Surgery FFP Flashcards
Fibroadenomas - presentation, examination, diagnosis, treatment
Aberrations of Normal Development and Involution (ANDI)
Benign breast condition
younger patients - 20s
smooth, very mobile, “breast mouse”, can be tender, firm rubbery, can change over menstruation
diagnoses using triple assessment; US, mammogram, clinically and core biopsy
left alone or removed if too big; surgery/vacuum excision
Breast cysts - presentation, examination, diagnosis, treatment
Aberrations of Normal Development and Involution (ANDI)
Benign breast condition
30-50; 50+ if on HRT
Lump +/- pain with cyclical fluctuation
Smooth, mobile lump, can be tender
Triple assessment; US, mammogram, clinically and core biopsy
Left alone if asymptomatic or simple drainage
Fibroadenosis presentation, examination, diagnosis, treatment
Aberrations of Normal Development and Involution (ANDI)
“Benign breast changes” - Benign breast condition
Lumpiness +/- pain with cyclical fluctuation
Thickening +/- tenderness
Fat necrosis presentation, examination, diagnosis,
Any age
Trauma (surgery, accident) except in older women; can be small hits
Could feel benign (solid/cystic) or malignant +/- bruise
Triple assessment
What tests should be done for pts less than 40 vs those older than 40 with suspected breast cancer
<40 => Ultrasound
40< => Ultrasound and mammogram
This is due to younger patients breasts being too dense for mammograms to be of use.
Types of nipple discharge and when it may be significant
Milky discharge or galactorrhoea is often due to hyperprolactinaemia, which may point to an underlying endocrine condition so the patient should be managed accordingly.
Pus discharging from the nipple is often part of an infection such as periductal mastitis, so should be managed accordingly.
Significant/Pathological :
Spontaneous
Persistent
Unilateral
Single-duct
Insignificant/Physiological :
Provoked
intermittent
bilateral
multi-duct
For unilateral and single-duct discharge, the commonest underlying pathology is …..
and treatment
For unilateral and single-duct discharge, the commonest underlying pathology is a duct papilloma, which is again a benign condition. However ductal carcinoma in situ (DCIS) could also present this way.
In the absence of any abnormal radiological findings (mammogram and ultrasound), if we are still worried, we will tend to operate by removing the discharging duct (a procedure called microdochectomy) for histological examination. That will also treat the symptom of discharge.
Breast pain - facts and questions to ask, next steps
Pain alone is rarely due to breast cancer
- Is it Disturbing vs non-disturbing life activities
- Cyclical vs non-cyclical
We do not normally have to carry out radiological examination except for a screening mammogram if the patient falls into the age group who will benefit from this (40 years onward).
Breast infections (two main ones)
History
Physical findings
Pathogens
Investigations
Management
Lactational mastitis/abscess
History of lactation
Found Peripherally, Deep with Acute inflammation
S. aureus
US if ?abscess
Antibiotic (flucloxacillin) +/- drainage* + C/ST
Breast feeding can continue
Periductal mastitis/abscess
20s-40s, Chronic smoker, Recurrent episodes
Found Peri-areolar, Superficial, Chronic inflammation (scarring, fistula)
Mixed, including anaerobes
US if ?abscess
Antibiotic (co-amoxiclav) +/- drainage* + C/ST
↓Smoking
?Surgery
Most common types of breast cancer
Invasive Ductal carcinoma, followed by lobular
DC in situ
Breast cancer risk factors
Female
Age
BRCA
Direct family history
Radiation
Past breast surgeries
alcohol
Combined contraceptives
increased exposure to oestrogen
Breast cancer presentation, examination, diagnosis
Hard, immobile lump, rough borders, non-tender
Triple assessment
At risk pathologies for breast cancer
At-risk pathology: Atypical Ductal hyperplasia, ALH, LCIS, papillomatosis.
Types of pathology tests for breast cancer
Pathological assessment is done by biopsy.
Fine needle aspiration (FNA) cytology - gives you cell morphology
Needle core biopsy, which is now preferred, gives you tissue architecture.
Angles for mammogram
The standard views are cranio-caudal (CC) and oblique, so you broadly cover two dimensions, but also include the axilla – pectoral muscles as shown here in an oblique view, which shows a mass with irregular border in the upper aspect of the breast near the axilla.
Following radiology, the results for a breast lump are defined as either (5)
Normal
Benign Indeterminate
Suspicious
Malignant
TMN Staging for breast cancer
T (Primary Tumor):
T0: No evidence of primary tumor.
Tis: Carcinoma in situ (non-invasive cancer).
T1: Tumor size ≤2 cm
T2: Tumor size >2 cm but ≤5 cm
T3: Tumor size >5 cm
T4: Tumor of any size invading nearby structures (e.g., chest wall or skin)
N (Regional Lymph Nodes):
NX: Regional lymph nodes cannot be assessed.
N0: No regional lymph node involvement.
N1: regional lymph node involvement.
N2: distant nodes
M (Distant Metastasis):
M0: No distant metastasis.
M1: Distant metastasis present.
Manchester 4 stage classification of breast cancer
1 - confined to breast
2 - breast and mobile axillary nodes
3 - growth beyond mammary parenchyma
4 - growth beyond breast area
What is the commonest first site of distant metastasis in breast cancer?
Bone
Two broad groups of inoperable breast cancers and management
Locally advanced primary disease – The tumour is inoperable e.g. fungating or ulcerated tumour, tumour fixed to the pectoralis major muscle or chest wall, or inflammatory cancer, but has NOT yet spread to distant sites. There are two distinct points in terms of the principles of managing this group – (i) Since the chance of asymptomatic distant metastases is higher than in early operable disease, we normally do some staging investigations like a CT scan of the chest, abdomen and pelvis, prior to starting treatment; (ii) the initial treatment tends to be systemic such as chemotherapy (or we call it neoadjuvant chemotherapy) with a view of down-staging the cancer to allow surgery.
- Metastatic breast cancer – The disease is no longer curable so the goal of treatment is palliative aiming at improving quality of life.
Management of primary breast cancer - surgery
In general, surgery is performed as the INITIAL treatment, followed by what we call adjuvant therapies.
Locoregional control
Obtaining information»_space;> Adjuvant therapies
Cosmesis
Breast - masectomy or wide local incision; if unifocal and small
Axilla - sentinel lymph node (first to spread to) biopsy; identified using radioisotopes or a dye which fails to clear and can be identified by a surgeon.
- If positive: axillary clearance
Management of primary breast cancer - adjuvant therapies
Radiotherapy to affected area if tolerated;
Reasons that they might not tolerate could be previous radiotherapy (like a previous breast cancer, radiotherapy to treat mediastinal lymphoma as a child, or some collagen vascular disease associated with increased skin toxicity eg scleroderma, or that the patient has significant shoulder restriction so the external beam radiation can’t be delivered with her arm stretched
Factors to consider endocrine therapy
The most important ones which we use clinically for making a decision about adjuvant systemic therapies are oestrogen receptor (ER) and human epidermal growth receptor 2 (HER2).
Most invasive breast carcinomas are ER+ (about one-third overall) and only about 15% are HER2+.
Systemic therapies for breast cancer
Chemotherapy
Endocrine therapy (oestrogen +ve) e.g. tamoxifen pre-menopausal, aromatase inhibitors post menopausal (anastrozole, letrozole, exemestane)
Anti-HER2 targeted therapy e.g. trastuzumab (Herceptin)
Reducible, irreducible, obstructed, incarcerated, strangulated hernias
Reducible
Contents of the hernia can be manipulated back into its original position through the defect from which it emerges
Irreducible
Cannot be reduced without surgery
Incarcerated
Irreducible hernia, contents trapped due to adhesions
Strangulated
Compression of bowel -> Ischaemia as blood supply cut off -> necrosis -> sepsis
Obstructed
Hernias containing bowel -> contents compressed -> bowel lumen is no longer patent
Presents as triad of symptoms
Hernia repair
Open for strangulation
laparoscopic otherwise
mesh repair
Spigelian hernia
Spigelian – through spigelian fascia (aponeurotic layer between the rectus abdominus mm medially and semilunar line laterally).
Below and lateral to umbilicus.
“6 pack hernia”
Hernia risk factors
Increased intraabdominal pressure from: lifting, chronic constipation, chronic cough, obesity
Protein deficiencies and older patient: less collagen for tensile strength of gut lining
Inguinal canal borders
Anterior wall – aponeurosis of the external oblique, reinforced by the internal oblique muscle laterally.
Posterior wall – transversalis fascia.
Roof – transversalis fascia, internal oblique, and transversus abdominis.
Floor – inguinal ligament (a ‘rolled up’ portion of the external oblique aponeurosis), thickened medially by the lacunar ligament.
Which border do inguinal hernias break through?
Posterior wall – transversalis fascia. - only has one layer
Indirect inguinal hernias
Indirect inguinal hernias result from bowel passing through the deep ring of the inguinal canal due to an incomplete closure of the processus vaginalis.
Indirect hernias are more likely to strangulate than direct hernias.
Both types of hernia can exit the superficial ring and pass into the scrotum but this is more common with indirect hernias as the path through both inguinal rings, rather than a muscle defect, has less resistance.
Direct inguinal hernias
Direct inguinal hernias are less common than indirect inguinal hernias.
Direct inguinal hernias are where bowel enters into the inguinal canal through a weakness in the posterior wall (called Hesselbach’s triangle).
Direct hernias tend to reduce easily and do not rarely strangulate.
Less likely to pass through to the scrotum
Determining indirect vs direct inguinal hernia
Reduce the hernia
Press over the deep ring (just above midpoint of the inguinal ligament)
Ask the patient to cough
If the hernia reappears it is…
DIRECT
Technically, we can only be certain that the inguinal hernia is direct or indirect via surgical exploration.
Indirect inguinal hernias are lateral to the inferior epigastric vessels.
Direct inguinal hernias are medial to the inferior epigastric vessels.
Femoral hernias
Femoral hernias occur when abdominal viscera or omentum pass through the femoral ring into the potential space of the femoral canal; lies medial to the femoral vein and it’s purpose is allow space for the vein to expand.
HIGH risk of strangulation due to narrow neck of the femoral canal
Relatively uncommon (5% of all hernias)
Risk Factors:
Female (due to wider anatomy of pelvis)
Pregnancy
Raised intra-abdominal pressure
How can you tell the difference between inguinal and femoral hernias on clinical examination?
Inguinal hernias are SUPERIOMEDIAL to the pubic tubercle
Femoral hernias are INFEROLATERAL to the pubic tubercle
Umbilical hernia
Defect in the transversalis fascia = Umbilical ring
Where the umbilical vessels passed in-utero
More common in children
Occur in adults due to pregnancy or gross ascites
Low strangulation risk
Para-umbilical hernia
Occur adjacent to the umbilicus due to a weakness in the linea alba
More common in 35-50yo women; Usually caused by obesity or gross ascites
High risk of strangulation
Epigastric hernia
Herniation of fat which overlies the bowel through the linea alba above the umbilicus
Usually small – 1cm diameter
Usually occur in young males
Can cause discomfort on exercise or eating
Relieved by reclining
Divarication of recti
Separation of rectus abdominus due to linea alba laxity
Men – weight gain (truncal obesity)
Women – pregnancy
Also repeated midline operations and chronically raised intra abdominal pressure
Ultrasound diagnosis
Incisional hernia
Common risk of any abdominal surgery
5% at 1 year, 25% at 2 years
Risk factors are those that affect wound healing – poor blood supply, reduced ability to produce collagen, factors relating to reduced immunity
Emergency surgery is twice as likely to result in incisional hernia.
Smokers are twice as likely to get a wound infection post operatively
Early - midterm complication
Due to risk factors, normally repair these with mesh but often these reoccur after repair.
Should form part of the consent process along with a scar in abdominal surgery
Do not have to intervene surgically if patient assymptomatic
Articular cartilage has all of the following properties except:
Avascular
Alymphatic
Aneural
Acellular
Articular cartilage is Avascular, Alymphatic and Aneural
Which zones of cartilage resist which direction of forces
Superficial and deep withstand horizontal
intermediate withstands vertical forces
Hyaline cartilage composition and function
type II collagen for tensile strength
proteoglycans for compressive strength
chondrocytes in lacunae
How does synovial joint cartilage receive nutrition?
synovial fluid and subchondral bone marrow blood
How does cartilage repair in acute trauma?
Bleeding from subchondral bone
clot fills defect
becomes fibrous by 8 weeks
fibrocartilage by 4 months
OA on xray
4 features OA: Joint space narrowing, marginal osteophytes, subchondral sclerosis, subchondral cysts. Additionally, varus/valgus deformities can develop in more severe cases.
OA vs RA vs psoriatic arthritis features in hand
OA: diffuse osteopenia, no erosion, osteophytes, asymmetrical joint space loss, no swelling, PIP & DIP
RA: juxta-articular osteopenia, marginal erosion, no osteophytes, uniform joint space loss, swelling, PIP & MCP
PA: minimal osteopenia, proliferative erosion, no osteophytes, uniform joint space loss, swelling, DIP
OA causes
Abnormal concentration of force on normal cartilage
e.g. CAM deformity, loss of menisces
Normal concentration of force on abnormal cartilage
e.g. inflamm or crystal arthropathy
Normal concentration of force on normal cartilage supported by stiffened subchondral bone
e.g. Pagets
Normal concentration of force on normal cartilage supported by weakened subchondral bone
e.g. avascular necrosis
OA treatment
Non pharma: physio, weight loss etc.
Topical NSAIDs then Oral NSAIDs then intra-articular steroids
No opiates (NICE)
Surgical: hip/knee/shoulder = hemi, partial, complete arthroplasty
Hand = cortiva implant, trapeziotomy
Causes for extensive internal bleeding and what can it lead to
AAA rupture most serious cause
Ruptured ectopic pregnancy
Bleeding
Gastric ulcer
Trauma
Hypovolaemic shock:
Hypotension
Tachycardia
Pale and clammy
Cool to touch
Peritonitis presentation
Patients lay completely still
Tachycardia and potential hypotension / pyrexial
Percussion / rebound tenderness
Involuntary guarding
Reduced or absent bowel sounds
Ischaemic bowel presentation
Diffuse and constant pain reported
Examination may be unremarkable
Acidaemia with raised lactate on blood gases
Colic definition
Colic is an abdominal pain thatcrescendosto become very severe and thengoes away completely.
list of investigations for an acute abdomen
Bedside
Basic obs – lots of information in your NEWS2 score – indication of how unwell the patient is
ECG – Exclude MI, baseline ECG if surgery required
Urine dip - For signs of infection or haematuria. +/- MC+S.
Pregnancy test- (bHCG) Include a pregnancy test for all women of reproductive age
BM – DKA can present with abdominal pain
Bloods
Routine bloods
FBC – infection, bleeding
UE – dehydration(AKI), obstructive hydroneprhosis e.g kidney stone
LFT – gallbladder or liver pathology (further talk)
Amylase/lipase +/- serium calcium – in suspected pancreatitis.
Note amylase needs to be 3x higher than the upper limit to be diagnostic of pancreatitis. Values lower than this might be due to other pathology e.g. perforated bowel, ectopic pregnancy or DKA.
CRP - inflammation
G+S and co-ag – If the patient is bleeding or is likely to need surgery soon
Blood cultures – if considering infection as a potential diagnosis
Basic Imaging – Depends on what you think the likely cause is!
Erect CXR - for evidence of bowel perforation
AXR/ USS discussed on the next slide
Specialist Imaging - best discussed with a senior depending on the suspected underlying diangosis
When to do an abdo xray
Bowel obstruction
Toxic megacolon
Foreign body ingestion or insertion
Appendicitis presentation and signs on examination
Patients typically complain of a vague abdominal pain which intensifies and moves to the RIF in mcburneys point (1/3 of line between asis and umbilicus)
There is usually associated nausea and anorexia
Fever
There may be some vomiting, urinary symptoms or loose stools
Rovsing’s sign: RIF fossa pain on palpation of the LIF
On examination, patients may betachycardic,tachypnoeic, andpyrexial.
There is likelyrebound tendernessandpercussion painover McBurney’s point, as well as potentialguarding(especially if perforated).
Anappendiceal abscessmay also present with a RIF mass.
Mr Wright, a 67 year old gentleman, presents to A and E with a tender, swollen abdomen. He is vomiting and hasn’t opened his bowels for 6 days
Differentials?
Bowel obstruction
Constipation
Paralytic ileus - Functional obstruction of the bowel due to temporary paralysis
Usually affects the whole bowel
Extremely common post-op
Toxic megacolon - Acute colonic distension
Acute colitis and system toxicity
Secondary to IBD or colonic infections such as C.Diff
Symptoms of bowel obstruction
differences between sbo and lbo
Vomiting
Absolute constipations
Abdo distension
Colicky abdo pain
Large bowel obstruction (LBO) - Absolute constipation and pain are more prominent early. Vomiting often late. Symptoms generally are more gradual due to the large volume of colon and caecum and its resorptive activity
Small bowel obstruction (SBO) – Vomiting is the predominant early feature. Constipation often late.
Ileus
Functional obstruction of the bowel due to temporary paralysis
Usually affects the whole bowel
There is no pain and the bowel sounds are absent
Extremely common post-op complication
Can occur secondary to:
Hypokalaemia
Sepsis
Intra- abdominal inflammation
Bowel obstruction on examination
Abdo distension
Abdo tenderness
Central resonance to percussion
Tinkling bowel sounds
Dehydration
Why does bowel obstruction cause dehydration
‘Third spacing’ from increased electrolyte fluid in the bowel
Vomiting ++
Lack of fluid intake – patients with bowel obstruction commonly develop anorexia
Strangulating obstructions
Strangulating obstructionsare characterised by interruption of the intestinal blood supply with simultaneousblockageof the intestinal lumen
Closed loop obstruction
Obstruction at two points which forms a loop of grossly distended bowel
SURGICAL EMERGENCY
Bowel will continue to distend, stretching the bowel wall until it becomes ischaemic and ultimately perforates
Large bowel obstruction with competent or incompetent ileo-ceocal valve
Ileocaecal valve
Normally prevents backflow of bowel contents from large bowel to small bowel
If ileocaecal valve is competent closed-loop obstruction forms
If ileocaecal valve is incompetent bowel content flows from large to small bowel
Sigmoid volvulus
Twisting of bowel on itself
Small or large bowel obstruction more common?
Causes
SBO 80% - Adhesions, hernias, crohns
LBO 20% - malignancy, diverticular disease, volvulus
List of tests for bowel obstruction
Bedside
Observations – ?dehydrated ?shocked ?infection or peritonitis
Abdominal exam – signs of bowel obstruction (Abdominal distension, Abdominal tenderness, Central resonance to percussion, Tinkling bowel sounds, Dehydration).
Also scars ?adhesional bowel obstruction
Hernia – Examine groin. If a strangulated hernia is present may have overlying red and tender skin. More likely to cause SBO.
PR – obstructing mass / faecal impaction
Bloods
FBC - Raised WBC count may indicate an infective or inflammatory cause O complication such as perforation or impending perforation. Microcytic (iron deficency) anaemia may be found in the presence of an underlying malignancy.
U+E Colon secretes potassium and bicarbonate in exchange for sodium chloride and water absorption. If this is disrupted in the obstructed colon may have resulting hypokalaemia.
An increase in the urea shows the severity of dehydration/renal failure
CRP- raised in infection or perforation
G+S and co-ag- pre-surgery
VBG - metabolic derangement (secondary to dehydration or excessive vomiting).High lactate ?ischaemia
Basic Imaging
AXR – diagnosis (May have rectal gas if PR performed)
Erect CXR – looking for free air under the diaphragm if ?perforation
Specialist Imaging
CT more sensitive than AXR
Differentiate mechanical vs. pseudo-obstruction;
Site and cause of obstruction can be seen on a CT which is helpful for operation planning
If malignant cause for obstruction may be able to see presence of metastases on a CT
SBO and LBO on x ray
SBO
Tends to lie centrally in the X-ray
Normal diameter is <3cm
‘Conniventes are continuous’ – cross the entire diameter of the bowel
LBO
Tends to lie around the edge of the abdomen
Normal diameter is <6cm (<9cm at caecum)
May contain faeces, which has a mottled appearance
Haustra go half way’ – incomplete crossing of the bowel
Bowel obstruction management
NBM, IVI, fluid balance and or catheter
Analgesia, antiemetic’s
SBO: Usually Drip and Suck
LBO: Surgery
Volvulus: Initial management is a flatus tube
Recurrent or unresolving disease may necessitate surgery
Gallstone risk factors
Female
Forty
Fat
Fair
Fertile
Family History
Increased plasma oestrogen → Obesity, pregnancy, OCP, female
Depletion of the bile acid pool → Terminal ileum resection or disease
Lack of stimulus to GB emptying → Fasting, TPN
Haemolytic Disorders → Spherocytosis, sickle cell disease or malaria
Gallstone types
20% Cholesterol
Often solitary
Large (>2.5cm)
Smooth
75% Mixed
Predominantly cholesterol
Multiple stones
‘Generations’ Range of colours and shapes
5% Bile pigments
Multiple
Small
Irregular and fragile
Biliary colic
PATHOPHYSIOLOGY
Stone impacted in neck of GB or cystic duct
PAIN
Sudden, sharp, stabbing, RUQ-epigastric pain. Typically radiates to right shoulder and lasts <6 hours
ASSOCIATIONS
Pain may be precipitated by eating, (especially fatty foods)
May have associated N+V
EXAMINATION
Typically unremarkable. Apyrexial.
INVESTIGATIONS
Typically unremarkable other than presence of stones on USS
MANAGEMENT
Analgesia
Outpatient cholecystectomy
Cholecystitis
PATHOPHYSIOLOGY
Stone impacted in neck of the GB or CD results in super concentrate, irritant, bile +/- infection via ascending gut bacteria (Klebsiella, E.coli)
PAIN
Constant RUQ-epigastric pain which persists
Radiates to right shoulder
ASSOCIATIONS
May have N+V
Likely to have fever and or lethargy
EXAMINATION
Tender RUQ with possible guarding.
Murphy’s sign
INVESTIGATIONS
Raised inflammatory markers
Mildly deranged AST/ALT/ ALP
USS shows enlarged gall bladder with stone(s) and thickened walls
MANAGEMENT
Analgesia, NBM, IVI, IV Abx (cef + met)
Cholecystectomy within one week
Cholangitis
PATHOPHYSIOLOGY
CBD biliary outflow obstruction and ascending infection (most common E. coli)
PAIN
RUQ pain, persistent, may be colicky in nature
ASSOCIATIONS
Patient is jaundiced, typically unwell and pyrexial with rigors
May also have pruritis, pale stool and dark urine
Often causes sepsis
EXAMINATION
Tender RUQ with possible guarding
Pyrexial, jaundiced
INVESTIGATIONS
Raised white cell count, blood cultures
Raised Bilirubin
Raised ALP/ GGT > AST/ALT
USS will show dilated bile ducts +/- gall bladder stones +/-ductal stones
MANAGEMENT
Analgesia, NBM, IVI, IV Abx
May need ERCP / open or lap stone removal
Gallstone Ileus
Inflammation of the gallbladdercan cause afistula between the gallbladder wall and the duodenum allowing gallstones to pass into the small bowel directly
If a the stone impacts at the terminal ileum this results in small bowel obstruction
Causes of acute pancreatitis
(Drugs in particular)
I-idiopathic
G-gallstones (most common cause)
E-ethanol (alcohol-2nd most common cause)
T-trauma (esp stabs)
S-steroids
M-mumps
A-autoimmune (eg: Lupus, Sjogrens)
S-scorpion stings
H-hypercalcaemia/hypertriglyceridaemia
E-ERCP
D-drugs (eg: azathioprine, furosemide, immunosuppressants, thiopurines, thiazides, furosemide, sodium valproate, steroids)
Acute Pancreatitis- Symptoms and Signs
N+V
Epigastric pain with radiation to the back, relieved by sitting forward
Cullen’s sign - Bruising around periumbilical region
Grey-Turner’s sign - Bruising around flanks
Sepsis
Pancreatitis investigations
Bloods;
Amylase -> usually elevated
Lipase -> these are elevated as well and are specific for pancreatitis
Bone profile-> to look at calcium levels (for hypercalcaemia)
Triglycerides-> to check for elevated triglyceride levels
(and do normal bloods such as FBC, U+Es, LFTs, CRP)
ABG- used for checking lactate and PaO2
Abdo X-ray-> may show ileus
Ultrasound-> used to confirm or exclude gallstones
CT abdo-> not done routinely but can be used to confirm diagnosis when uncertainty present and also used to look for complications
Glasgow scoring system - acute pancreatitis
PaO2 <7.9 kPa
Age >55
Neutrophils >15
Calcium <2mmol/L
Renal Urea >16mmol/L
ERCP
Albumin <32 G/L
Sugar >10mmol/L
Management of Acute Pancreatitis
Fluids
Analgesia (IV opiates) and anti-emetics
NG tube if needed
O2
Antibiotics if ?infection
ERCP if GS induced
Complications of pancreatitis
Necrosis.
This happens when the inflammatory process causes blood vessels to become leaky and then rupture leading to pancreatic tissue swelling.
This causes premature activation of lipases which then starts to destroy peripancreatic fat.
The fat and tissues liquefy and can start necrosing (process called Liquefactive Haemorrhagic Necrosis)
Pseudocyst
>4 weeks
This is when fibrous tissue surrounds necrotic tissues and fills with pancreatic juices.
The pseudocyst can also become infected to become an abscess and presents as sepsis
This may cause abdominal pain, loss of appetite and a palpable tender mass.
Abdominal CT scan is best way to assess for a pseudocyst/abscess
Systemic
hypovolemic shock
ARDS
DIC
