Abdominal Aortic Aneurysm Flashcards
List the common causes for severe abdominal pain of sudden onset accompanied by the clinical signs mentioned above (fast pulse, low BP, cold/clammy hands, pale, CRT > 5s)
- Perforated viscus (i.e. perforated gastric/duodenal ulcer)
- Acute pancreatitis
- Biliary colic/acute cholangitis
- Acute mesenteric occlusion
- Ruptured/leaking abdominal aortic aneurysm
- Basal pneumonia (rare)
- Inferior MI (rare)
What are the branches of the celiac trunk?
- L gastric artery
- Splenic artery
- Common hepatic artery
Discuss the relevance of AAA clamping on patient outcome
Supra-coeliac clamping: highest stress on the heart, iscahemia to all organs below the coeliac artery with subsequent reperfusion injury.
Supra-renal clamp: high stress on the heart, ischaemia to all organs below the superior mesenteric artery with subsequent reperfusion injury.
Infra-renal clamp: relatively less stress on the heart, ischaemia to all organs below the kidneys with subsequent reperfusion injury.
What are the signs of ruptured AAA? Dissection/PVD?
Shock + bilateral limb schema
Shock + unilateral limb ischemia
What should you suspect in a male > 60y with first presentation of renal colic?
Aortic aneurysm rupture
What should you suspect in a patient with GI bleed + PMH of aortic surgery?
Aorto-enteric fistula (until proven otherwise)
What is the transfusion management of major hemorrhage?
- Reverse anticoagulation (vitamin K, prothrombin complex concentrate)
- Tranexamic acid (antifibrinolytic agent) within 1st hour
- Bloods (FBC, U&E, Ca2+, LFTs, PT, APTT, Fibrinogen, crossmatch)
- Request (Red cells, FFP, platelets)
- Request O RhD negative = extreme emergency only!
- Within 15min from sample arriving in the lab = can receive group specific (ABO + RhD compatible)
- Safest product if time allows (45-60min after arriving in lab) = Crossmatched (fully screened for antibodies)
Pack 1: 4U red cells, 4U fresh frozen plasma
Pack 2: 4U red cells, 4U FFP, 1 dose platelets, 2 packs cryoprecipitate
** Red cells don’t control coagulopathy!!
Try to keep blood results at the following ranges: Fibrinogen > 1.5g/L PT/APTT < 1.5 Hb 80-100g/L Platelets > 75 x 10^9L
How do cardiac output and blood pressure change in a patient who is losing blood?
As shown in the figure, the body is able to maintain pressure (at the expense of cardiac output and tissue blood flow) until a large volume of blood has been lost. In other words, it is only when the compensatory mechanisms are unable to cope that the blood pressure begins to fall. Therefore, any person (particularly young subjects with good physiological reflexes) who have a low blood pressure in the context of acute blood loss, is extremely ill and needs urgent medical attention.
What causes the formation of an atherosclerotic plaque?
- Smooth muscle proliferation/migration
- Inflammation
- Lipid deposit
What is the cause of chronic ischemia? Acute ischemia?
Chronic ischemia = decreased diameter of lumen due to atherosclerosis
Acute ischemia = rupture of atherosclerotic plaque
What are risk factors for PVD?
- Increased age
- Male
- Family history
- Smoking
- HTN
- Cholesterol
- Diabetes
What are the 6Ps of limb ischemia?
- Pale
- Perishingly cold
- Pulseless
(onset within 4h of acute ischemia) - Paraesthesia
- Pain
(within 6h) - Paralyzed (irreversible)
How is chronic ischemia classified?
Fontaine Classification system
I = asymptomatic II = claudication III = rest pain IV = tissue loss (i.e. ulcers, gangrene)
What is the treatment of limb ischemia?
- Stop smoking
- Antiplatelet therapy (aspirin)
- BP control
- Cholesterol control
- Exercise
- Lose weight
- Strict diabetic control
What is the cause of cerebrovascular disease?
Atheroma
- Affects the carotids
- Leads to stroke, TIA, Amaurosis fugax (transient blindness in ipsilateral eye)
What investigations are done in CVD?
- Duplex
- Angiography
- MR/CT
What are the indications for carotid surgery?
- Symptomatic patients (in last 6mo)
- > 70% stenosis of ICA
- 2yr life expectancy
- Fit for surgery (2.6% risk of stroke, 2% risk of death, 1% risk of nerve palsy - CN 9/10)
What are abdominal aneurysms? How are they treated?
> 50% of normal transverse diameter.
Ectasia = dilation of up to 50%
Either saccular or fusiform in shape
Above umbilicus = AAA
Below umbilicus = iliac aneurysm
Small AAA < 4.5cm
Large AAA > 5.5cm -> requires surgery!
EVAR: endovascular aneurysm repair
- 70% pts suitable on anatomical basis: proximal infrarenal aortic neck, iliac arteries
- Lifelong CT/duplex follow-up
- 8% chance of 2nd procedure needed -> endoleak: sac repressurization
What signs would lead you to believe there was a suspected rupture
- collapse
- hypotension
- low back/flank pain
What is an aortic dissection?
- Separation of layers in wall of aorta
- Layers of artery (adventitia, media-muscle layer, intima)
- Tear in intima, blood enters between intimacy + media = increased tearing OR exit tear allowing blood to re-enter aorta (false lumen formed) -> hypotension, shock
What are the causes of aortic dissection?
- Chronic HTN
- Connective tissue disorder (Marfan’s, Ehler-Danlos)
- Aneurysm
- Chest trauma
- Males
- Increased age (50-65y)
How are aortic dissections classified?
Stanford System
Type A: ascending aorta (surgical treatment)
Type B: Descending aorta after L subclavian artery (medical treatment)
- Most common site = 2cm above aortic root (type A)
What are the symptoms of aortic dissection?
- Severe central chest pain “tearing” to the back
- Sweating, Nausea, SOB, Syncope, Weakness
- Abdo pain (if abdominal aortic dissection)
How is an aortic dissection diagnosed?
- CT scan with contrast (GOLD STANDARD!)
- MR angiogram
- Transesophageal echocardiogram (TEE) - shows thoracic aorta + aortic valve only
What is shock?
An acute clinical syndrome initiated by ineffective perfusion and cellular hypoxia, resulting in severe dysfunction of organs vital to survival
What are the key features of shock?
- Acute tissue/organ hypo-perfusion
- Impaired delivery of oxygen to cells
- Supply inadequate to meet demand
- Generalised cellular hypoxia
- Consequences for cellular respiration
- Hemodynamic abnormalities but shock isn’t simply the presence of hypotension
- Oxygen utilization may be abnormal
What are the 4 types of shock?
- Hypovolemic (reduced intravascular volume)
- Cardiogenic (intrinsic cardiac pump failure)
- Distributive (Vasodilation + malperfusion)
- Obstructive (failure of circulatory flow)
What are clinical examples of each of the 4 types of shock?
- Hypovolemic:
- Hemorrhage
- Burns
- GI losses (vomiting, diarrhea, fistula)
- Dehydration (heat exposure, polyuria - DKA) - Distributive:
- SIRS related - sepsis, pancreatitis, trauma, burns
- Neurogenic - spinal cord injury
- Anaphylaxis - Cardiogenic:
- Myocardial infarction/ischemia
- Arrhythmia
- Acute valve pathology - Obstructive:
- Tension pneumothorax
- Pericardial tamponade
- Pulomonary embolism
What is the pathophysiology of hypovolemia?
- Sudden, severe blood loss
- Reduction in venous return
- Fall in stroke volume + cardiac output
- Hypotension
- Hypoperfusion of organs
- Onset of organ dysfunction
What is Starling’s law of the heart?
A relationship between stroke volume and ventricular end-diastolic volume (preload).
As blood loss increases, preload and stroke volume decreases.
What are the physiological responses to blood loss?
- Sympathetic system activated
- Adrenal catecholamine release
- Compensatory cardiovascular responses
- Sodium + water retention
- Coagulation system activation
- Cortisol release
What are the signs of organ hypoperfusion?
- Skin (pale, CRT > 2s)
- Oliguria
- Cognitive changes
- Metabolic acidosis
What are the management principles for hypo perfusion?
- Restore tissue perfusion + oxygen delivery to cells as rapidly as possible
- ABC (2x large bore IV cannulas 14/16G)
- Administer oxygen
- Give IV fluids (1L warmed Hartmann’s given stat, colloids, blood requested)
- Treat the cause
- Resuscitation begins concurrently or ahead of the diagnostic process
- Aiming to prevent irreversible organ injury + failure
- Blood tests (crossmatch 6u red cells, FBC, clotting, U&E, glucose, LFTs, bone, lactate)
- Ultrasound of abdomen (FAST scan)
- ECG
- Measure core temperature + maintain
How can other types of shock be diagnosed?
Cardiogenic:
- History
- Signs of cardiac failure
- ECG evidence
Obstructive:
- Impaired cardiac filling
- Obstructed forward flow
- Specific symptoms + signs
Distributive:
- Vasodilated
- Markers of infection
- Capillary leak
What are further management strategies for shock?
- Surgery
- Fluid management = increase preload
- Invasive lines
- Drugs (inotropes) = increase contractility
- Monitoring
- ICU
What is the result of administrating inotropes on Starling’s law? Fluids?
Inotropes:
- Increase stroke volume without large increase in preload
Fluids:
- Increase both preload + stroke volume
What are the consequences of shock?
- Mortality (cariogenic > septic)
- Prolonged organ hypo perfusion + tissue hypoxia
- Multi-organ dysfunction then failure
- Cellular injury + death
What is sepsis?
- Widespread inflammation due to infection
- Vasodilation and capillary leak
- When severe can rapidly progress to shock
- Treatment principles the same, plus: - piperacillin/tazobactam
- Noradrenaline
- IV fluids
Define allogenic and autologous
Allogenic = blood product donated from another person
Autologous = re-infusion of the person’s own blood products for transplant
What is transfusion associated acute lung injury? What is Transfusion Associated Circulatory Overload?
Transfusion Associated Acute Lung Injury:
- Sudden acute respiratory distress following transfusion
- Occurs within 6h of blood transfusion
Transfusion Associated Circulatory Overload:
- Common transfusion reaction in which pulmonary oedema
- Develops primarily due to volume excess or circulatory overload.
- Typically occurs in patients who receive a large volume of a transfused product over a short period of time, or in those with underlying cardiovascular or renal disease.
- Respond well to diuretics
Why did Mr Simpson develop abnormal clotting after his blood transfusion?
Abnormalities in clotting is a common complication associated with massive blood transfusion. Dilution of platelets and clotting factors are recognised causes for this state of coagulopathy. Which is why patients who receive massive transfusions require careful monitoring of their coagulation status and transfusion of blood products - including Platelets, FFP, Cryoprecipitate and single clotting factors. This is a complex area and such patients should be managed in consultation with the Haematologists.
List 5 recognized complications of ICU patients once discharged
- Muscle weakness + wasting
- Nutritional deficits
- Recurrent chest infections
- Sleep disorders
- Inability to swallow effectively and microaspiration of food
What are 5 complications that can occur due to a transfusion?
Transfusion coagulopathy can occur due to increased circulatory toxins leading to:
- Acute lung injury
- Renal failure
- Gut sepsis
- DIC (coagulation failure)
- ACoTS (acute coagulation of trauma shock)
What is PT? What is APTT?
PT:
- Looks at extrinsic pathway
- Monitor warfarin
- Increased in liver disease
- Blood clot test produced within 12s
APTT:
- Looks at intrinsic pathway
- Monitor heparin therapy (not DOACs)
- Increased in hemophilia/vWB disease
- Blood clot test -> clotting within 42s
What are the 3 stages of cell-based model of hemostasis?
Need tissue factor (TF) and platelets
- Initiation
- TF binds to VIIa
- Activates IV + X
- Factor Xa activates V
- Small amounts of thrombin generated - Amplification
- Thrombin activates platelets
- FV + FIX activated (activated platelets)
- Va removes vWF from VIII - Propagation
- IVa + VIIIa on platelets surface activate factor X
- Activation occurs on platelet surface
- Factor Xa generates large amounts of thrombin = thrombin burst
- Thrombin splits fibrinogen into fibrin monomers
List 4 groups of antiplatelet drugs
- Aspirin (thromboxane A2 - prostaglandin)
- Clopidogrel/ticlopidine (ADP inhibitor)
- Thrombin inhibitor
- Glycoprotein IIb/IIIa inhibitors
*Multiplate = to monitor platelet function
What does the fibrinolytic system do? Name a antifibrinolytic and thrombolytic agent.
Breaks down clot (i.e. FDP = fibrin degradation product, D-dimer)
Thrombolytic = tPA = streptokinase
Antifibrinolytics = increase clotting of blood = tranexamic acid
How is clot forming limited?
- Location of initiation and amplification (Tissue factor then platelets)
- Serum protease inhibitors
- Healthy endothelium secretes thrombomodulin (especially smaller vessels)
- TM-thrombin-aPC complexes cleave factor Va to factor VIIIa
What occurs in DIC?
- Increased thrombin, increased fibrin, increased clots
- Increased FDP + D-dimer
Causes:
- Trauma
- Cytokines (IL1, endotoxin)
DIC Shock:
- Hypoperfusion
- Increased protein C
- Hyperfibrinolysis
What is the treatment for transfusion coagulopathy?
- FFP, platelets (gently rocked to prevent aggregation)
- Blood transfusion (“cell-saver” = heperanize patients own cells then transfuse back into the patient)
- Potential for viral transmission + immunosuppression
- Keep patient warm
- Reverse anticoagulation
- Inhibit fibrinolysis (tranexamic acid)
- All of the above = “shock packs”
- *DVT prophylaxis post-tx of DIC (i.e. Heparin)
- Look out for HIT (heparin induced thrombocytopenia)!
Name 2 medications where ankle oedema is a common side effect
- Sitagliptan
2. Amlodipine
What are the components of Tazocin?
Tazobactam + Piperacillin
** Contains penicillin!
A patient who is in hypovolemic shock has the following clinical signs:
Heart rate 120 beats/minute, systolic blood pressure 80mmHg and urine output 20mL. After administering an IV fluid bolus, what is the best indication of improved tissue perfusion?
Urine output improves to > 30mls/hr
The same patient with hypovolaemic shock is transfused 2 units of blood. What measurement indicates his plasma volume is adequately restored to prevent a cardiac arrest?
Lactate < 2mmol/l
List 5 complications of a massive blood transfusion
- Hypocalcemia (citrate binds with ionized calcium)
- Hypothermia
- DIC
- Transfusion related acute lung injury
- Hemolytic reactions - immediate and delayed
- Immediate = ABO incompatability
- Delayed = Rhesus antibody reactions
What are the symptoms of local compression of AAA on neighbouring structures?
- Early satiety
- N/V
- Urinary symptoms
- Venous thrombosis from venous compression
What are the symptoms of embolic disease from aneurysm?
Blue toes, thromboembolism lodges and ischemia distally
Which organs are affected by PVD?
- Brain
- Eyes
- Heart
- Kidneys
- Gut (mesenteric ischemia)
- Muscles
- PVD
What medications will a patient be put on if found to have an AAA < 5.5cm?
Aspirin + statin + quit smoking
- Thought to reduce growth of aneurysm
What is the triad indicative of cardiac tamponade?
- Increased JVP
- Muffled heart sounds
- Syncope
What is the gold standard imaging for AAA?
CT scan
USS
What is the lethal triad?
- Hypothermia
- Coagulopathy
- Metabolic acidosis
What classifications are used to grade aortic dissections?
- DeBakey (I-III)
- Stanford (1 or 2)
What are the signs of aortic dissection?
- > 20mmHg difference between arms
- Aortic regurgitation
- Cardiac tamponade
- Acute occlusion of arteries arising from aorta (malperfusion)
- Brachiocephalic (UL limb ischemia)
- Stroke (spinal artery)
- Celiac trunk (mesenteric ischemia)
- Renal artery (oliguria - renal artery stenosis)
- SMA, IMA (abdo pain)
- Ischemic leg
- Widened mediastinum on xray (i.e. cardiac tamponade)
What’s the treatment for aortic dissection?
- Lower BP + surgery!
What is mesenteric ischemia?
- Ischemia/infarct affecting any/all 3 mesenteric arteries (SMA, IMA)
- Sudden pain + metabolic acidosis = acute presentation
- Post-prandial pain + weight loss (‘fear of food’) = chronic presentation
