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Upper GIT - Surgery - Week 3 - Coggle Diagram
Upper GIT - Surgery - Week 3
PREOPERATIVE ASSESSMENT - estimating the patient’s ability to respond to these stresses of surgery and anaesthesia
FUNCTION/AIM OF PREOPERATIVE ASSESSMENT
• Obtain informed consent,
• Ensure correct patient; correct surgery; correct anatomical site
• Assess fitness for anaesthesia and operative procedure,
• Address patient concerns and fears
• Identify signs & symptoms indicating recent patient deterioration,
• Allay patient anxiety and ensure symptoms of pain, dyspnoea and nausea are managed appropriately,
• Check appropriate preoperative investigations (
screening tests
) have been performed or ordered
HAEM: FBC (o2 carryign capacity, clotting capacity, immune capacitiy), COAGS (INR, aPTT), CROSS MATHC GROUPS AND HOLD
BIOCHEM: EUC hypokal, hyperuremia, LFT
CARDIC: ECG (MALES > 40, FEMALES >50, Ssymptomatic CVD, HTN, diabetes), CXR (CCF)
RESP: CXR, PFT (if indicated/Hx of pulm disease)
Pregnancy screening
fastign BGL
• Identify possible issues that will prolong postoperative hospital admissions;,i.e.,home, environment, social, support, rehabilitation,
Identify known health problems
screen for commonly undiagnosed problems (HTN, T2DM)
identify other risk factors (smoking, high alcohol intake, obesity)
identify drug allergies (including anesthetics)
initiate standard perioperative regimes (antibiotics, DVT prophylaxis.
Cardiac and Pulmonary Risk:
Cardiac evaluation: Consider: Characteristics of patient, risk of procedure, functional capacity of patient
Hx: congenital, acquired pathology, intervention, MI, pacemakers, palps, syncope, arrythmias Aotic stenosis (
Ex: Vitals, JVP, slow carotid upstroke, bruits, edema, heart displacement, S3, systolic murmurs, rubs,
Pulmonary evalutaion
Smoking, asthma , COPD sleep apneoa, CHF, previosu complication, exercise toelracne, coughing, wheezing, sputum, dyspnoea, snoring, orthopnea (if porrrly controlled = high risk.
Cardiovascular Risk:
Low Risk
No CVS conditions
Stable coronary syndromes (angina, arrtyhmias, HTN)
Mild to moderate HTN (DBP <90)
Mild cardiac failure EF >40%
Normal chol, BGL, Hba1c
High Risk
Unstable coronary syndromes
ADCHF
Sever valvuar disease
Sinificant arrythmias
Sever HTN (DBP > 110, SBP >180
congentital heart abnormalties
Perioperative Medication Management
Full,list,of,current,medica
ons,incl.,dosages,and,indica
ons,for,each,should, be,obtained,
• In,general,,medica
ons,should,be, con
nued,as,normal, i.e d o not stop if goign to put patietn at risk
• LongBterm,steroids,–,hypoaldrenalism ! inability,to,mount,effec*ve,response,to, surgical,stress.,,,
• An
platelet/an
coags,–,weigh,risk,of,withdrawal,against,risk,of, thromboembolic event
OCP/HRT,–,risk,of,thromboembolism.,,Cease,6/52,prior,to,surgery;,weigh,risk,of, pregnancy,against,risk,of,complica*on.,
• Psychiatric,drugs,–,complica*on,to,general,anaesthesia
Cease oral hypoglycemic, antidepressants, ACE inhibitors on day of surgery . Warfarin/antiplatelet therapy also
Adjust insulin, prednisone, bronchodilators
Emergency situation = AMPLE:
a
llergies,
m
edications,
p
ast HX,
l
ast eaten, preceding
e
vents
Renal dysfunction
Increased risk of complications in the peri-operative period
• Mx. of fluid balance and specific arrangements for dialysis
• Dialysis dependent Pt.
– Fluid,balance
Maintain access for dialysis (e.g. protect fistula site)
Frequent monitoring of electrolytes
• Non-dialysis dependent Pt.
Optimise,fluid,balance,
Avoid nephrotoxic drugs and radio-contrast agents,
Treat sepsis aggressively,
Protect renal perfusion by avoiding hypotension,
Avoid build up of renally excreted drugs (e.g., morphine, metabolites
Hepatic dysfunction
Identify cause as pre-hepatic hepatic or post-hepatic
• Hepatitis
– Ascertain status (following consent), protect staff
Consider if elevated aminotransferases or cirrhosis,
• Coagulopathy,
coagulopathy due to lack of Vitamin,K reduced factors,II VII,,IX,,X,
Obstructive jaundice and hepatocellular dysfunction
– Administer Vitamin or fresh frozen plasma pre-operatively
• Acute renal failure
Hepatorenal syndrome
• Cirrhosis,
– ICU postoperatively
Pregnancy
Do not administer general anaesthetic
• Elective surgery should be delayed
• Weigh risk of delaying surgery against risk to foetus
• Increased risk of infection
Diabetes
Comorbidites
Vascular,disease,
Renal,disease,
Neuropathy,
Infec*on,and,impaired,wound,healing,
• Management,
Maintain stable circulating glucose levels ensure adequate supply to cells
Monitor,glycaemic,control,!,oral,hypoglycaemics,or,insulin,
Administer sufficient K+ - insulin increases cellular K+ uptake
Obesity
GIT
Risk,of,aspira*on,of,gastric,contents,(#abdominal,pressure,,hiatus,hernia,,GORD),
– Difficult,mask,ven
la
on,! #ven
la
on,pressures,!,predisposes,to,gastric,
insuffla
on,!,regurgita
on
Pharm
Alters,pharmacokine*cs,of,most,drugs,
– Altered,responses,to,some,medica
ons,(#sensi
vity,to,BZD,
&,other,seda*ves,
– Dosing,difficul*es:,IBW,(underdose),,TBW,(overdose),
• Lean,Body,Weight,(IBW,+,20B40%,excess,body,weight),
– Soluble,inhala
on,agents,accumulate,in,adipose,
ssue,!
longer,clearance,*me,!,prolonged,emergence,compared,
with,lessBsoluble,agents,
Cardiac
Bod
y,weight,&,#lean,body,mass,! #Metabolic,demands,!,larger,total,blood,
– Lying,supine,#central,circula*ng,volume,! #stress,on,le[,ventricle,
Postinoning
Respiratory
"Chest,wall,,compliance,(#adipose,*ssue,on,chest,&,abdomen),! "FRC
– "Lung,compliance,(#pulmonary,blood,flow,,viscosity),
– Chronic,hypoxaemia
– #Oxygen,requirements,due,to,metabolic,demands,of,excess,adipose,*ssue,
pain management
Adequate,postBop,pain,control,a,challenge,
– Opiods,mainly,used,but,issues,with,sideBeffects,+,obesity,risks,
(OSA,,sensi
sa
on,+,dosing,challenges),
Airway management
– Difficulty,with,mask,ven
la
on,,larygoscopy,,intuba*on,
–
High,mallampa
,classifica
on&,neck,circumference,
Predictors of increased perioperative risk
Cardiac
major
Unstable,coronary,
syndromes,(MI,or,
unstable,angina,
• Heart,failure,
• Significant,arrhythmia,
• Severe,valvular,disease,
intermediate
Mild,angina,pectoris,
• Previous,MI,
• Diabetes,
• Renal,insufficiency,
Minor
Advanced,age,
• Abnormal,ECG,
• Rhythm,other,than,sinus,
• Low,func*onal,capacity,
• History,of,stroke,
• Uncontrolled,HTN,
Pulmonary
APPENDICITIS
Hx: SOCRATES
Ex: GIT
General inspection: do they look unwell? ABCDE
• Vitals:,HR,,RR,,Temp,,O2,,BP,
• Abdomen:,inspect, palpate, percuss, auscultate,
• Groin exam + DRE
• Special Tests: – Murphy’s sign (acute cholecystitis), Boas’ sign (acute cholecystitis) pain radiates to scapula, Grey Turner’s & Cullen’s sign (pancreatitis) bruising around umbilicus & in L flank, Rovsing’s sign (appendicitis) palpation in LIF produces pain in Right IF, Psoas sign, Obturator sign,
DDx:
Appendicitis!
• Salpingitis!
• Ovarian cyst (rupture or torsion)
• Mesenteric adenitis
• Terminal ileitis (Crohn’s disease, Yersinia infection, tuberculosis)
• Ureteric calculus
• Meckel’s diverticulum (inflammation, perforation or torsion)
• Cholecystitis
• Perforated duodenal ulcer
Investigations
Bloods: FBE, UEC, CRP (reference, hydration status)
• Serum Lipase/amylase: pancreatitis (lipase more sensitive
• Ultrasound: gallstones, cholecystitis, Common Bile Duct, appendicitis
• LFTs: hepatitis, obstruction of Common Bile Duct
• Urine,dipstick: exclude renal cause (e.g.,UTI)
• Pregnancy test: BHCG
Complications and how managed
Generalised peritonitis
• Perforation --> surgery
• Gangrenous appendicitis -->resection
• Perforation abscess --> drainage
• Infection following surgery --> Antibiotics
Management
Rest, antibiotics, analgesics & fluids
• Laparoscopic v's open appendicectomy.
Structures affected in Appendicectomy
McBurney’s Point incision
1/3,distance,between,ASIS,&,umbilicus,(Right,side),
• 2,perpendicular,lines,that,split,muscle,fibres,!,allows,for,good healing
• Structures,at,risk:,
– Inferior,epigastric,vessels
Ilioinguinal,and,iliohypogastric,nerves,
Midline!incision!
• Through,linea,alba,!,poorly,vascularised,!,minimum,blood, loss,&,major,nerves,avoided,
• Structures,at,risk:,
Upper:,Falciform,ligament,,
Lower:,Bladder
Pfannensteil!(suprapubic)!incision!
• 5cm,superior,to,pubic,symphysis
• Access,to,pelvic,organs,
• Structures,at,risk:,
– Bladder
Superficial,epigastric,vessels,,
– Inferior,epigastric,vessels,
LAYERS PIERCED
Skin & Superficial fascia
External!oblique!/aponeurosis!
Internal!oblique!/aponeurosis!
Transversis!abdominus!/aponeurosis!!
Transversalis!fascia!
Extraperitoneal!fat!
Parietal!peritoneum
Indications
OPEN APPENDECTOMY
Difficult placement of the appendix
Diagnosis not certain, children <30kg
LAPAROSCOPIC APPENDECTOMY
When prior diagnostic laparoscopy has established the diagnosis
Risks
OPEN APPENDECTOMY
Right inguinal hernias
Infection risk; Vessels & nerve injury
LAPAROSCOPIC APPENDECTOMY
Cost. Operation may take longer
Less ability to assess and management accidental tissue damage
Benefits
OPEN APPENDECTOMY
Relatively cost effective
LAPAROSCOPIC APPENDECTOMY
Less post-operative pain. Quicker return to normal activity.
Less chance of wound infection & dehiscence (in routine cases); less Scarring
POST OPERATIVE CARE
PROMROTE/RESTORE BOWEL FUNCTION
PREVENT DVT
PREVETN INFECTION
ANALGESIA
Appendiceal carcinoid tumors
Carcinoid, carcinoma, mucocoele
• Carcinoids = ~50% GIT carcinoids
• Majority benign can be source of luminal obstruction and appendicitis
• Usually<2cm simple appendicectomy
• >2cm R. hemicolectomy (↑ risk of malignancy & lymphatic spread)
• Overall cure rate = 50>60% at 5>year follow up
WOUND HEALING WOUND: a disruption of normal anatomic relations as a result of injury. The injury may be intentional (eg elective surgical incision) or unintentional (trauma)
PHASES
2ND INTENTION
"Spontaneous healing"
wound is left open and allowed to heal close by re-epithelialization and contraction by myofibroblasts
Permitted in management of contaminated wounds
More complicated reapair process. More inetnse inflammatory reaction (subtrate pahse). Abbundant granualtion tisseue and extensive collagen deposition
All phase of wound healing are increased
THIRD INTENTION
Used for wounds that are too heavily contaminated for primary closure but appear cleaner and well vascularized after 4-5 days inflammatory process of substrate phase = antibacterial = enabled safe closure.
Wound apporxiation is permited after 3 -5 days
Indications: infected or unhealthy wounds.; wounds with a long lapse time since injury; Wounds with sever crush component
Combination of 1st and 2nd intension. Left open with increased inflam (substrate phase) but reduced remodeling phase due to primary closure process
1ST INTENTION
wound closed by approximation of wound margins or by placement of a graft or flap, or wounds that are surgically created & closed
Best choice for clean, fresh wounds in well vascularized areas. Fastest healing and most cosmetically please
Final appearance dependent on: initial injury/nature of injury; amount of contamination/ischemia; method and accuracy of wound closure.
Minimal death of cells and tissue disruption. Less inflammatory response (substrate phase) and thereby less proliferative phase and maturation phase resulting quicker wound healing
GENERAL:
PROLIFERATIVE PHASE
Fibroblast andn macrophages
4 days - 1 month
Commences once wound is cover by epithelium. production of collagen.
Decreased edema and erythema. Scar raised, red, hard
MATURATION PHASE
Remodeling - fibroblast
No net collagen gain. Collagen deposited an exsting collaen remodelled adn removed
Flattens, pale, supple
SUBSTRATE PHASE
PMN's ¯ophages,
First 4 days
Tissue matyrix metalloprotienases degrad collagen adn necrotic cells.
macrophages release growth factors (TGF-b for fibrobalst proliferation, IL-1 induces fever, pormotes haemotstais
Wound is edematous and erythematous
GRANULATION TISSUE: Friable, reddish granules or tiny capillary buds forming the base of wounds
Most richly vascularized tissue in body
Highly resistant to infection
Cells: Fibroblasts, myofibroblasts, macrophages
GROWTH FACTORS
TGF-a
Cell of origin:
Monocytes/macrophages
Target Cells/Tissue:
fibroblasts, epithelial cells, endothelial cells
Effect:
Migration, Matrix proteins, proliferation, capillary formation
TGF-b
Cell of origin:
platelets, macrophages, fibroblasts, keratinocytes
Target Cells/Tissue:
Inflam cells, fibroblasts, endothelial cells
Effect:
Chemotactic, migration of cells, matrix proteins, proliferation, capillary formation
IL-8
PDGF
IL-1
IFN-g
IL-6
EGF
IL-2
TNF-a
Retardation of wound healing
Causations
Contamination
Time
Systemic factors
metabolic status (DM)
Circulatory status
Nutrition
Hormones glucocorticoid/corticosteroids
Lcoal factors
Infection
mechanical
foreign bodies
Size. location, type of wound
SUTURES
Absorbable
broekn down by proteolysi of hyrolysi
Do not persist as foerign body
not suitable for wound under great tension/mechanical load
used for Bowel anastomoses, skin and sub cut tissue
Non-absorbable
used where loss of strength could compromise wound
Vascualr anastomes, hernia mesh,tendon repair
Variable foreign body reaction
maintains tensile strength for longer
Wound Dehiscence: Management:
Causes: Sepsis; failure of healing process, distractive forces; poor surgical technique, immunosuppression, steroid use
Classification:
Superficial and revealed
2 weeks at suture removal. Common cause = hematoma or cellulitis
Deep and concealed
Occurs gradually with separation of all layers of abdo wall excepts skin. Lead to incisional hernia
Complete and revealed
Occurs day 10. exposure/protrusion of of knuckle or loop of bowel (evisceration)
Symptoms and signs:
usually painless, open wound, visible fat and/or viscera. maybe associated with organ dysfunction and infection
Management
IV access, clam patient, cover exposed viscera with saline soaked dressing, IV antibiotics, drain pus, lightly pack with absorbent dressing, vacuum assisted closure for large defects, re-suturing in theater or allow closure by secondary intention
POST-OPERATIVE FEVER
ASSESSMENT
TIMING
ACUTE
SUBACUTE
IMMEDIATE
DELAYED
SYMPTOMS:
PAIN AT WOUND SITE
ABDO PAIN, DISTENTION, FLUID COLLECTION OR BASCESS
RESP: sob, PRODUCTIVE COUGH, PLEURITIC PAIN
DYSURIA, HAEMATURIS, FOUL SMELLING
CALF PAIN AND SWELLING
SIGNS:
WOUND: CELLULTITIS, ERYTMEA, EDEMA, FLUCTUANCE, DISCHARGE
SWINGING FEVER (ABSCESS, TNEERNESS AWAY FROMSCAR, PERITONITIS, PALPABLE SWELLING,ABSENT BOWEL SOUNDS
RATE, OXYGEN, ACCESSORY MUSCLE USE, INPSECTION, PALPATION, PERCUSSION ADN AUSCULTATION
LEGS: UNILATERAL SWELLING , HEAT, TENDERNESS - SUSPECT DVT
SEPSIS - SHAKING, HIGH TEMPERATURE, TACHYCARDIA, HYPOTENSION, DECREASED URINE OUTPUT WARM EXREMETIES
CATHETER
CANNULA SITE
CAUSES:
MEDICATIONS
MOST COMMON CAUSES - ANTIMICROBIALS/HEPARIN
NON-INFECTION
CVS
MI
Aostic dissection
pericaristis
Fat emboli
DVT
phlebitis
RESP
atelectasisi
ARDS
aspiration pneumoitis
PE
infarction
GIT
Cholecyctitis,
hepatitis
IBD
Ischaemic colitis
pancreatitis
CNS
Caverous sinus thrombois
non haemorrahgoc infacrtion
Stoke
seizures
SAH
TBI
HAEM
VTE
haemorrhage
Transfusion reaction
Haematoma
ENDO/MET
Alchool/drug withdawal
hyperthyroidism
Adrenal insufficiency
INFLAM
Gout
Pseudogout
Transplant rejection
Vascualrtiis
IV contrast reaction
NEOPLASM
metastaici diseas
Primary tumour
MISC
Allergic drug reaction
Drug fever
Tissue ischemia/infarction
INFECTIOUS
ENDOGENOUS BOWEL FLORA
REACTIVATION OF CMV/HSV
PNEUMONIA
PATHOPHYSIOLOGY
ENDOCRINE
Pyrogens presented to host macrophage development of pyrogenic cytokines (IL-1,TNF-α,IL-6, IFN-Y)
Cytokines activate phospholipase and arachidonic acid released from plasma membranes
• Arachidonic acid COX-2 Prostaglandin E2 (PGE2)
• PGE2 --> hypothalamus internal thermostat increases the desire Body temperature thereby initiating heat creation & heat preservation mechanisms
METABOLIC
Body!heat!is!generated!by!basal!metabolic!activity!&!muscle!movement.
• ↑!muscle!contractions!=!↑!heat!pdn!=!↑!energy!requirements!
• ∴!more!energy!is!spent!on!maintaining!a!higher!body!temperature!than!would!normally!be!spent.!
• To compensate for his energy demand skeletal muscle is broken down into amino acids and used by the liver in gluconeogenesis to make more energy. This increased metabolic activity also generates heat
AUTONOMIC
The autonomic nervous system works to increase body temperature by increasing heat production & reducing heat loss
• Heat production mechanisms:↑!muscle contractions (seen as rigors) increase the amount of heat produced
• Heat loss mechanisms – revolves around sympathetic control of vascular diameter. Vasoconstriction of peripheral vessels reduces heat loss through conduction, convection & radiation thereby preserving body heat
BEHAVIOURAL
Act!in!ways!to!conserve!heat.!
" Increased!amount!&!thickness!of!clothing!!!jumpers!!
" Increased!external!heat!sources!!!heaters!!
" Consume!hot!foods!&!beverages!!soups!&!teas!
Investigations:
Screen for transfusion reaction
Blood cultures
UA (UTI)
ABG
FBC, EUC, CRP (will be elevated post surgery but if >100 do sepsis workup
head CT
ECG/cardiac enzymes
CXR
Ultrasound
TIMING OF FEVER
DAY5-7
ENTERIC ANASTOMTIC SHOCK
DVT
DAY 7+
IntraBabdominal,collec*on,
• DVT,
• sep*caemia,
DAY 3-5
Sepsis,–,wound,infec*on,
• Biliary,or,urinary,sepsis,
• IntraBabdominal,collec*on,
• Pneumonia,
DAY 0-2
Physiological,as,a,response,to,*ssue, injury,(low,grade),
• Pulmonary,collapse/atelectasis,
• Blood,transfusions,
• Thrombophlebi*s,
PANCREATITIS
AETIOLOGY (I GET SMASHED)
IDIOPATHIC
GALLSTONES
ETHANOL
TRAUMA/TUMOUR
STERIODS
MICROBES
AUTOIMMUNE
SCORPION VENOM
HYPERLIPIDEMAI, HYPOTHERMIA, HYEPRCALCAEMIA
ECRP (SCOPE) & EMBOLI
DRUGS
MOST COMMON - GALLSTONES, ALCOHOL, IDOPATHIC, POST ERCP
HISTORY
Ask about alcohol consumption, lipid status, medication, gallstones, blunt or penetrating injury, surgery
Non crampy, epigastric pain, raditating to LUQ, RUQ or back, alleviated by sitting or standing
Nausea, vomiting, worsens with food consumption
EXAMINATION
Appears unwell
Fever
tachycardia
upper abdo tenderness and guarding
dyspnoea, tachypnea, possible rales
haemodynaic instability - hematemesis, malena
absent bowel sounds
Grey-turns, cullen's signs
RANSON CRITERIA
BGL > 11
55 Y.O
LDH > 350
AST >250
WBC> 16 X 10
Ca++ < 2
hematocrit drop > 10 %
arterial Po2 < 60
base defcit > 4
BUN rise > 1.8
fluid sequestration >6 L
jaundice
INVESTIGATIONS
FBC (mild leukocytosis with left shift and elevate hematocrit (dehydration))
Increased amylase/lipases (> 3 & >2 times upper limit or normal respectively)
hyper/ogycaemia
increased BUN
ABG (hypoxemia
U/S (stones) or CT (imaging of choice) AXR/CXR (to exclude other causes of pain and to see pathology stemming from pancreatitis i.e. pleural effusion, bowel obstruction etc)
LFTs (ALT > 150 = gallstone)
CRP elevated . 200 = pancreatic necrosis
UEC: increase ur/cr ratio. Decreased calcium
Diagnostic Features (at least two)
Atlanta classification
Acute onset of persistent, severe epigastric pain
Elevation in pancreatic enzymes (> 3 times upper limit or normal)
Imaging confirmation (U/S CT)
SEVERITY SCORES: RANSON (0 & 48 hrs), Glasgow (within 48 hrs) and APACHE criteria (on admission then daily)
PATHOPHYSIOLOGY
1
. Defective transport and secretion of zymogens,
2
. duct obstruction (stones/tumor),
3
. hyperstimulation (alcohol),
4
. Reflux of bile or duodenal contents
Zymogens activatation cascade
autodigestion/damage
systemic inflammatory response
fluid loss.vascular alteration
organ failure
MANAGEMENT
ACUTE
analgesia morphine les desirable - go with tramadol, NSAIDS,paracetemol
antiemetics (metoclopramide, prochlorperazine, ondansetron)
fluids (resus, replacement, maintenance)
SEVERE
hIGH DEPENDENCY UNIT/ICU
NGT
INSULIN INFUSION
CA++ REPLACEM,ENT
IV ANTIBIOTICS
MONITIRING
map 65, URINE VOL 0.5 ML/KG/HR, CLEAR FLUIDS, ADEQUATE ANALGESIA
Assess using scoring systems
early identification fo deterioration
early imaging
early introduction of enteral nutrition (if indicated)
COMPLICATIONS
LOCAL
pseudocyst
abscess
NECORIS
haemorrhage
ascites
SYSTEMIC
shock
parlytic ileus
pulmonary effusoins
ARDS
Acutre renal failure
Hypcalceamia
ostrucitve jaundice
erosion of the GIT
Acute v's Chronic
acute
alchol/gallstones
elevated lipas/amylase
reversible
painful
chronic
alcohol/genetic
may be aymptomatic
irreveersible structireal changes, patchy fibrosis
normal amylase/lipase
CHOLESCYSTITIS/BILARY COLIC
PATHOGENESIS
TYPES
BLACK
2%,
• Deep,black/brown colour
• O[en,associated,with,haemoly*c,diseases,+ cirrhosis,
Hyperbilirubinaemia ! biliary,secre
on,of,bile !,favours,precipita
on, of,pigment,stones,
*RadioBopaque,
BROWN
Muddy,colour,
alterna
ng,brown,&,tan,layers,on,X-sec
on,
• Calcium,biblrubinate
Denovo,forma
on, following,biliary,stasis,&,infec
on,
*Radiolucent,
MIXED
ΔRa
o,of,biliary, cholesterol,,bile,salts,&,phospholipids,2. Nuclea
on,of,cholesterol, 3. Gallbladder, hypomobility *Radiolucent,
• 50-100% cholesterol,
GREEN, WHITE, YELLOW
80-90%
Cholesterol concentrations - solubilising capacity of bile (supersaturation)
• CHOLESTEROL STONES: o Bile supersaturate with cholesterol, o Hypomotility of gallbladder promotes nucleation, o Cholesterol nucleation in bile accelerated, o Hypersecretion of mucus in the gallbladder
PIGEMENTED STONES:
1.
Mixture of abnormal insoluble calcium salts of unconjugated bilirubin + inorganic calcium salts.
2.*
Disorders with ↑!unconjugated bilirubin: haemolytic syndromes severe ileal dysfunction (or bypass), bacterial contamination of the biliary tree
RUQ PAIN DDX:
Dyspepsia
Duodenal ulver
Acute cholecystitis
Hepatic abscess
Biliary colic
MI
INVESTIGATIONS
AMYLASE/LIPASE - pancreatitis
LFT'S - increased ALP, increased billrubin --> obstuction, cholangitits, or pancreatitis
FBC - increased WCC Acute cholecytitis
CRP
ULTRASOUND
CT ANGIOCRAM
HIDA
BOOD CULTURES if pyrexic
5 F's
female
fertiel
forty
fair
Fat
CHOLESCYSTITIS v's BILARY COLIC
ASsociated symptoms
Acute Cholecystitis
:
Fat intolerance
FEVER
N & V
Biliary colic
N & V
Dyspepsia, bloating
Fat intolerance
Pain:
Acute Cholecystitis
:
unremitting
RUQ . Sever constant crescendo.
Exacerbated by movement
, post prandial. Radiates to T7 intrascapular region +/- C4 shoulder tip.
Biliary colic
=
RUQ/epigastric <6hrs
. Crescendo.
not exacerbated by movement
, post prandial. Radiates to T7 intrascapular region
PHYSICAL EXAM
Acute Cholecystitis
Mass
M<urphey's postive
Tneder
Febrile
jaundice
Biliary colic
Abdo exam unremarkable
A febrile
Murphey's Negative
CHOLEDOCOLITHIASIS + CHOLECYSTECTOMY
ACUTE INFLAMMATION
Leakage of plasma proteins oedema: contraction of endothelial cells
Neutrophil emigration: margination, rolling and adhesion to endothelium migration across endothelium and vessel
wall towards chemotactic stimulus
Vascular dilation + ↑blood flow: histamine + NO release ↑ permeability of microvasculature, vascular congestion
(rubor), adhesion molecules
