Treatment for light bruises is minimal and may include RICE (rest, ice, compression, elevation), painkillers (particularly NSAIDs) and, later in recovery, light stretching exercises. Particularly, immediate application of ice while elevating the area may reduce or completely prevent swelling by restricting blood flow to the area and preventing internal bleeding. Rest and preventing re-injury is essential for rapid recovery. Applying a medicated cream containing mucopolysaccharide polysulfuric acid (e.g., Hirudoid) may also speed the healing process. Other topical creams containing skin-fortifying ingredients, including but not limited to retinol or alpha hydroxy acids, such as DerMend, can improve the appearance of bruising faster than if left to heal on its own.

Very gently massaging the area and applying heat may encourage blood flow and relieve pain according to the gate control theory of pain, although causing additional pain may indicate the massage is exacerbating the injury. As for most injuries, these techniques should not be applied until at least three days following the initial damage to ensure all internal bleeding has stopped, because although increasing blood flow will allow more healing factors into the area and encourage drainage, if the injury is still bleeding this will allow more blood to seep out of the wound and cause the bruise to become worse.

In most cases hematomas spontaneously revert, but in cases of large hematomas or those localized in certain organs ("e.g.", the brain), the physician may optionally perform a puncture of the hematoma to allow the blood to exit.

Hematomas can be subdivided by size. By definition, ecchymoses are 1 centimeter in size or larger, and are therefore larger than petechiae ( less than 2 millimeters in diameter) or purpura (2 millimeters to 1 centimeter in diameter). Ecchymoses also have a more diffuse border than other purpura.

There are many causes of subcutaneous hematomas including ecchymoses. Coagulopathies such as Hemophilia A may cause ecchymosis formation in children. The medication betamethasone can have the adverse effect of causing echhymosis.

Bruises can be scored on a scale from 0-5 to categorize the severity and danger of the injury.

The harm score is determined by the extent and severity of the fractures to the organs and tissues causing the bruising, in turn depending on multiple factors. For example, a contracted muscle will bruise more severely, as will tissues crushed against underlying bone. Capillaries vary in strength, stiffness and toughness, which can also vary by age and medical conditions.

An alternate bruise severity ranking system called the Chien Intensity Scale is slowly growing in popularity in some research circles. Although not widely used, the Chien Intensity Scale is used by institutes including the Ryan Mackey Memorial Research Institute and the Sydney Medical Center.

Low levels of damaging forces produce small bruises and generally cause the individual to feel minor pain straight away. Repeated impacts worsen bruises, increasing the harm level. Normally, light bruises heal nearly completely within two weeks, although duration is affected by variation in severity and individual healing processes; generally, more severe or deeper bruises take somewhat longer.

Severe bruising (harm score 2-3) may be dangerous or cause serious complications. Further bleeding and excess fluid may accumulate causing a hard, fluctuating lump or swelling hematoma. This has the potential to cause compartment syndrome as the swelling cuts off blood flow to the tissues. The trauma that induced the bruise may also have caused other severe and potentially fatal harm to internal organs. For example, impacts to the head can cause traumatic brain injury: bleeding, bruising and massive swelling of the brain with the potential to cause concussion, coma and death. Treatment for brain bruising may involve emergency surgery to relieve the pressure on the brain.

Damage that causes bruising can also cause bones to be broken, tendons or muscles to be strained, ligaments to be sprained, or other tissue to be damaged. The symptoms and signs of these injuries may initially appear to be those of simple bruising. Abdominal bruising or severe injuries that cause difficulty in moving a limb or the feeling of liquid under the skin may indicate life-threatening injury and require the attention of a physician.

Petechiae on the face and conjunctiva (eyes) can be a sign of a death by asphyxiation, particularly when involving reduced venous return from the head (such as in strangulation). Petechiae are thought to result from an increase of pressure in the veins of the head and hypoxic damage to endothelia of blood vessels.

Petechiae can be used by police investigators in determining if strangulation has been part of an attack. The documentation of the presence of petechiae on a victim can help police investigators prove the case. Petechiae resulting from strangulation can be relatively tiny and light in color to very bright and pronounced. Petechiae may be seen on the face, in the whites of the eyes or on the inside of the eyelids.

A petechia, plural petechiae, is a small (1–2 mm) red or purple spot on the skin, caused by a minor bleed from broken capillary blood vessels.

"Petechia" refers to one of the three descriptive types of bleeding into the skin differentiated by size, the other two being purpura and ecchymosis. Petechiae are by definition less than 3 mm.

The term is almost always used in the plural, since a single lesion is seldom noticed or significant.

Some hematomas are visible under the surface of the skin (commonly called bruises) or possibly felt as masses/lumps. Lumps may be caused by the limitation of the blood to a sac, subcutaneous or intramuscular tissue space isolated by fascial planes. This is a key anatomical feature that helps prevent injuries from causing massive blood loss. In most cases the hematoma such as a sac of blood eventually dissolves; however, in some cases they may continue to grow such as due to blood seepage or show no change. If the sac of blood does not disappear, then it may need to be surgically cleaned out/repaired.

The slow process of reabsorption of hematomas can allow the broken down blood cells and hemoglobin pigment to move in the connective tissue. For example, a patient who injures the base of his thumb might cause a hematoma, which will slowly move all through the finger within a week. Gravity is the main determinant of this process.

Hematomas on articulations can reduce mobility of a member and present roughly the same symptoms as a fracture.

In most cases, movement and exercise of the affected muscle is the best way to introduce the collection back into the blood stream.

A mis-diagnosis of a hematoma in the vertebra can sometimes occur; this is correctly called a hemangioma (buildup of cells) or a benign tumor.

A hematoma (US spelling) or haematoma (UK spelling) is a localized collection of blood outside the blood vessels, due to either disease or trauma including injury or surgery and may involve blood continuing to seep from broken capillaries. A hematoma is initially in liquid form spread among the tissues including in sacs between tissues where it may coagulate and solidify before blood is reabsorbed into blood vessels. An ecchymosis is a hematoma of the skin larger than 10mm.

They may occur among/within many areas such as skin and other organs, connective tissues, bone, joints and muscle.

A collection of blood (or even a hemorrhage) may be aggravated by anticoagulant medication (blood thinner). Blood seepage and collection of blood may occur if heparin is given via an intramuscular route; to avoid this, heparin must be given intravenously or subcutaneously.

It is not to be confused with hemangioma, which is an abnormal buildup/growth of blood vessels in the skin or internal organs.

When there is post-operative swelling after breast surgery or core needle biopsy, a breast ultrasound examination may be indicated in order to differentiate between a hematoma and other possible post-surgical complications such as abscess or seroma, A recent hematoma is usually visible in a mammogram. and it also shows typical signal intensities on MR imaging. If a differentiation from breast cancer is necessary, a hematoma biopsy may be indicated.

A careful consideration of the case history is important for the diagnosis of a breast hematoma.

Small breast hematomas that cause no discomfort often require merely clinical observation, with ultrasound being used to monitor the resolution of the hematoma.

Large breast hematomas, or those that are not becoming smaller or that are causing discomfort, usually require drainage. Also hematomas that occur after surgery for excision of a malignant tumor are drained, because a hematoma to which irradiation is applied is unlikely to ever resolve. A recent hematoma can be drained by means of needle aspiration or (rarely) open surgical drainage.

A diagnosis of TTP is based on the clinical symptoms with the concomitant presence of thrombocytopenia (platelet count below 100×10/L) and microangiopathic hemolytic anemia with schistocytes on the blood smear, a negative direct antiglobulin test (coombs test), elevated levels of hemolysis markers (such as total bilirubin, LDH, free hemoglobin and an unmeasurable haptoglobin), after exclusion of any other apparent cause.

USS can present similar to the following diseases which have to be excluded: fulminant infections, disseminated intravascular coagulation, autoimmune hemolytic anemia, Evans syndrome, the typical and atypical form of hemolytic uremic syndrome (HUS), HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome, pre-eclampsia, heparin-induced thrombocytopenia (HIT), cancer that is often accompanied with metastasis, kidney injury, antiphospholipid antibody syndrome and side effects from hematopoietic stem cell transplantation.

Of note is that pregnancy associated affections like pre-eclampsia, eclampsia and HELLP syndrome can overlap in their presentation as pregnancy can trigger TTP episodes.

Patients with fulminant infections, disseminated intravascular coagulation, HELLP syndrome, pancreatitis, liver disease and other active inflammatory conditions may have reduced ADAMTS13 activity but almost never a relevant severe ADAMTS13 deficiency <10% of the normal.

A severe ADAMTS13 deficiency below 5% or <10% of the normal (depending on the definitions) is highly specific for the diagnosis of TTP. ADAMTS13 activity assays are based on the direct or indirect measurement of VWF-cleavage products. Its activity should be measured in blood samples taken before therapy has started, to prevent false high ADAMTS13 activity. If a severe ADAMTS13 deficiency is present an ADAMTS13 inhibitor assay is needed to distinguish between the acquired, autoantibody-mediated and the congenital form of TTP (USS). The presence of antibodies can be tested by ELISA or functional inhibitor assays. The level of ADAMTS13 inhibitor may be fluctuating over the course of disease and depends on free circulatory antibodies, therefore an onetime negative test result does not always exclude the presence of ADAMTS13 inhibitors and thereby an autoimmune origin of TTP. A severe ADAMTS13 deficiency in the absence of an inhibitor, confirmed on a second time point in a healthy episode of a possible USS patient, usually sets the trigger to perform a molecular analysis of the "ADAMTS13" gene to confirm a mutation. In unclear cases a plasma infusion trial can be done, showing an USS in the absence of anti-ADAMTS13-antibodies a full recovery of infused plasma-ADAMTS13 activity as well as a plasma half-life of infused ADAMTS13 activity of 2–4 days. A deficiency of ADAMTS13 activity in first-degree relatives is also a very strong indicator for an Upshaw-Schulman Syndrome.

The incidence of acute TTP in adults is around 1.7–4.5 per million and year. These cases are nearly all due to the autoimmune form of TTP, where autoantibodies inhibit ADAMTS13 activity. The prevalence of USS has not yet been determined but is assumed to constitute less than 5% of all acute TTP cases. The syndrome's inheritance is autosomal recessive, and is more often caused by compound heterozygous than homozygous mutations. The age of onset is variable and can be from neonatal age up to the 5th–6th decade. The risk of relapses differs between affected individuals. Minimization of the burden of disease can be reached by early diagnosis and initiation of prophylaxis if required.

Kaposiform hemangioendothelioma (KHE) is a rare vascular neoplasm that is locally aggressive but without metastatic potential. It occurs particularly in the skin, deep soft tissue, retroperitoneum, mediastinum, and rarely in bone. Although lesions occur solitary, they often involve large areas of the body, such as the head/neck region (40%), trunk (30%), or extremity (30%).

Usually, it is present at birth as a flat, reddish-purple, tense and edematous lesion.

Although half of lesions are congenital, 58% of KHE develop during infancy, 32% between age 1 and 10 years (32%) and 10% after 11 years of age. Moreover, adult onset has been described too with mainly males being affected. Both sexes are affected equally in children.

Lesions are often greater than 5 cm in diameter and can cause visible deformity and pain. During early childhood, KHE may enlarge and after 2 years of age, it may partially regress. Though, it usually persists longterm. In addition, 50% of patients suffer from coagulopathy due to thrombocytopenia (<25,000/mm3), presenting with petechiae and bleeding. This is called the Kasabach-Merritt Phenomenon, which is caused by trapping of platelets and other clotting factors within the tumor. Kasabach-Merritt Phenomenon is less likely in patients with lesions less than 8 cm. As two-thirds of adult-onset KHE tumors are less than 2 cm, KHE in adults is rarely associated with Kasabach-Merritt Phenomenon.

Patients with KHE and Kasabach-Merritt Phenomenon present with petechiae and ecchymosis.

Most KHE tumors are diffuse involving multiple tissue planes and important structures. Resection of KHE is thus often difficult. Treatment of kaposiform hemangioendothelioma is therefore medical. The primary drug is interferon alfa, which is successful in 50% of children. Another option is vincristine, which has lots of side-effects, but has a response rate of 90%. Drug therapy is often used in shrinking the tumor and treating the coagulopathy. However, many of these kaposiform hemangioendotheliomas do not completely regress and remain as a much smaller asymptomatic tumor. However, KHE still has a high mortality rate of 30%. Although complete surgical removal with a large margin has the best reported outcome, it is usually not done because of the risk of bleeding, extensiveness, and the anatomic site of the lesion.

Operative management may be possible for small or localized lesions. Removal of larger areas also may be indicated for symptomatic patients or for patients who have failed farmacotherapy. Resection is not required for lesions that are not causing functional problems, because KHE is benign and because resection could cause deformity.

Congenital hemangioma can be distinguished from infantile hemangioma because it is fully developed at birth. It forms during prenatal life and has reached its maximal size at birth. Congenital hemangioma can even be diagnosed in utero by prenatal ultrasound. Unlike IH, CH is more common in the extremities, has an equal sex distribution, and is solitary, with an average diameter of 5 cm. It commonly presents in the head and neck and in the lower extremities.

Congenital hemangioma are divided into 2 subgroups: the rapidly involuting congenital hemangiomas (RICHs) and the non-involuting congenital hemangiomas(NICHs).

The rapidly involuting congenital hemangioma, RICH, presents at birth as a solitary raised tumor with a central depression, scar, or ulceration surrounded by a rim of pallor. It is noted for its involution, which typically begins several weeks after birth and is completed no later than 14 months of age. After regression RICH may cause a residual deformity, such as atrophic skin and subcutaneous tissue. It mainly affects the limbs (52%), but also the head and neck region (42%) and the trunk (6%).

The non-involuting congenital hemangioma, NICH, presents as a solitary, well-circumscribed reddish-pink to purple plaque with central telangiectasia and hypopigmented rim. In contrast to RICH, NICH does not involute and rarely ulcerates. It persists into late childhood and can even mimic a vascular malformation by growing commensurately with the child. Although NICH can resemble RICH in its external appearance, it can be differentiated from RICH by a greater elevation and coarse telangiectases. It mainly affects the head and neck region (43%), but also the limbs (38%) and the trunk (19%).

Surgical resection for congenital hemangiomas is rarely needed, because RICH undergoes postnatal regression and NICH is benign and often asymptomatic. Resection may be indicated to improve the appearance of the affected area, as long as the surgical scar is less noticeable than the lesion. Other indications are problematic ulcers with persistent bleeding or chronic infection.

Although most NICH lesions are non-problematic and do not cause significant deformity, the threshold for resection of NICH is lower, because it neither involutes, nor responds to pharmacotherapy. RICH tumors are observed until involution is completed. Involuted RICH may leave behind atrophic tissue, which can be reconstructed with autologous grafts. It is often best to postpone excision until regression is complete.

There are effective pharmacologic treatments, which include intralesional corticosteroid injection, systemic corticosteroid injection, interferon α-2a or α-2b and angiogenic inhibitors. The use of corticosteroids leads to accelerated regression in 30%, stabilization of growth in 40%, lightening of color and softening of the tumor. However, 30% shows minimal or no response. Another drug treatment is interferon α-2a or α-2b. It is often used for patients who did not respond to corticosteroids. Although the response rate is much slower, it has been successful for 80% of children treated. The most serious side effect of interferon is a spastic diplegia. Other therapeutic options are embolization and pulsed-dye laser, which improves residual telangiectasias in RICH and in NICH.

The U.S. Preventive Services Task Force recommends a single screening ultrasound for abdominal aortic aneurysm in males age 65 to 75 years who have a history of smoking. There is an estimated number needed to screen of approximately 850 people. It is unclear if screening is useful in women aged 65 to 75 who have smoked and they recommend against screening in women who have never smoked.

Repeat ultrasounds should be carried out in those who have an aortic size greater than 3.0 cm. In those whose aorta is between 3.0 and 3.9 cm this should be every three years, if between 4.0 and 4.4 cm every two year, and if between 4.5 and 5.4 cm every year.

In the United Kingdom one time screening is recommended in all males over 65 years of age. Australia has no guideline on screening.

Raccoon eye/eyes (also known in the United Kingdom and Ireland as panda eyes) or periorbital ecchymosis is a sign of basal skull fracture or subgaleal hematoma, a craniotomy that ruptured the meninges, or (rarely) certain cancers. Bilateral hemorrhage occurs when damage at the time of a facial fracture tears the meninges and causes the venous sinuses to bleed into the arachnoid villi and the cranial sinuses. In layman's terms, blood from skull fracture seeps into the soft tissue around the eyes. Raccoon eyes may be accompanied by Battle's sign, an ecchymosis behind the ear. These signs may be the only sign of a skull fracture, as it may not show on an X-ray. They may not appear until up 2–3 days after the injury. It is recommended that the patient not blow their nose, cough vigorously, or strain to prevent further tearing of the meninges.

Raccoon eyes may be bilateral or unilateral. If bilateral, it is highly suggestive of basilar skull fracture, with a positive predictive value of 85%. They are most often associated with fractures of the anterior cranial fossa.

Raccoon eyes may also be a sign of disseminated neuroblastoma or of amyloidosis (multiple myeloma).

Depending on cause, raccoon eyes always require urgent consultation and management, that is surgical (facial fracture or post-craniotomy) or medical (neuroblastoma or amyloidosis).

Abdominal aortic aneurysms are commonly divided according to their size and symptomatology. An aneurysm is usually defined as an outer aortic diameter over 3 cm (normal diameter of the aorta is around 2 cm), or more than 50% of normal diameter. If the outer diameter exceeds 5.5 cm, the aneurysm is considered to be large.

A ruptured AAA is a clinical diagnosis involving the presence of the triad of abdominal pain, shock, and a pulsatile abdominal mass. If these conditions are present, indicating AAA rupture, no further clinical investigations are needed before surgery.

Predicts mortality risk in pancreatitis with fewer variables than Ranson's criteria. Data should be taken from the first 24 hours of the patient's evaluation.

- BUN >25 mg/dL (8.9 mmol/L)

- Abnormal mental status with a Glasgow coma score <15

- Evidence of SIRS (systemic inflammatory response syndrome)

- Patient age >60 years old

- Imaging study reveals pleural effusion

Patients with a score of zero had a mortality of less than one percent, whereas patients with a score of five had a mortality rate of 22 percent. In the validation cohort, the BISAP score had similar test performance characteristics for predicting mortality as the APACHE II score. As is a problem with many of the other scoring systems, the BISAP has not been validated for predicting outcomes such as length of hospital stay, need for ICU care, or need for intervention.

Regarding selection on these tests, two practice guidelines state:

Most, but not all individual studies support the superiority of the lipase. In one large study, there were no patients with pancreatitis who had an elevated amylase with a normal lipase. Another study found that the amylase could add diagnostic value to the lipase, but only if the results of the two tests were combined with a discriminant function equation.

It is not an easy task determining whether or not a bite by any species of snake is life-threatening. A bite by a North American copperhead on the ankle is usually a moderate injury to a healthy adult, but a bite to a child's abdomen or face by the same snake may be fatal. The outcome of all snakebites depends on a multitude of factors: the size, physical condition, and temperature of the snake, the age and physical condition of the person, the area and tissue bitten (e.g., foot, torso, vein or muscle), the amount of venom injected, the time it takes for the person to find treatment, and finally the quality of that treatment.

Identification of the snake is important in planning treatment in certain areas of the world, but is not always possible. Ideally the dead snake would be brought in with the person, but in areas where snake bite is more common, local knowledge may be sufficient to recognize the snake. However, in regions where polyvalent antivenoms are available, such as North America, identification of snake is not a high priority item. Attempting to catch or kill the offending snake also puts one at risk for re-envenomation or creating a second person bitten, and generally is not recommended.

The three types of venomous snakes that cause the majority of major clinical problems are vipers, kraits, and cobras. Knowledge of what species are present locally can be crucial, as is knowledge of typical signs and symptoms of envenomation by each type of snake. A scoring system can be used to try to determine the biting snake based on clinical features, but these scoring systems are extremely specific to particular geographical areas.

Although not yet formally incorporated in the generally accepted classification systems, molecular profiling of myelodysplastic syndrome genomes has increased the understanding of prognostic molecular factors for this disease. For example, in low-risk MDS, "IDH1" and "IDH2" mutations are associated with significantly worsened survival.

Non-displaced or minimally displaced fractures may be treated conservatively. Open reduction and internal fixation is reserved for cases that are severely angulated or comminuted. The purpose of fixation is to restore the normal appearance of the face. Specific attention is given to the position of the malar eminence and reduction of orbital volume by realigning the zygoma and sphenoid. Failure to correct can result in rotational deformity and increase the volume of the orbit, causing the eye to sink inwards.

Fractures with displacement require surgery consisting of fracture reduction with miniplates, microplates and screws. Gillie's approach is used for depressed zygomatic fractures. The prognosis of tripod fractures is generally good. In some cases there may be persistent post-surgical facial asymmetry, which can require further treatment.

A compound elevated skull fracture is a rare type of skull fracture where the fractured bone is elevated above the intact outer table of the skull. This type of skull fracture is always compound in nature. It can be caused during an assault with a weapon where the initial blow penetrates the skull and the underlying meninges and, on withdrawal, the weapon lifts the fractured portion of the skull outward. It can also be caused the skull rotating while being struck in a case of blunt force trauma, the skull rotating while striking an inanimate object as in a fall, or it may occur during transfer of a patient after an initial compound head injury.

A fracture in conjunction with an overlying laceration that tears the epidermis and the meninges—or runs through the paranasal sinuses and the middle ear structures, putting the outside environment in contact with the cranial cavity—is a compound fracture.

Compound fractures may either be clean or contaminated. Intracranial air (pneumocephalus) may occur in compound skull fractures.

The most serious complication of compound skull fractures is infection. Increased risk factors for infection include visible contamination, meningeal tear, loose bone fragments and presenting for treatment more than eight hours after initial injury.