Case Protocol 38 Flashcards
You are an “on call” surgical resident asked to see a 73 y/o man who died in his sleep 12hrs after undergoing surgery to bypass an occluded right popliteal artery. You have not seen him previously. His wife, who is very keen for you to sign the death certificate, tells you that he was known to have suffered from I/T claudication in the right leg for the previous six months, with recent onset of nocturnal pain in the right calf. He had received treatment for systemic hypertension for the past 18 years, and had a history of angina for the past 2 years.
Is a coronial autopsy necessary in this case, and if so, why? What legal obligations must be satisfied before performing an autopsy under these circumstances?
The coroner must be notified and an autopsy may be performed as the patient died within 24 hrs of an anaesthetic.
What is the likely pathological basis of his I/T calf pain, and what may have occurred to precipitate the nocturnal calf pain present in the days before his death?
Peripheral arterial disease
Stenosis or occlusion in the vessels supplying the lower limbs - 70-80% occlusion
Most commonly due to occlusive atherosclerotic lesions in the arterial vessels of the legs.
Lesions tend to occur at arterial branch points (site of turbulence, shear stress and intimal injury). Can be caused by thrombosis, embolism, vasculitis, entrapment.
Progressive occlusion causes vascular insufficiency. Early on this manifests only on exertion (intermittent claudication), progressing to insufficiency at rest (critical limb ischaemia) and ultimately causing gangrene.
Intermittent claudication - pain starts after walking a certain distance, and subsides quickly after stopping. Pain is typically severe, cramping pain, most commonly in the calf and may extend into the thigh and buttocks with continued walking. Pain never felt at rest, at rest blood is sufficient to meet the metabolic demands of the tissues.
Critical limb ischaemia (chronic severe limb ischaemia) - decrease in limb perfusion that causes a potential threat to limb viability (manifested by ischaemic rest pain, ischaemic ulcers and/or gangrene) that is >2 weeks. Due to severe arterial luminal narrowing. Likely progressed to rest pain due to plaque complication –> thrombus formation –> increased stenosis. Occurs at night. During the day, gravity assists blood flow to the lower limbs. This is eliminated when the patient is in the supine position (likely at night). Also, decreased cardiac output at night.
Describe the abnormalities you would expect to find at autopsy in the blood vessels of the abdomen and legs.
Macroscopic: atherosclerosis of the abdominal aorta, femoral and popliteal arteries - yellow/grey raised plaques. Usually involve partial circumference of arterial wall. Patchy and variable along vessel length - may have superimposed thrombus, associated with aneurysm dilation, common at branch points). Hypertrophy of vascular SM (secondary to HTN).
Microscopic: atherosclerosis - intimal thickening (necrotic lipid core; fibrous cap; neovascularisation at periphery - vasa vasorum - these thing vesseled walls are prone to disruption –> haemorrhage in the plaque; chronic inflammation [CD4+ T cells, macrophages at shoulder]; granulation tissue and calcification at base), medial thinning and atrophy, luminal narrowing
How might the finding of atherosclerosis involving the origin of the right renal artery explain the development of hypertension at the age of 55?
Atherosclerosis of the right renal artery would decrease kidney function.
Decreased perfusion of the kidney results in activation of the RAS that causes increased systemic vascular resistance and sodium retention.
Renal artery atherosclerosis –> luminal narrowing –> decreased renal perfsuion –> JG apparatus secretes renin –> activation of RAS –> angiotensin II production:
Arteriolar vasoconstriction –> increased BP
Tubular Na reabsorption and H20 retention –> increased vascular volume –> increased BP
Aldosterone secretion from adrenals –> Na/H20 absorption
Sympathetic activity
ADH secretion from the posterior pituitary –> H20 absorption in collecting duct –> increased vascular volume –> increased BP
Clinically: age of onset of HTN (55 years suggests atherosclerotic RAS), sudden or unexplained recurrent pulmonary oedema, HTN (accelerated, malignant, resistant), kidney dysfunction or AKI.
Hypertension will result in atherosclerosis in the kidney unaffected by the RAS while the kidney with the RAS will be spared from the systemic effect of HTN (due to decreased perfusion).
Primary HTN: essential hypertension
Secondary HTN: primary renal disease, drug induced, pheochromocytoma, primary aldosteronism, Cushing’s, other endocrine - hypo/hyperthyroid
What factors predispose to atherosclerotic peripheral vascular disease?
Strong: smoking (independently associated with the development of PVD), DM (increases risk by 2-4x), hyperchromocysteinaemia (30-40% of patients with PVD have high levels of homocysteine, increases progression risk), hyperlipidaemia, age >40, hx of CAD/CVD, low levels of exercise
Weak: HTN, elevated CRP, vasculitis/inflammatory conditions, arterial fibrodysplasia, trauma
Which organs are likely to undergo pathological changes as a result of long-standing hypertension, and what is the nature of the changes in each of those organs?
Heart - systemic HTN –> increased afterload –> LVH (concentric), systloic and diastolic dysfunction –> HF, increased myocardial mass –> increased oxygen demand –> ischaemia/infarction
Kidneys - neprhosclerosis - hyaline arteriosclerosis –> arteriolar narrowing –> impaired blood supply –> loss of nephrons –> symmetric contraction of kidneys
Eyes - hypertensive retinopathy:
Mild - retinal arteriolar narrowing due to vasospasm, arteriolar wall thickening, nipping
Moderate - haemorrhages, cotton wool spots, hard exudates, microaneurysms
Severe - optic disc oedema
Brain - aneurysms (Charcot Bouchard aneurysm) and wall defects - lipohyalinosis, increased risk of CVS (both ischaemic and haemorrhagic), vascular dementia
What do you consider to be the most likely causes of death in this case?
MI Arrhythmia - secondary to MI or LVH CVS (haemorrhagic) PE (unlikely as it is too early post-op) Adverse reaction to anaesthetic
What factors may have increased the risk of myocardial infarction in the peri-operative period?
Hypertension is a common occurrence in the operative and post-operative period.
Others: blood loss, decreased oral fluid intake, vasodilatory action of anaesthetic agents, decreased venous return caused by mechanical ventilation, narcotic analgesics
Hypotension is of particular concern in patients with LVH as decreased BP –> decreased perfusion of myocardium –> increased risk of ischaemia and infarction.
Post-operative hypoxia (secondary to narcotics and pulmonary atelectasis) will decrease myocardial oxygen supply.
