Hepatic fremitus is a vibration felt over the person's liver. It is thought to be caused by a severely inflamed and necrotic liver rubbing up against the peritoneum. The name 'Monash sign' has been suggested for this clinical sign, after the Monash Medical Centre in Melbourne, Australia.

When a person speaks, the vocal cords create vibrations ("vocal fremitus") in the tracheobronchial tree and through the lungs and chest wall, where they can be felt ("tactile fremitus"). This is usually assessed with the healthcare provider placing the flat of their palms on the chest wall and then asking a patient to repeat a diphthong such as "blue balloons" or "toys for tots" (the original diphthong used was the German word Neunundneunzig but the translation to the English 'ninety nine' was not a diphthong and thus not as effective in eliciting fremitus). An increase in tactile fremitus indicates denser or inflamed lung tissue, which can be caused by diseases such as pneumonia. A decrease suggests air or fluid in the pleural spaces or a decrease in lung tissue density, which can be caused by diseases such as chronic obstructive pulmonary disease or asthma.

Once a pleural effusion is diagnosed, its cause must be determined. Pleural fluid is drawn out of the pleural space in a process called thoracentesis, and it should be done in almost all patients who have pleural fluid that is at least 10 mm in thickness on CT, ultrasonography, or lateral decubitus X-ray and that is new or of uncertain etiology. In general, the only patients who do not require thoracentesis are those who have heart failure with symmetric pleural effusions and no chest pain or fever; in these patients, diuresis can be tried, and thoracentesis is avoided unless effusions persist for more than 3 days. In a thoracentesis, a needle is inserted through the back of the chest wall in the sixth, seventh, or eighth intercostal space on the midaxillary line, into the pleural space. The use of ultrasound to guide the procedure is now standard of care as it increases accuracy and decreases complications. After removal, the fluid may then be evaluated for:

1. Chemical composition including protein, lactate dehydrogenase (LDH), albumin, amylase, pH, and glucose

2. Gram stain and culture to identify possible bacterial infections

3. White and red blood cell counts and differential white blood cell counts

4. Cytopathology to identify cancer cells, but may also identify some infective organisms

5. Other tests as suggested by the clinical situation – lipids, fungal culture, viral culture, tuberculosis cultures, lupus cell prep, specific immunoglobulins

A pleural effusion appears as an area of whiteness on a standard posteroanterior chest X-ray. Normally, the space between the visceral pleura and the parietal pleura cannot be seen. A pleural effusion infiltrates the space between these layers. Because the pleural effusion has a density similar to water, it can be seen on radiographs. Since the effusion has greater density than the rest of the lung, it gravitates towards the lower portions of the pleural cavity. The pleural effusion behaves according to basic fluid dynamics, conforming to the shape of pleural space, which is determined by the lung and chest wall. If the pleural space contains both air and fluid, then an air-fluid level that is horizontal will be present, instead of conforming to the lung space. Chest radiographs in the lateral decubitus position (with the patient lying on the side of the pleural effusion) are more sensitive and can detect as little as 50 mL of fluid. At least 300 mL of fluid must be present before upright chest X-rays can detect a pleural effusion (e.g., blunted costophrenic angles).

Chest computed tomography is more accurate for diagnosis and may be obtained to better characterize the presence, size, and characteristics of a pleural effusion. Lung ultrasound, nearly as accurate as CT and more accurate than chest X-ray, is increasingly being used at the point of care to diagnose pleural effusions, with the advantage that it is a safe, dynamic, and repeatable imaging modality. To increase diagnostic accuracy of detection of pleural effusion sonographically, markers such as boomerang and VIP signs can be utilized.

Ultrasound is commonly used in the evaluation of people who have sustained physical trauma, for example with the FAST protocol. Ultrasound may be more sensitive than chest X-rays in the identification of pneumothorax after blunt trauma to the chest. Ultrasound may also provide a rapid diagnosis in other emergency situations, and allow the quantification of the size of the pneumothorax. Several particular features on ultrasonography of the chest can be used to confirm or exclude the diagnosis.

Computed tomography (CT, or "CAT scan") is not necessary for the diagnosis of pneumothorax, but it can be useful in particular situations. In some lung diseases, especially emphysema, it is possible for abnormal lung areas such as bullae (large air-filled sacs) to have the same appearance as a pneumothorax on chest X-ray, and it may not be safe to apply any treatment before the distinction is made and before the exact location and size of the pneumothorax is determined. In trauma, where it may not be possible to perform an upright film, chest radiography may miss up to a third of pneumothoraces, while CT remains very sensitive.

A further use of CT is in the identification of underlying lung lesions. In presumed primary pneumothorax, it may help to identify blebs or cystic lesions (in anticipation of treatment, see below), and in secondary pneumothorax it can help to identify most of the causes listed above.

A pulmonary consolidation is a region of (normally compressible) lung tissue that has filled with liquid, a condition marked by induration (swelling or hardening of normally soft tissue) of a normally aerated lung. It is considered a radiologic sign. Consolidation occurs through accumulation of inflammatory cellular exudate in the alveoli and adjoining ducts. Simply, it is defined as alveolar space that contains liquid instead of gas. The liquid can be pulmonary edema, inflammatory exudate, pus, inhaled water, or blood (from bronchial tree or hemorrhage from a pulmonary artery). It must be present to diagnose pneumonia: the signs of lobar pneumonia are characteristic and clinically referred to as consolidation.

Signs that consolidation may have occurred include:

- Expansion of the thorax on inspiration is reduced on the affected side

- Vocal fremitus is increased on the side with consolidation

- Percussion is dull in affected area

- Breath sounds are bronchial

- Possible medium, late, or pan-inspiratory crackles

- Vocal resonance is increased. Here, the patient's voice (or whisper, as in whispered pectoriloquy) can be heard more clearly when there is consolidation, as opposed to in the healthy lung where speech sounds muffled.

- A pleural rub may be present.

- A lower expected Pa02 than calculated in the alveolar gas equation

Diagnosis relies on the characteristic cytopathology of the exudative pleural fluid, which contains elongated and giant multinucleated macrophages in a sea of amorphous granular material. The absence of mesothelial cells is also characteristic (Champion, 1968). While these findings are highly specific for rheumatoid pleuritis (Nosanchuk et al., 1968; Geisinger, 1985; Engel, 1986; Montes, 1988; Shinto, 1988), rheumatoid pleuritis must be considered if more than one of the above cytologic findings are detected.

Steroids are the mainstay of treatment for rheumatoid arthritis, and have been shown to improve rheumatoid pleuritis. This would seem to be an outdated view of the treatment for this disease. More modern methods form the mainstay of treatment today. (no references?)

Some CAP patients require intensive care, with clinical prediction rules such as the pneumonia severity index and CURB-65 guiding the decision to hospitalize. Factors increasing the need for hospitalization include:

- Age greater than 65

- Underlying chronic illnesses

- Respiratory rate greater than 30 per minute

- Systolic blood pressure less than 90 mmHg

- Heart rate greater than 125 per minute

- Temperature below 35 or over 40 °C

- Confusion

- Evidence of infection outside the lung

Laboratory results indicating hospitalization include:

- Arterial oxygen tension less than 60 mm Hg

- Carbon dioxide over 50 mmHg or pH under 7.35 while breathing room air

- Hematocrit under 30 percent

- Creatinine over 1.2 mg/dl or blood urea nitrogen over 20 mg/dl

- White-blood-cell count under 4 × 10^9/L or over 30 × 10^9/L

- Neutrophil count under 1 x 10^9/L

X-ray findings indicating hospitalization include:

- Involvement of more than one lobe of the lung

- Presence of a cavity

- Pleural effusion

Patients with symptoms of CAP require evaluation. Diagnosis of pneumonia is made clinically, rather than on the basis of a particular test. Evaluation begins with a physical examination by a health provider, which may reveal fever, an increased respiratory rate (tachypnea), low blood pressure (hypotension), a fast heart rate (tachycardia) and changes in the amount of oxygen in the blood. Palpating the chest as it expands and tapping the chest wall (percussion) to identify dull, non-resonant areas can identify stiffness and fluid, signs of CAP. Listening to the lungs with a stethoscope (auscultation) can also reveal signs associated with CAP. A lack of normal breath sounds or the presence of crackles can indicate fluid consolidation. Increased vibration of the chest when speaking, known as tactile fremitus, and increased volume of whispered speech during auscultation can also indicate fluid.

When signs of pneumonia are discovered during evaluation, chest X-rays, are performed to support a diagnosis of CAP, and examination of the blood and sputum for infectious microorganisms and blood tests may be used to support a diagnosis of CAP. Diagnostic tools depend on the severity of illness, local practices and concern about complications of the infection. All patients with CAP should have their blood oxygen monitored with pulse oximetry. In some cases, arterial blood gas analysis may be required to determine the amount of oxygen in the blood. A complete blood count (CBC) may reveal extra white blood cells, indicating infection.

Chest X-rays and X-ray computed tomography (CT) can reveal areas of opacity (seen as white), indicating consolidation. CAP does not always appear on x-rays, because the disease is in its initial stages or involves a part of the lung an x-ray does not see well. In some cases, chest CT can reveal pneumonia not seen on x-rays. However, congestive heart failure or other types of lung damage can mimic CAP on x-rays.

Several tests can identify the cause of CAP. Blood cultures can isolate bacteria or fungi in the bloodstream. Sputum Gram staining and culture can also reveal the causative microorganism. In severe cases, bronchoscopy can collect fluid for culture. Special tests can be performed if an uncommon microorganism is suspected, such as urinalysis for Legionella antigen in Legionnaires' disease.

The ICSD-R also described three different types of sleep bruxism according to the duration the condition is present, namely acute, which lasts for less than one week; subacute, which lasts for more than a week and less than one month; and chronic which lasts for over a month.

Early diagnosis of bruxism is advantageous, due to the possible damage that may be incurred and the detrimental effect on quality of life. A diagnosis of bruxism is usually made clinically, and is mainly based on the person's history (e.g. reports of grinding noises) and the presence of typical signs and symptoms, including tooth mobility, tooth wear, masseteric hypertrophy, indentations on the tongue, hypersensitive teeth (which may be misdiagnosed as reversible pulpitis), pain in the muscles of mastication, and clicking or locking of the temporomandibular joints. Questionnaires can be used to screen for bruxism in both the clinical and research settings.

For tooth grinders who live in same household with other people, diagnosis of grinding is straightforward: Housemates or family members would advise a bruxer of recurrent grinding. Grinders who live alone can likewise resort to a sound-activated tape recorder. To confirm the condition of clenching, on the other hand, bruxers may rely on such devices as the Bruxchecker, Bruxcore, or a beeswax-bearing biteplate.

The Individual (personal) Tooth-Wear Index was developed to objectively quantify the degree of tooth wear in an individual, without being affected by the number of missing teeth. Bruxism is not the only cause of tooth wear. Another possible cause of tooth wear is acid erosion, which may occur in people who drink a lot of acidic liquids such as concentrated fruit juice, or in people who frequently vomit or regurgitate stomach acid, which itself can occur for various reasons. People also demonstrate a normal level of tooth wear, associated with normal function. The presence of tooth wear only indicates that it had occurred at some point in the past, and does not necessarily indicate that the loss of tooth substance is ongoing. People who clench and perform minimal grinding will also not show much tooth wear. Occlusal splints are usually employed as a treatment for bruxism, but they can also be of diagnostic use, e.g. to observe the presence or absence of wear on the splint after a certain period of wearing it at night.

The most usual trigger in sleep bruxism that leads a person to seek medical or dental advice is being informed by sleeping partner of unpleasant grinding noises during sleep. The diagnosis of sleep bruxism is usually straightforward, and involves the exclusion of dental diseases, temporomandibular disorders, and the rhythmic jaw movements that occur with seizure disorders (e.g. epilepsy). This usually involves a dental examination, and possibly electroencephalography if a seizure disorder is suspected. Polysomnography shows increased masseter and temporalis muscular activity during sleep. Polysomnography may involve electroencephalography, electromyography, electrocardiography, air flow monitoring and audio–video recording. It may be useful to help exclude other sleep disorders; however, due to the expense of the use of a sleep lab, polysomnography is mostly of relevance to research rather than routine clinical diagnosis of bruxism.

Tooth wear may be brought to the person's attention during routine dental examination. With awake bruxism, most people will often initially deny clenching and grinding because they are unaware of the habit. Often, the person may re-attend soon after the first visit and report that they have now become aware of such a habit.

Several devices have been developed that aim to objectively measure bruxism activity, either in terms of muscular activity or bite forces. They have been criticized for introducing a possible change in the bruxing habit, whether increasing or decreasing it, and are therefore poorly representative to the native bruxing activity. These are mostly of relevance to research, and are rarely used in the routine clinical diagnosis of bruxism. Examples include the "Bruxcore Bruxism-Monitoring Device" (BBMD, "Bruxcore Plate"), the "intra-splint force detector" (ISFD), and electromyographic devices to measure masseter or temporalis muscle activity (e.g. the "BiteStrip", and the "Grindcare").

In dentistry, occlusal trauma is the damage to teeth when they are not properly aligned when the jaw is closed.

When the jaws close, for instance during chewing or at rest, the relationship between the opposing teeth is referred to as occlusion. When trauma, disease or dental treatment alters occlusion by changing the biting surface of any of the teeth, the teeth will come together differently, and their occlusion will change. When that change has a negative effect on how the teeth occlude, this may cause tenderness, pain, and damage to or movement of the teeth. This is called traumatic occlusion.

Traumatic occlusion may cause a thickening of the cervical margin of the alveolar bone and widening of the periodontal ligament, although the latter is not pathognomonic for this condition.

Teeth are constantly subject to both horizontal and vertical occlusal forces. With the center of rotation of the tooth acting as a fulcrum, the surface of bone adjacent to the pressured side of the tooth will undergo resorption and disappear, while the surface of bone adjacent to the tensioned side of the tooth will undergo apposition and increase in volume.

In both primary and secondary occlusal trauma, tooth mobility might develop over time, with it occurring earlier and being more prevalent in secondary occlusal trauma. To treat mobility due to primary occlusal trauma, the cause of the trauma must be eliminated. Likewise for teeth subject to secondary occlusal trauma, though these teeth may also require splinting together to the adjacent teeth so as to eliminate their mobility.

In primary occlusal trauma, the cause of the mobility was the excessive force being applied to a tooth with a normal attachment apparatus, otherwise known as a "periodontally-uninvolved tooth". The approach should be to eliminate the cause of the pain and mobility by determining the causes and removing them; the mobile tooth or teeth will soon cease exhibiting mobility. This could involve removing a high spot on a recently restored tooth, or even a high spot on a non-recently restored tooth that perhaps moved into hyperocclusion. It could also involve altering one's parafunctional habits, such as refraining from chewing on pens or biting one's fingernails. For a bruxer, treatment of the patient's primary occlusal trauma could involve selective grinding of certain interarch tooth contacts or perhaps employing a nightguard to protect the teeth from the greater than normal occlusal forces of the patient's parafunctional habit. For someone who is missing enough teeth in non-strategic positions so that the remaining teeth are forced to endure a greater "per square inch" occlusal force, treatment might include restoration with either a removable prosthesis or implant-supported crown or bridge.

In secondary occlusal trauma, simply removing the "high spots" or selective grinding of the teeth will not eliminate the problem, because the teeth are already periodontally involved. After splinting the teeth to eliminate the mobility, the cause of the mobility (in other words, the loss of clinical attachment and bone) must be managed; this is achieved through surgical periodontal procedures such as soft tissue and bone grafts, as well as restoration of edentulous areas. As with primary occlusal trauma, treatment may include either a removable prosthesis or implant-supported crown or bridge.