The first symptom of compartment syndrome is pain. Loss of function and decreased pulses or pulselessness, however, are late signs. According to Shears, paresthesia in the distribution of the nerves transversing the affected compartment has also been described as relatively early sign of compartment syndrome, and later is followed by anesthesia (Shears, 2006).

- Pain is often reported early and almost universally. The description is usually of deep, constant, and poorly localized pain out of proportion with the findings on physical examination (often incorrectly described as pain out of proportion to the injury). The pain is aggravated by passively stretching the muscle group within the compartment or actively flexing it (though this finding is not specific to compartment syndrome alone) and is not relieved by analgesia up to and including morphine.

- Paresthesia (altered sensation e.g., "pins & needles") in the cutaneous nerves of the affected compartment is another typical sign.

- Paralysis of the limb is usually a late finding. The compartment may also feel very tense and firm (pressure). Some find that their feet and even legs fall asleep. This is because compartment syndrome prevents adequate blood flow to the rest of the leg.

- A lack of pulse rarely occurs in patients, as pressures that cause compartment syndrome are often well below arterial pressures and pulse is only affected if the relevant artery is contained within the affected compartment.

- Tense and swollen shiny skin, sometimes with obvious bruising of the skin.

- Congestion of the digits with prolonged capillary refill time.

The symptoms of chronic exertional compartment syndrome (CECS) are brought on by exercise and consist of a sensation of extreme tightness in the affected muscles followed by a painful burning sensation if exercise is continued. After exercise is ceased, the pressure in the compartment will decrease within a few minutes, relieving painful symptoms. Symptoms will occur at a certain threshold of exercise which varies from person to person but is rather consistent for a given individual and can range anywhere from 30 seconds of running to about 10–15 minutes of running. CECS most commonly occurs in the lower leg, with the anterior compartment being the most frequently affected compartment. Foot drop is a common symptom of CECS.

CCS is characterized by disproportionately greater motor impairment in upper compared to lower extremities, and variable degree of sensory loss below the level of injury in combination with bladder dysfunction and urinary retention. This syndrome differs from that of a complete lesion, which is characterized by total loss of all sensation and movement below the level of the injury.

In older patients, CCS most often occurs after acute hyperextension injury in an individual with long-standing cervical spondylosis. A slow, chronic cause in this age group is when the cord gets caught and squeezed between a posterior intervertebral disc herniation against the anterior cord and/or with posterior pressure on the cord from hypertrophy of the ligamentum flavum (Lhermitte's sign may be the experience that causes the patient to seek medical diagnosis). However, CCS is not exclusive to older patients as younger individuals can also sustain an injury leading to CCS. Typically, younger patients are more likely to get CCS as a result of a high-force trauma or a bony instability in the cervical spine. Historically, spinal cord damage was believed to originate from concussion or contusion of the cord with stasis of axoplasmic flow, causing edematous injury rather than destructive hematomyelia. More recently, autopsy studies have demonstrated that CCS may be caused by bleeding into the central part of the cord, portending less favorable prognosis. Studies also have shown from postmortem evaluation that CCS probably is associated with selective axonal disruption in the lateral columns at the level of the injury to the spinal cord with relative preservation of the grey matter.

Ebstein's anomaly is a congenital heart defect in which the septal and posterior leaflets of the tricuspid valve are displaced towards the apex of the right ventricle of the heart. Its classified as a Critical congenital heart defect accounting for <1% of all congenital heart defects presenting in ≈1 per 200,000 live births.

An enlargement of the aorta may occur; an increased risk of abnormality is seen in babies of women taking lithium during the first trimester of pregnancy (though some have questioned this) and in those with Wolff-Parkinson-White syndrome.

The classic signs and symptoms of measles include four-day fevers (the 4 D's) and the three C's—cough, coryza (head cold, fever, sneezing), and conjunctivitis (red eyes)—along with fever and rashes. Fever is common and typically lasts for about one week; the fever seen with measles is often as high as . Koplik's spots seen inside the mouth are pathognomonic (diagnostic) for measles, but are temporary and therefore rarely seen. Recognizing these spots before a person reaches their maximum infectiousness can help physicians reduce the spread of the disease.

The characteristic measles rash is classically described as a generalized red maculopapular rash that begins several days after the fever starts. It starts on the back of the ears and, after a few hours, spreads to the head and neck before spreading to cover most of the body, often causing itching. The measles rash appears two to four days after the initial symptoms and lasts for up to eight days. The rash is said to "stain", changing color from red to dark brown, before disappearing. Overall, the disease from infection with the measles virus usually resolves after about three weeks.

Complications with measles are relatively common, ranging from mild complications such as diarrhea to serious complications such as pneumonia (either direct viral pneumonia or secondary bacterial pneumonia), bronchitis (either direct viral bronchitis or secondary bacterial bronchitis), otitis media, acute brain inflammation (and very rarely SSPE—subacute sclerosing panencephalitis), and corneal ulceration (leading to corneal scarring). Complications are usually more severe in adults who catch the virus. The death rate in the 1920s was around 30% for measles pneumonia. People that are at high risk for complications are: Infants and children aged 20 years, pregnant women, and people with compromised immune systems, such as from leukemia and HIV infection.

Between 1987 and 2000, the case fatality rate across the United States was three measles-attributable deaths per 1000 cases, or 0.3%. In underdeveloped nations with high rates of malnutrition and poor healthcare, fatality rates have been as high as 28%. In immunocompromised persons (e.g., people with AIDS) the fatality rate is approximately 30%. Risk factors for severe measles and its complications include malnutrition, underlying immunodeficiency, pregnancy, and vitamin A deficiency. Even in previously healthy children, measles can cause serious illness requiring hospitalization. One out of every 1,000 measles cases will develop acute encephalitis, which often results in permanent brain damage. One or two out of every 1,000 children who become infected with measles will die from respiratory and neurologic complications.