The PESI and sPESI scoring tools can estimate mortality of patients. The Geneva prediction rules and Wells criteria are used to calculate a pre-test probability of patients to predict who has a pulmonary embolism. These scores are tools to be used with clinical judgment in deciding diagnostic testing and types of therapy. The PESI algorithm comprises 11 routinely available clinical variables. It puts the subjects into one of five classes (I-V), with 30-day mortality ranging from 1.1% to 24.5%. Those in classes I and II are low-risk and those in classes III-V are high-risk.

The most commonly used method to predict clinical probability, the Wells score, is a clinical prediction rule, whose use is complicated by multiple versions being available. In 1995, Philip Steven Wells, initially developed a prediction rule (based on a literature search) to predict the likelihood of PE, based on clinical criteria. The prediction rule was revised in 1998 This prediction rule was further revised when simplified during a validation by Wells "et al." in 2000. In the 2000 publication, Wells proposed two different scoring systems using cutoffs of 2 or 4 with the same prediction rule. In 2001, Wells published results using the more conservative cutoff of 2 to create three categories. An additional version, the "modified extended version", using the more recent cutoff of 2 but including findings from Wells's initial studies were proposed. Most recently, a further study reverted to Wells's earlier use of a cutoff of 4 points to create only two categories.

There are additional prediction rules for PE, such as the Geneva rule. More importantly, the use of "any" rule is associated with reduction in recurrent thromboembolism.

"The Wells score":

- clinically suspected DVT — 3.0 points

- alternative diagnosis is less likely than PE — 3.0 points

- tachycardia (heart rate > 100) — 1.5 points

- immobilization (≥ 3d)/surgery in previous four weeks — 1.5 points

- history of DVT or PE — 1.5 points

- hemoptysis — 1.0 points

- malignancy (with treatment within six months) or palliative — 1.0 points

Traditional interpretation

- Score >6.0 — High (probability 59% based on pooled data)

- Score 2.0 to 6.0 — Moderate (probability 29% based on pooled data)

- Score <2.0 — Low (probability 15% based on pooled data)

Alternative interpretation

- Score > 4 — PE likely. Consider diagnostic imaging.

- Score 4 or less — PE unlikely. Consider D-dimer to rule out PE.

Recommendations for a diagnostic algorithm were published by the PIOPED investigators; however, these recommendations do not reflect research using 64 slice MDCT. These investigators recommended:

- Low clinical probability. If negative D-dimer, PE is excluded. If positive D-dimer, obtain MDCT and based treatment on results.

- Moderate clinical probability. If negative D-dimer, PE is excluded. "However", the authors were not concerned that a negative MDCT with negative D-dimer in this setting has a 5% probability of being false. Presumably, the 5% error rate will fall as 64 slice MDCT is more commonly used. If positive D-dimer, obtain MDCT and based treatment on results.

- High clinical probability. Proceed to MDCT. If positive, treat, if negative, more tests are needed to exclude PE. A D-dimer of less than 750 ug/L does not rule out PE in those who are at high risk.

As a general rule, any diver who has breathed gas under pressure at any depth who surfaces unconscious, loses consciousness soon after surfacing, or displays neurological symptoms within about 10 minutes of surfacing should be assumed to be suffering from arterial gas embolism.

Symptoms of arterial gas embolism may be present but masked by environmental effects such as hypothermia, or pain from other obvious causes. Neurological examination is recommended when there is suspicion of lung overexpansion injury. Symptoms of decompression sickness may be very similar to, and confused with, symptoms of arterial gas embolism, however, treatment is basically the same. Discrimination between gas embolism and decompression sickness may be difficult for injured divers, and both may occur simultaneously. Dive history may eliminate decompression sickness in many cases, and the presence of symptoms of other lung overexpansion injury would raise the probability of gas embolism.

In addition to evaluating the symptoms above, the health care provider may find decreased or no blood pressure in the arm or leg.

Tests to determine any underlying cause for thrombosis or embolism and to confirm presence of the obstruction may include:

- Doppler ultrasound, especially duplex ultrasonography. It may also involve transcranial doppler exam of arteries to the brain

- Echocardiography, sometimes involving more specialized techniques such as Transesophageal echocardiography (TEE) or myocardial contrast echocardiography (MCE) to diagnose myocardial infarction

- Arteriography of the affected extremity or organ Digital subtraction angiography is useful in individuals where administration of radiopaque contrast material must be kept to a minimum.

- Magnetic resonance imaging (MRI)

- Blood tests for measuring elevated enzymes in the blood, including cardiac-specific troponin T and/or troponin I, myoglobins, and creatine kinase isoenzymes. These indicate embolisation to the heart that has caused myocardial infarction. Myoglobins and creatine kinase are also elevated in the blood in embolisation in other locations.

- Blood cultures may be done to identify the organism responsible for any causative infection

- Electrocardiography (ECG) for detecting myocardial infarction

- Angioscopy using a flexible fiberoptic catheter inserted directly into an artery.

If a patent foramen ovale (PFO) is suspected, an examination by echocardiography may be performed to diagnose the defect. In this test, very fine bubbles are introduced into a patient's vein by agitating saline in a syringe to produce the bubbles, then injecting them into an arm vein. A few seconds later, these bubbles may be clearly seen in the ultrasound image, as they travel through the patient's right atrium and ventricle. At this time, bubbles may be observed directly crossing a septal defect, or else a patent foramen ovale may be opened temporarily by asking the patient to perform the Valsalva maneuver while the bubbles are crossing through the right heart – an action which will open the foramen flap and show bubbles passing into the left heart. Such bubbles are too small to cause harm in the test, but such a diagnosis may alert the patient to possible problems which may occur from larger bubbles, formed during activities like underwater diving, where bubbles may grow during decompression. A PFO test may be recommended for divers intending to expose themselves to relatively high decompression stress in deep technical diving.

Prevention of atherosclerosis, which is a major risk factor of arterial embolism, can be performed e.g. by dieting, physical exercise and smoking cessation.

In case of high risk for developing thromboembolism, antithrombotic medication such as warfarin or coumadin may be taken prophylactically. Antiplatelet drugs may also be needed.

Early diagnosis still remains a challenge in CTEPH, with a median time of 14 months between symptom onset and diagnosis in expert centres. A suspicion of PH is often raised by echocardiography, but an invasive right heart catheterisation is required to confirm it. Once PH is diagnosed, the presence of thromboembolic disease requires imaging. The recommended diagnostic algorithm stresses the importance of initial investigation using an echocardiogram and V/Q scan and confirmation with right heart catheter and pulmonary angiography (PA).

Both V/Q scanning and modern multidetector CT angiography (CTPA) may be accurate methods for the detection of CTEPH, with excellent diagnostic efficacy in expert hands (sensitivity, specificity, and accuracy of 100%, 93.7%, and 96.5% for V/Q and 96.1%, 95.2%, and 95.6% for CTPA). However, CTPA alone cannot exclude the disease, but may help identify pulmonary artery distension resulting in left main coronary artery compression, pulmonary parenchymal lesions (e.g. as complications from previous pulmonary infarctions), and bleeding from bronchial collateral arteries. Today, the gold standard imaging remains invasive pulmonary angiography (PAG) using native angiograms or a digital subtraction technique.

Historically the prognosis for patients with untreated CTEPH was poor, with a 5-year survival of 40 mmHg at presentation. More contemporary data from the European CTEPH registry have demonstrated a 70% 3-year survival in patients with CTEPH who do not undergo the surgical procedure of pulmonary endarterectomy (PEA). Recent data from an international CTEPH registry demonstrate that mortality in CTEPH is associated with New York Heart Association (NYHA) functional class IV, increased right atrial pressure, and a history of cancer. Furthermore, comorbidities such as coronary disease, left heart failure, and chronic obstructive pulmonary disease (COPD) are risk factors for mortality.

Inferior vena cava filters (IVCFs) are not recommended in those who are on anticoagulants. IVCFs may be used in clinical situations where a person has a high risk of experiencing a pulmonary embolism, but cannot be on anticoagulants due to a high risk of bleeding, or they have active bleeding. Retrievable IVCFs are recommended if IVCFs must be used, and a plan should be created to remove the filter when it is no longer needed.

The use of heparin following surgery is common if there are no issues with bleeding. Generally, a risk-benefit analysis is required, as all anticoagulants lead to an increased risk of bleeding. In people admitted to hospital, thrombosis is a major cause for complications and occasionally death. In the UK, for instance, the Parliamentary Health Select Committee heard in 2005 that the annual rate of death due to thrombosis was 25,000, with at least 50% of these being hospital-acquired. Hence "thromboprophylaxis" (prevention of thrombosis) is increasingly emphasized. In patients admitted for surgery, graded compression stockings are widely used, and in severe illness, prolonged immobility and in all orthopedic surgery, professional guidelines recommend low molecular weight heparin (LMWH) administration, mechanical calf compression or (if all else is contraindicated and the patient has recently suffered deep vein thrombosis) the insertion of a vena cava filter. In patients with medical rather than surgical illness, LMWH too is known to prevent thrombosis, and in the United Kingdom the Chief Medical Officer has issued guidance to the effect that preventative measures should be used in medical patients, in anticipation of formal guidelines.

Evidence supports the use of heparin in people following surgery who have a high risk of thrombosis to reduce the risk of DVTs; however, the effect on PEs or overall mortality is not known. In hospitalized non-surgical patients, mortality decreased but not statistically significant. It does not appear however to decrease the rate of symptomatic DVTs. Using both heparin and compression stockings appears better than either one alone in reducing the rate of DVT.

In hospitalized people who have had a stroke and not had surgery, mechanical measures (compression stockings) resulted in skin damage and no clinical improvement. Data on the effectiveness of compression stockings among hospitalized non-surgical patients without stroke is scarce.

The American College of Physicians (ACP) gave three strong recommendations with moderate quality evidence on VTE prevention in non-surgical patients: that hospitalized patients be assessed for their risk of thromboembolism and bleeding before prophylaxis (prevention); that heparin or a related drug is used if potential benefits are thought to outweigh potential harms; and that graduated compression stockings not be used. As an ACP policy implication, the guideline stated a lack of support for any performance measures that incentivize physicians to apply universal prophylaxis without regard to the risks. Goldhaber recommends that people should be assessed at their hospital discharge for persistent high-risk of venous thrombosis, and that people who adopt a heart-healthy lifestyle might lower their risk of venous thrombosis.

In those with cancer who are still walking about yet receiving chemotherapy, LMWH decreases the risk of VTE. Due to potential concerns of bleeding its routine use is not recommended. For people who are having surgery for cancer, it is recommended that they receive anticoagulation therapy (preferably LMWH) in order to prevent a VTE. LMWH is recommended for at least 7–10 days following cancer surgery, and for one month following surgery for people who have a high risk of VTEs.

In adults who have had their lower leg casted or placed in a brace for more than a week, LMWH decreased the risk of VTEs. LMWH is recommended for adults not in hospital with an above-knee cast and a below-knee cast, and is safe for this indication.

Following the completion of warfarin in those with prior VTE, long term aspirin is beneficial.

The diagnosis of an individual suspected of having "fat embolism syndrome" can be done via the following tests and methods:

The treatment for thrombosis depends on whether it is in a vein or an artery, the impact on the person, and the risk of complications from treatment.

Professional divers are screened for risk factors during initial and periodical medical examination for fitness to dive. In most cases recreational divers are not medically screened, but are required to provide a medical statement before acceptance for training in which the most common and easy to identify risk factors must be declared. If these factors are declared, the diver may be required to be examined by a medical practitioner, and may be disqualified from diving if the conditions indicate.

Asthma, Marfan syndrome, and COPD pose a very high risk of pneumothorax. In some countries these may be considered absolute contraindications, while in others the severity may be taken into consideration. Asthmatics with a mild and well controlled condition may be permitted to dive under restricted circumstances.

A significant part of entry level diver training is focused on understanding the risks and procedural avoidance of barotrauma. Professional divers and recreational divers with rescue training are trained in the basic skills of recognizing and first aid management of diving barotrauma.

Prevention consists of walking, drinking fluids and if currently hospitalized, changing of IV lines. Walking is especially suggested after a long period seated, particularly when one travels.

Arterial embolism can cause occlusion in any part of the body. It is a major cause of infarction, tissue death due to the blockage of blood supply.

An embolus lodging in the brain from either the heart or a carotid artery will most likely be the cause of a stroke due to ischemia.

An arterial embolus might originate in the heart (from a thrombus in the left atrium, following atrial fibrillation or be a septic embolus resulting from endocarditis). Emboli of cardiac origin are frequently encountered in clinical practice. Thrombus formation within the atrium occurs mainly in patients with mitral valve disease, and especially in those with mitral valve stenosis (narrowing), with atrial fibrillation (AF). In the absence of AF, pure mitral regurgitation has a low incidence of thromboembolism.

The risk of emboli forming in AF depends on other risk factors such as age, hypertension, diabetes, recent heart failure, or previous stroke.

Thrombus formation can also take place within the ventricles, and it occurs in approximately 30% of anterior-wall myocardial infarctions, compared with only 5% of inferior ones. Some other risk factors are poor ejection fraction (<35%), size of infarct, and the presence of AF. In the first three months after infarction, left-ventricle aneurysms have a 10% risk of emboli forming.

Patients with prosthetic valves also carry a significant increase in risk of thromboembolism. Risk varies, based on the valve type (bioprosthetic or mechanical); the position (mitral or aortic); and the presence of other factors such as AF, left-ventricular dysfunction, and previous emboli.

Emboli often have more serious consequences when they occur in the so-called "end circulation": areas of the body that have no redundant blood supply, such as the brain and heart.

Passage of a clot (thrombus) from a systemic vein to a systemic artery. When clots in systemic veins break off (embolize), they travel first to the right side of the heart and, normally, then to the lungs where they lodge, causing pulmonary embolism. On the other hand, when there is a hole at the septum, either upper chambers of the heart (an atrial septal defect) or lower chambers of the heart (ventricular septal defects), a clot can cross from the right to the left side of the heart, then pass into the systemic arteries as a paradoxical embolism. Once in the arterial circulation, a clot can travel to the brain, block a vessel there, and cause a stroke (cerebrovascular accident).

Embolism can be classified as to where it enters the circulation either in arteries or in veins. Arterial embolism are those that follow and, if not dissolved on the way, lodge in a more distal part of the systemic circulation. Sometimes, multiple classifications apply; for instance a pulmonary embolism is classified as an arterial embolism as well, in the sense that the clot follows the pulmonary artery carrying deoxygenated blood away from the heart. However, pulmonary embolism is generally classified as a form of venous embolism, because the embolus forms in veins, e.g. deep vein thrombosis.

The diagnosis for thrombophlebitis is primarily based on the appearance of the affected area. Frequent checks of the pulse, blood pressure, and temperature may be required. If the cause is not readily identifiable, tests may be performed to determine the cause, including the following:

- Doppler ultrasound

- Extremity arteriography

- Blood coagulation studies (Blood clotting tests)

Treatment for this condition entails the maintenance of intravascular volume. Additionally, the following can be done as a means of managing FES in an individual:

- Albumin can be used for volume resuscitation

- Long bone fractures should be attended to immediately (surgery)

- Mechanical ventilation

As with other chest injuries such as pulmonary contusion, hemothorax, and pneumothorax, pulmonary laceration can often be treated with just supplemental oxygen, ventilation, and drainage of fluids from the chest cavity. A thoracostomy tube can be used to remove blood and air from the chest cavity. About 5% of cases require surgery, called thoracotomy. Thoracotomy is especially likely to be needed if a lung fails to re-expand; if pneumothorax, bleeding, or coughing up blood persist; or in order to remove clotted blood from a hemothorax. Surgical treatment includes suturing, stapling, oversewing, and wedging out of the laceration. Occasionally, surgeons must perform a lobectomy, in which a lobe of the lung is removed, or a pneumonectomy, in which an entire lung is removed.

The microscopic examination of tissue (histology) gives the definitive diagnosis. The diagnostic histopathologic finding is intravascular cholesterol crystals, which are seen as cholesterol clefts in routinely processed tissue (embedded in paraffin wax). The cholesterol crystals may be associated with macrophages, including giant cells, and eosinophils.

The sensitivity of small core biopsies is modest, due to sampling error, as the process is often patchy. Affected organs show the characteristic histologic changes in 50-75% of the clinically diagnosed cases. Non-specific tissue findings suggestive of a cholesterol embolization include ischemic changes, necrosis and unstable-appearing complex atherosclerotic plaques (that are cholesterol-laden and have a thin fibrous cap). While biopsy findings may not be diagnostic, they have significant value, as they help exclude alternate diagnoses, e.g. vasculitis, that often cannot be made confidently based on clinical criteria.

A paradoxical embolism, also called a crossed embolism, refers to an embolus which is carried from the venous side of circulation to the arterial side, or vice versa. It is a kind of stroke or other form of arterial thrombosis caused by embolism of a thrombus (blood clot), air, tumor, fat, or amniotic fluid of venous origin, which travels to the arterial side through a lateral opening in the heart, such as a patent foramen ovale, or arteriovenous shunts in the lungs.

The opening is typically an atrial septal defect, but can also be a ventricular septal defect.

Paradoxical embolisms represent two percent of arterial emboli.

Pulmonary laceration may not be visible using chest X-ray because an associated pulmonary contusion or hemorrhage may mask it. As the lung contusion clears (usually within two to four days), lacerations begin to become visible on chest X-ray. CT scanning is more sensitive and better at detecting pulmonary laceration than X-rays are, and often reveals multiple lacerations in cases where chest X-ray showed only a contusion. Before CT scanning was widely available, pulmonary laceration was considered unusual because it was not common to find with X-ray alone. On a CT scan, pulmonary lacerations show up in a contused area of the lung, typically appearing as cavities filled with air or fluid that usually have a round or ovoid shape due to the lung's elasticity.

Hematomas appear on chest radiographs as smooth masses that are round or ovoid in shape. Like lacerations, hematomas may initially be hidden on X-ray by lung contusions, but they become more apparent as the contusion begins to heal. Pneumatoceles have a similar shape to that of hematomas but have thin, smooth walls. Lacerations may be filled completely with blood, completely with air, or partially with both. Lacerations filled with both blood and air display a distinctive air-fluid level. A single laceration may occur by itself, or many may be present, creating an appearance like Swiss cheese in the radiography of the lung.

Pulmonary laceration is usually accompanied by hemoptysis (coughing up blood or of blood-stained sputum).

Thoracoscopy may be used in both diagnosis and treatment of pulmonary laceration.

A healing laceration may resemble a pulmonary nodule on radiographs, but unlike pulmonary nodules, lacerations decrease in size over time on radiographs.