Common types of emboli: An embolus is either a dislodged thrombus, air, cholesterol or fat droplets, amniotic fluid components etc. that lodge in a blood vessel and block it.
| Type of embolization | Characteristic features |
| Air embolism | Seen in central venous catheterization; cardiac bypass; childbirth; trauma; head and neck surgery; acute cardiac failure; hypoxia, hypercapnia; right ventricular strain; dyspnea, chest pain, headache, confusion, arrhythmias, collapse |
| Amniotic fluid embolism | Amniotic fluid, fetal cells or hair embolize to pulmonary vessels; occur in labour, C sections; amnio-infusions etc; vasoactive and procoagulant products including platelet-activating factor, cytokines, bradykinin, thromboxane, leukotrienes, and arachidonic acid in amniotic fluid lead to anaphylactoid reaction; DIC; acute dyspnea, tachypnea, circulatory collapse, cardiac arrest. |
| Fat embolism | Fat embolizes to capillaries blocking microcirculation most commonly of the lungs, brain, skin, eyes, heart; seen in long bone fractures, pancreatitis, liposuction, bone marrow transplant; elevated free fatty acids cause systemic inflammation, fat globules released from bone marrow cause mechanical obstruction; respiratory distress, altered mental status, DIC, fever, petechial rash, ARDS; prevented by early operative fixation of long bone fracture |
| Cholesterol embolism or atheroembolism | Cholesterol embolizes from an atherosclerotic plaque from a large proximal artery to smaller distal arteries; symptoms from ischemia due to occlusion and inflammatory response; may be spontaneous or follow cardiac catheterization, surgery in or around the aorta; typically multiple small embolizations occur over time; blue toes, fever, malaise, fatigue, weight loss, livedo reticularis, end organ damage like renal failure, amaurosis fugax, hypereosinophilia, Hollenhorst plaques on ophthalmoscopy are seen. |
Hypertension:
Hypertension is sustained elevation of systolic and/or diastolic blood pressure. It is classified as follows:
Classification: Normal Blood Pressure
Classification: Elevated Blood Pressure
Classification: Stage 1 HT
Classification: Stage 2 HT
There is an increased risk of developing HT in individuals with blood pressure readings at the high end of normal range, obese or overweight individuals, African Americans and in older age group. Blood pressure can be erroneously high due to stress, emotion, pain, physical activity, reading errors, improper technique of measurement, caffeine or nicotine. “White coat hypertension” is high blood pressure only seen in a medical setting or in the presence of medical staff. If a non-hypertensive person has high BP readings in an office visit, then the BP should be measured outside of the medical office by ambulatory BP monitoring (more accurate) or by home blood pressure monitors. If the BP is very high, or there are signs of end-organ damage or there are underlying conditions known to cause HT such as chronic renal disease, then home and ambulatory monitoring is not essential and diagnosis and treatment of HT can be begun early. Screening is done every 3-5 years for the age group 18-39 years and every year for the above 40 years age group (in the absence of signs and symptoms or conditions predisposing to HT; screen more frequently if these risks present).
HT may be primary or secondary. Primary or essential HT is the most common type. It is idiopathic. Increased stroke volume, blood volume and cardiac output correlates with rise in systolic blood pressure, while decreased elasticity of arteries, increased vascular tone and increased total peripheral resistance correlates with increase in diastolic blood pressure. Changes in the function of sarcolemmal membrane ion channels on vascular smooth muscle may cause increased vascular tone. Dysfunction of Na+K+ATPase pump, with increased permeability to Na+ and increased intracellular Na+ and Ca++ can increase vascular tone. An increase in cardiac output and/or total peripheral resistance affect the blood pressure. Hypokalemia can lead to HT by causing vasoconstriction. Deficiency of vasodilators like nitric oxide due to endothelial dysfunction cause increased BP. Genetic predisposition is seen. Secondary HT can result from primary hyperaldosteronism (Conn’s syndrome), Cushing’s syndrome, renovascular HT, obstructive sleep apnea, chronic renal disease like chronic glomerulonephritis, polycystic kidney disease, pheochromocytoma, thyroid dysfunction, acromegaly, coarctation of the aorta etc. Drugs that can cause HT are corticosteroids, excess alcohol, OCPs, cocaine, licorice etc.
Renovascular hypertension: Renovascular hypertension is hypertension caused by occlusive lesions in the renal arteries, also called renal artery stenosis. As a result of reduced blood supply, there is activation of the renin-angiotensin-aldosterone system leading to HT. Typically more than 70-75% luminal narrowing of the renal artery should occur before renovascular HT sets in. Most common causes are atherosclerosis of the renal arteries (about 75% cases), fibromuscular dysplasia, compression by tumors, trauma, aortic dissection, emboli etc. HT appearing in children or young adults, or the recent onset of HT in previously normotensive older individuals above age 55 years should raise the suspicion of renal HT.
Fibromuscular dysplasia of the renal arteries is typically seen in young females, sometimes during pregnancy. Smoking is a risk factor.
Presentation is with resistant HT. Plasma renin activity is increased, increased renin in the renal vein of the affected kidney, compensatory decrease in renal vein renin of unaffected kidney, renal bruits are heard. “Beaded” appearance of renal artery is seen on angiography, in cases of fibromuscular dysplasia. ACE inhibitors are contraindicated in bilateral renal artery stenosis.
Complications of HT: Long standing, uncontrolled HT can cause LVH, heart failure, chronic renal disease, peripheral artery disease, stroke, IHD, retinopathy, aneurysms and vascular dementia.
HT emergency and urgency: Hypertensive crisis or accelerated HT or malignant HT, is defined as an acute and critical increase of blood pressure > 180/110 mmHg. These terms have now been replaced by HT emergency and urgency depending on the presence or absence of acute end-organ damage respectively. Presence of acute hypertensive target organ damage, such as stroke, myocardial infarction or heart failure in a hypertensive crisis defines a “hypertensive emergency”. In these patients, immediate lowering of blood pressure (about 25 % within one to two hours) in an intensive care setting is mandatory to prevent further progression of target organ damage. In contrast to hypertensive emergencies, hypertensive urgencies are characterized by an acute and critical increase in blood pressure without signs or symptoms of acute hypertensive target organ damage. In these patients, blood pressure should be lowered within 24 to 48 hours in order to avoid hypertensive target organ damage. End-organ damage can be heart failure, AMI, HT encephalopathy, aortic dissection, ICH, SAH, acute renal failure, unstable angina etc.
Antidepressants, when taken along with MAOIs can precipitate a HT crisis. Because MAOIs inhibit the breakdown of tyramine, patients taking them should avoid tyramine-containing foods and herbal supplements like St. John’s wort, ginseng, and yohimbine.
** Hypertensive retinopathy:** HT causes endothelial damage of retinal blood vessels, sclerosis and vasoconstriction leading to retinopathy. It is aggravated by DM and smoking. Flame shaped hemorrhages are due to rupture of blood vessels or micro-aneurysms. Cotton wool spots or soft exudates are small, gray-white foci of retinal ischemia. Hard exudates have clear margins and result from protein leak from blood vessels. Yellow exudates are from intraretinal lipid deposits from leaking retinal vessels. Copper wiring and silver wiring are from sclerosis of blood vessels, changes being more pronounced in the latter. Similar changes cause AV or arterio-venous nicking.
| Grade | Changes seen |
| Grade 1 | Arteriolar constriction only, AV nicking |
| Grade 2 | Constriction and sclerosis of arterioles, more severe AV nicking, copper wiring |
| Grade 3 | Hemorrhages and exudates seen, soft and hard exudates, silver wiring |
| Grade 4 | Papilledema, plus grade 3 findings |
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