Surgical emergency due to its sudden onset and rapid progression. Most commonly it affects the perineum (Fournier’s gangrene).
32
How is necrotising fasciitis classified?
Classification is based on causative organism
1. Type 1 is caused by mixed anaerobes and aerobes (often post-surgery in diabetics) and is most common.
2. Type 2 occurs due to streptococcus pyogenes
33
What are the risk factors for necrotising fasciitis?
Skin – recent trauma, burns or soft tissue infection
Diabetes mellitus (particularly if on SGLT-2 inhibitors)
Intravenous drug use
Immunosuppression
34
What are the clinical features of necrotising fasciitis?
Acute onset pain, swelling and erythema at sight (rapidly worsening cellulitis with pain out of keeping with physical features)
Extremely tender over infected tissue
Fever
Swelling
```
Later on:
Bullae
Dark haematomas
Colouration of red to purple to black
Gas bubbles in skin
Parasthesia
```
Note immunocompromised patients may not show any signs at all
35
How should necrotising fasciitis be investigated?
Diagnosis of suspicion
If high suspicion, then small incision made and if the finger easily separates the tissue along the fascial plane then the diagnosis is confirmed.
36
How is necrotising fasciitis managed?
Sepsis 6 pathway
Surgical debridement
Amputation
Mortality is around 20%
37
What are fistulas?
Definition – abnormal connection between two epithelial surfaces. The abdominal cavity has the potential for many fistula to form and most arise from diverticula disease and Crohn’s.
38
What is an enterocutaneous fistula?
This is a connection from intestine to the skin. They can be high output (>500ml) or low output (<250ml) depending on their source. Duodenal/jejunal fistulae tend to produce high volume, electrolyte rich secretion causing skin excoriation. Colo-cutaneous fistula will tend to leak faeculent material.
39
What is an enteroenteric or enterocoli fistula?
Fistula that involves the large or small intestines and can arise from spontaneous rupture of abscess or with iatrogenic input. These types of fistula bring about serious problems with bacterial overgrowth causing malabsorption problems. Enterovaginal share a similar aetiology.
40
What is an enterovesicular fistula?
Connection between bowel and bladder. This results in frequent urinary tract infection or the passage of gas from the urethra during urination.
41
What are the principles of managing a fistula?
* Fistulas will heal provided there is no underlying inflammatory bowel disease or distal obstruction so conservative management is the best option.
* If skin is involved this must be protected as it is difficult to treat so use well-fitting stoma bags
* Octreotide can be used to manage high output fistulas
* Nutritional complications are common especially with high out put fistulas and may necessitate the use of TPN to provide nutritional support along with octreotide and reduce volume and protect the skin
* In perianal fistulas caused by Crohn’s it is often best to drain the acute abscess and maintain drainage through use of setons whilst medical management is implemented.
42
What is meckel's diverticulum?
Definition – Congenital abnormality of the small bowl causing a small out pouching from remnant of the vitellointestinal duct (omphalomesenteric duct). The diverticula will contain ectopic ileal, gastric or pancreatic mucosa.
43
What are the rules of 2 in relation to meckel's diverticulum?
Rule of 2s: 2% of the population, 2 feet proximal to the Ileocaecal valve, 2 inches in length, 2 years at presentation and 2:1 male: female.
44
What are the clinical features of meckel's diverticulum?
Most are symptomless
If there are symptoms this includes
Abdominal pain mimicking appendicitis
Rectal bleeding usually as malaena (most common cause of painless bleeding requiring transfusion between ages of 1 and 2)
This is shortly followed by intestinal obstruction (due to an omphalomesenteric band), volvulus, and intussusception
Can mimic pancreatitis if pancreatic tissue is present
45
How should meckel's diverticulum be investigated?
Technetium-99m pertechetate scan – scan for gastric/pancreatic tissue as 50% of Meckel’s diverticulum contain gastric or pancreatic tissue
USS if suspecting appendicitis
CT
46
How are meckel's diverticulum managed?
If symptomless then conservative
| If symptomatic or narrow neck then laparoscopic resection
47
What causes small bowel obstruction?
```
Adhesions (most common)
Hernia (second most common)
Volvulus
Tumours (caecal cancer not small bowl as they are uncommon)
Foreign body
Strictures from Crohn’s
Gall stone ileus (uncommon) usually due to fistula from gall bladder to small bowl
Intussusception
```
48
What are the clinical features of small bowel obstruction?
```
Abdominal pain that is colicky in nature
Nausea and vomiting (earlier than in large bowel obstruction)
Abdominal distention
Absolute constipation (including flatus)
Small bowel distention that is greater than 3cm on X-ray
```
49
How should small bowel obstruction be investigated?
CXR erect looking for perforation
ABX looking for dilated bowl loops. Small > 3cm large > 6cm caecum > 9cm. Large bowl in peripheral generally and has haustra that do not cross the full diameter. Small is central and has valvulae conniventes across the whole diameter.
CT abdo, pelvis
50
How should small bowel obstruction be managed?
ABCDE
```
If adhesions:
Will definitely need fluids
FBC, Us and Es, lactate, CRP
Drip and Suck NG tube with suction this is compulsory
Catheter is essential
Give 48hours to get better
```
Other cases are very similar but will almost definitely require surgery.
51
What causes large bowel obstruction?
```
Tumours
Volvulus (especially sigmoid colon)
Diverticular disease
Constipation
Crohn’s strictures
Foreign body
Intussusception
```
52
What are the clinical features of large bowel obstruction?
Coffee bean sign on AXR
Abdominal pain that is colicky in nature
Vomiting
Abdominal distention
Absolute constipation (including flatus)
Bowl distention that is larger than 6cm on x-ray (or 9 for caecum)
53
How should suspected large bowel obstruction be investigated?
CXR erect looking for perforation
ABX looking for dilated bowl loops. Small > 3cm large > 6cm caecum > 9cm. Large bowl in peripheral generally and has haustra. Small is central and has valvulae conniventes
CT abdomen and pelvis
It is very important to work out whether the ileal caecal valve is competent or not. If competent – closed bowl loop obstruction – absolute emergency, if not competent then open bowl loop obstruction – less of an emergency.
54
How is large bowel obstruction managed?
ABCDE
Will definitely need fluids due to secretion of large volumes of electrolyte rich fluid by bowl
FBC, Us and Es, lactate, CRP
Drip and Suck NG tube with suction this is compulsory
Catheter is essential
Analgesia
Allow 48 hours to improve otherwise you will need to do a laparotomy
Can do an endoscopic stent for cancer
55
When is surgery required for bowel obstruction?
Surgical Intervention for Bowl obstruction should take place if:
1. Suspicion of intestinal ischaemia or with closed loop large bowl obstruction
2. Small bowl obstruction on patient with virgin abdomen
3. Strangulated hernia, volvulus or obstructing cancer is the cause
4. Patient fails to improve after 48 hours
56
What is a hernia?
A Hernia is the abnormal protrusion of an organ or fascia through the wall that usually contains it.
57
What are the risk factors for any abdominal hernia?
* Obesity
* Ascites
* Increasing age
* Surgical wounds
58
What is a femoral hernia?
Bowel tissue passes through the femoral ring (below the inguinal ligament and lateral to the pubic tubercle) and into the potential space of the femoral canal which normally only contains lymphatic vessel nodes.
59
Why are femoral hernias of particular concern and who most commonly gets them?
They are prone to being surgical emergencies due to the rigidity of the borders of the canal. Femoral account for 5% and are most common in older multiparous women.
60
What are the borders of the femoral canal?
Lateral – femoral vein
Medial – lacunar ligament
Anteriorly – inguinal ligament
Posterior – pectineal ligament
61
What causes femoral hernias?
Increase age
Have had pregnancies
Increase intrabdominal pressure from lifting, constipation and coughing
62
What are the clinical features of femoral hernias?
Usually, asymptomatic
Infero-lateral to the pubic tubercle
Obstruction
Strangulation leading to infarction
63
How should femoral hernias be investigated?
USS
64
How are femoral hernias managed?
All femoral hernias should be surgically managed due to the high risk of strangulation this requires reduction of the hernia and surgical narrowing of the femoral ring.
This can be done via a low approach or a high approach above the inguinal canal which allows better access to any compromised bowl but can cause a weakness in the inguinal canal resulting more hernias.
65
Describe these other hernias: epigastric, umbilical, periumbilical, incisional, Richter's, Spigelian and obturator hernias
Epigastric – through the linea alba in the midline above the umbilicus and below the xiphisternum, usually in middle-aged men and are fairly common with 10% prevalence. Note this is note divarication of the recti
Umbilical – symmetrical bulge under the umbilicus
Paraumbilical – asymmetrical bulge, half the sac is covered by skin of the abdomen directly above or below the umbilicus
Incisional – may occur in up to 10% of abdominal operations
Richter’s – rare herniation of small bowl where only the anti-mesenteric border becomes strangulate and so care must be taken during surgery. Presents with strangulation without symptoms of obstruction
Spigelian – also known as lateral ventral hernia, rare and seen most often in the elderly. Hernia through the spigelian fascia (aponeurotic layer between the rectus abdominis muscle medially and semilunar line laterally
Obturator – hernia passes through the obturator foramen, more common in females and typically presents with bowel obstruction.
66
How common are inguinal hernias?
These account for 75% of abdominal wall hernias and 95% of patients are male giving men a 25% lifetime risk of developing an inguinal hernia.
67
What is the difference between a direct and indirect inguinal hernia?
Direct – directly through the abdominal wall (through Hesselbach’s triangle) and can be via the superficial ring. They are medial to the inferior epigastric vessels. This occurs as a result of defects or weakness in the transversalis fascia of the Hesselbach’s triangle. They have a low risk of strangulation and are seen in adults.
Indirect – through the deep ring along the inguinal canal then out the superficial ring and are lateral to the inferior epigastric vessels. These occur because of incomplete closure of the processus vaginalis. They have a high risk of strangulation and can occur in children.
68
Which type of inguinal hernia are most common
20% are direct and 80% are indirect
69
What are the boundaries of hesselbach's triangle?
Medial – rectus abdominis
Lateral – inferior epigastric vessels
Inferior – inguinal ligament
70
What are the risk factors for inguinal hernias?
Males
Increasing age
Raised intrabdominal pressure from chronic cough, lifting or chronic constipation
Obesity
71
What are the clinical features of inguinal hernias?
Reducible lump in the groin supero-medial to the pubic tubercle that may disappear when patient lies down (should examine standing up if possible)
If non reducible then incarcerated and at high risk of strangulation
Some general discomfort and ache
Cough impulse
Non pulsatile and non-expansile (unlike false or true aneurysms)
72
How should inguinal hernias be investigated?
Diagnosis is mostly clinical
Check if mass expands on coughing
Check for pulsatility and expansibility – to rule out aneurysms
Lipoma – soft, small and very superficial
Hernia enters the scrotum if swelling in scrotum that does not transilluminate and you can not get above it
Hernia can be reducible or non-reducible. If reducible then you can determine whether it is indirect or direct by applying pressure to the mid inguinal point (over the inguinal canal) and then trying to reduce it. If it is no longer reducible then this is an indirect hernia.
USS is the only useful imaging technique
Erect CXR or CT if strangulated and suspecting perforation
73
How are inguinal hernias managed?
General consensus is to treat all hernias as long as patient medically fit. Management of direction and indirect are exactly the same
If not fit for surgery a hernia truss
Mesh repair is associated with the lowest recurrence rates
Open repair generally done for first hernia and laparoscopic for recurrent or bilateral
After open repair – 2-3 weeks off and after laparoscopic repair 1-2 weeks
74
If an inguinal hernia is left what is the yearly risk of strangulation?
3% risk per year of strangulation
75
How does a strangulated hernia present?
Episodes of pain in a previously asymptomatic hernia suggest high risk
Pain
Fever
Increase in size of hernia or erythema of the overlying skin
Peritonitic features such as guarding and localised tenderness
Bowel obstruction
Bowel ischaemia – lose stools
76
How is a strangulated hernia managed?
Management – immediate surgery which may involve removal of dead bowel then repairing the hernia itself.
77
What is appendicitis and who does it present in?
Inflammation of the appendix due usually presenting aged 10-20, more common in Caucasians and in the summers.
78
What can cause appendicitis?
Faecolith
Lymphoid hyperplasia
Impacted stool
Appendiceal or caecal tumour
79
What are the clinical features of appendicitis?
Dull and poorly localised abdominal pain that starts in the umbilical region and then moves towards the RIF becoming localised and sharp (visceral pain to midgut, peritoneal irritation causes localisation)
Pain worse on coughing or jolting movements
Children – inability to hop on right leg due to the pain
Nausea and vomiting after the pain
Anorexia
Diarrhoea
Mild pyrexia
Rebound tenderness and percussion pain at McBurney’s point (2/3rd between umbilicus and the ASIS)
Signs of peritonitis if perforation
Rovsing’s sign – RIF pain on palpation of the LIF
Psoas sign – RIF pain with extension of the right hip (suggesting retrocaecal position which usually has few symptoms)
80
How should suspected appendicitis be investigated?
Raised inflammatory markers
Urinalysis for pregnancy test but also to exclude renal colic and UTI
Transabdominal USS – useful in younger patients and females for pelvic pathology. Presence of free fluid in males is always pathological
CT scan (older patients)
81
How is appendicitis managed?
Laparoscopic appendicectomy and prophylactic appendicectomy
If perforated copious peritoneal lavage
Some evidence to suggest uncomplicated cases can be treated with antibiotics
82
What is cholelithiasis?
Gall stones
83
Why do gallstones form?
Gall stones form as a result of an imbalance in the makeup of bile in the gall bladder usually due to raised cholesterol, low bile salts and biliary stasis.
84
What are the risk factors for cholelithiasis?
```
The 4 F’s
Fat and high cholesterol
Female – gall stones are 2-3 times more common in women probably because oestrogen increases activity of HMG-CoA reductase
Fertile (pregnant) or on COCP
Forty
```
```
Other Risk factors
Diabetes mellitus
Crohn’s disease
Rapid weight loss e.g. weight reduction surgery
Drug – fibrates and COCP
```
85
What are the clinical features of symptomatic gall stones
Biliary colic – contraction of the biliary tree against the gall stone
Pain induced/worst post prandially especially with fatty foods
Jaundice
Deranged LFTs
But may be asymptomatic
86
How should suspected cholelithiasis be investigated?
FBC and Us and Es
LFTs
USS
ERCP/MRCP
87
What are the complications of ERCP?
Pancreatitis
Bleeding
Duodenal perforation
Ascending cholangitis
88
How should cholelithiasis be managed?
If asymptomatic then no action required
ERCP
Laparoscopic cholecystectomy
89
What complications can occur from gallstones based on their location?
```
Hepato-biliary
Biliary colic
Acute cholecystitis
Mucocele
Empyema
Carcinoma
Mirizzi’s syndrome
```
Bile ducts
Pancreatitis
Ascending cholangitis
Obstructive jaundice
Gut
Gallstone ileus – gall stone erodes into the bowel and block terminal ileum
90
What is ascending or acute cholangitis?
Infection of the bile duct due to bacteria ascending from duodenum. 15% of people have gall stones and 15-26% will suffer from biliary colic at some point.
91
Waht can cause cholangitis?
Most commonly occurs when gall stones obstruct the bile duct. Benign structures
Post-operative damage
Tumours.
92
Which organisms are usually involved in cholangitis?
E coli, klebsiella and Enterobacter.
93
What are the clinical features of cholangitis?
```
Charcot’s Triad
• RUQ pain
• Fever
• Jaundice
• Reynold’s Pentad = Above 3 as well as hypotension and confusion
```
Raised inflammatory markers
Sepsis
94
How should suspected cholangitis be investigated?
Raised ALT and APT
Routine bloods including inflammatory markers
MCRP or ERCP
95
How is cholangitis managed?
IV fluids
Antibiotics (co-amoxiclav and metronidazole)
Relief of the underlying obstruction by ERCP
ERCP after 24-48 hours to relieve any obstruction
96
How does a gallbladder abscess present and how should it be investigated?
Usually, prodromal illness and right upper quadrant pain with a swinging pyrexia, patient may be systemically unwell.
Imaging with USS +/- CT Scanning
97
How are gall bladder abscesses managed?
Ideally, drain via surgery although subtotal cholecystectomy may be required. In unfit patients, percutaneous drainage may be considered.
98
What is cholecystitis?
Inflammation of the gallbladder most commonly as a result of gall stones.
99
What causes cholecystitis?
Gallstones blocking the cystic duct (90%) – calculous cholecystitis
Everything else – acalculous cholecystitis
Tumour blocking the cystic duct
Bile duct blockage due to stasis
Poor perfusion
Infection – AIDS and other viral infections such as cryptosporidium or cytomegalovirus
100
What are the risk factors for cholecystitis?
5Fs risk factors – Fat, Female, fertile, Forty and Family History
Pregnancy
Oral contraceptives as oestrogens cause more cholesterol to be secreted
101
What are the clinical features of cholecystitis?
Severe pain in RUQ or epigastric region which may spread to right shoulder or back
Tender abdomen
Nausea and vomiting
Fever and systemic upset
Biliary colic describes waves of pain as the biliary tree or gallbladder contracts when this becomes constant this indicates acute cholecystitis.
102
What are Murphy's and Boas sign?
Murphy’s sign – patient breaths in deeply whilst your hand is pressed up below the liver. As patient breaths in the liver and gall bladder move down into your hand causing pain.
Boas sign – hypersensitivity below the right scapula
103
How should cholecystitis be investigated?
Raised inflammatory markets
LFTs are typically normal, if deranged may indicate Mirizzi syndrome – gallstone impacted in the distal cystic duct causing extrinsic compression of common bile duct
USS is first line to assess for gallstones and may show a thickened gall bladder wall
Cholescintigraphy (HIDA scan) – technetium labelled HIDA (hepatobiliary iminodiacetic acid) is injected and taken up by the liver then excreted into bile, if acute cholecystitis is present then cystic duct is obstructed and so the gallbladder will not be visualised
MRCP
104
How is cholecystitis managed?
Patient should be NBM
Rehydration and Analgesia
IV Antibiotics – Co-Amoxiclav and metronidazole
Early laparoscopic cholecystectomy within 1 week of diagnosis
If gallbladder perforation, then open surgery is required
105
How can you prevent gall stones?
Lose weight slowly
Maintain healthy weight
Eat healthily avoid high fat and fibre diets
106
What is a hiatus hernia?
A hiatus hernia describes the herniation of part of the stomach above the diaphragm.
107
What are the two types of hiatus hernia?
There are two types:
• Sliding – accounts for 95% of hiatus hernias, the gastroesophageal junction moves above the diaphragm and so no longer receives intrabdominal pressure to assist in its function
• Rolling (paraesophageal) – the gastroesophageal junctions remains below the diaphragm, but a separate part of the stomach herniates through the oesophageal hiatus causing the diaphragm to become less tight around the sphincter
108
What are the clinical features of a hiatus hernia?
```
Reflux and/or oesophagitis
Halitosis
Excessive belching
Belatedness
Nausea and vomiting
Dysphagia and Odynophagia
```
109
How should hiatus hernias be investigated?
Erect CXR may show a retrocardiac air bubble or simply be normal
Oesophago-gastro-duodenoscopy
May order a CT or MRI but rarely indicated
110
How are hiatal hernias managed?
Change eating habits i.e. eating smaller, more frequent meals
Cease smoking
Reflux medications
Surgery – usually only if other treatment have not worked
