The amount of fresh frozen plasma required to reverse disseminated intravascular coagulation associated with purpura fulminans may lead to complications of fluid overload and death, especially in neonates, such as transfusion-related acute lung injury. Exposure to multiple plasma donors over time increases the cumulative risk for transfusion-associated viral infection and allergic reaction to donor proteins found in fresh frozen plasma.

Allergic reactions and alloantibody formation are also potential complications, as with any protein replacement therapy.

Concomitant warfarin therapy in subjects with congenital protein C deficiency is associated with an increased risk of warfarin skin necrosis.

Treatment focuses on monitoring and should be accomplished with inpatient floor service for individuals responsive to commands or neurological ICU observation for those with impaired levels of consciousness. Extra attention should be placed on intracranial pressure (ICP) monitoring via an intraventricular catheter and medications to maintain ICP, blood pressure, and coagulation. In more severe cases an external ventricular drain may be required to maintain ICP and evacuate the hemorrhage, and in extreme cases an open craniotomy may be required. In cases of unilateral IVH with small intraparenchymal hemorrhage the combined method of stereotaxy and open craniotomy has produced promising results.

Diagnosis is based on the symptoms the patient is experiencing and the appearance of the tissues of the mouth following chemotherapy, bone marrow transplants or radiotherapy. Red burn-like sores or ulcers throughout the mouth is enough to diagnose mucositis.

The severity of oral mucositis can be evaluated using several different assessment tools.

Two of the most commonly used are the World Health Organization (WHO) Oral Toxicity score and the National Cancer Institute Common Toxicity Criteria (NCI-CTC) for Oral Mucositis. While the NCI system has separate scores for appearance (erythema and ulceration) and function (pain and ability to eat solids, liquids, or nothing by mouth), the WHO score combines both elements into a single score that grades the severity of the condition from 0 (no oral mucositis) to 4 (swallowing not possible such that patient needs supplementary nutrition). Another scale developed in 1999, the Oral Mucositis Assessment Scale (OMAS) has been shown to be highly reproducible between observers, responsive over time, and accurate in recording symptoms associated with mucositis. The OMAS provides an objective assessment of oral mucositis based on assessment of the appearance and extent of redness and ulceration in various areas of the mouth.

Purpura fulminans lesions, once established, often progress within 24 to 48 hours to full-thickness skin necrosis or soft-tissue necrosis. Once purpura fulminans lesions progress to full-thickness skin necrosis, healing takes between 4–8 weeks and leaves large scars.

Without treatment, necrotic soft tissue may become gangrenous, leading to loss of limbs. Purpura fulminans is often accompanied by micro-vascular thrombosis and haemorrhagic infarction in other tissues, such as the lungs, kidneys, central nervous system and adrenal glands, leading to multiple organ failure, and causes initial high mortality and long-term morbidity in survivors.Purpura fulminans may also lead to severe large vessel venous thrombosis if untreated in its early stages.

Purpura fulminans secondary to severe infection is self-limiting. In cases of homozygous protein C deficiency, episodes of purpura fulminans and other thrombotic events are recurrent. Moreover, infant survival due to maintenance replacement therapy is often associated with mental retardation and/or visual impairment. For post-infection purpura fulminans, new lesions will occur while neutralising autoantibodies are present (1–2 weeks after presentation).

A multi-disciplinary care team is usually required for rehabilitation after purpura fulminans.

IVH in the preterm brain usually arises from the germinal matrix whereas IVH in the term infants originates from the choroid plexus. However, it is particularly common in premature infants or those of very low birth weight. The cause of IVH in premature infants, unlike that in older infants, children or adults, is rarely due to trauma. Instead it is thought to result from changes in perfusion of the delicate cellular structures that are present in the growing brain, augmented by the immaturity of the cerebral circulatory system, which is especially vulnerable to hypoxic ischemic encephalopathy. The lack of blood flow results in cell death and subsequent breakdown of the blood vessel walls, leading to bleeding. While this bleeding can result in further injury, it is itself a marker for injury that has already occurred. Most intraventricular hemorrhages occur in the first 72 hours after birth. The risk is increased with use of extracorporeal membrane oxygenation in preterm infants. Congenital cytomegalovirus infection can be an important cause.

The amount of bleeding varies. IVH is often described in four grades:

- Grade I - bleeding occurs just in the germinal matrix

- Grade II - bleeding also occurs inside the ventricles, but they are not enlarged

- Grade III - ventricles are enlarged by the accumulated blood

- Grade IV - bleeding extends into the brain tissue around the ventricles

Grades I and II are most common, and often there are no further complications. Grades III and IV are the most serious and may result in long-term brain injury to the infant. After a grade III or IV IVH, blood clots may form which can block the flow of cerebrospinal fluid, leading to increased fluid in the brain (hydrocephalus).

There have been various therapies employed into preventing the high rates of morbidity and mortality, including diuretic therapy, repeated lumbar puncture, streptokinase therapy and most recently combination a novel intervention called DRIFT (drainage, irrigation and fibrinolytic therapy).

In 2002, a Dutch retrospective study analysed cases where neonatologists had intervened and drained CSF by lumbar or ventricular punctures if ventricular width (as shown on ultrasound) exceeded the 97th centile as opposed to the 97th centile plus 4 mm. Professors Whitelaw's original Cochrane review published in 2001 as well as evidence from previous randomised control trials indicated that interventions should be based on clinical signs and symptoms of ventricular dilatation. An international trial has instead looked an early (97th centile) versus late (97th centile plus 4 mm) for intervening and draining CSF.

DRIFT has been tested in an international randomised clinical trial; although it did not significantly lower the need for shunt surgery, severe cognitive disability at two years Bayley (MDI <55) was significantly reduced. Repeated lumbar punctures are used widely to reduce the effects in increased intracranial pressure and an alternative to ventriculoperitoneal (VP) shunt surgery that cannot be performed in case of intraventricular haemorrhage. The relative risk of repeated lumbar puncture is close to 1.0, therefore it is not statistically therapeutic when compared to conservative management and does raise the risk of subsequent CSF infection.

A pregnant woman with a history of haemophilia in her family can test for the haemophilia gene. Such tests include:

- chorionic villus sampling (CVS) – a small sample of the placenta is removed from the womb and tested for the haemophilia gene, usually during weeks 11-14 of pregnancy

- amniocentesis – a sample of amniotic fluid is taken for testing, usually during weeks 15-20 of pregnancy

There's a small risk of these procedures causing problems such as miscarriage or premature labour, so the woman may discuss this with the doctor in charge of her care.

Genetic testing and counselling are available to help determine the risk of passing the condition onto a child. This may involve testing a sample of tissue or blood to look for signs of the genetic mutation that causes haemophilia.

The diagnosis of hemophilia A may be suspected as coagulation testing reveals an increased PTT in the context of a normal PT and bleeding time. PTT tests are the first blood test done when haemophilia is indicated. However, the diagnosis is made in the presence of very low levels of Factor VIII. A family history is frequently present, although not essential. Recently, genetic testing has been made available to determine an individual's risk of attaining or passing on hemophilia. Diagnosis of haemophilia A also includes a severity level which can range from mild to severe based on the amount of active and functioning factor VIII detected in the blood. Factor VIII levels do not typically change throughout an individual's life. Severe haemophilia A is the most common form occurring in the majority of affected people. Individuals with mild haemophilia often experience few or no bleeding episodes except in the case of serious trauma (i.e. tooth extraction, or surgery).

Diagnosis of mouth ulcers usually consists of a medical history followed by an oral examination as well as examination of any other involved area. The following details may be pertinent: The duration that the lesion has been present, the location, the number of ulcers, the size, the color and whether it is hard to touch, bleeds or has a rolled edge. As a general rule, a mouth ulcer that does not heal within 2 or 3 weeks should be examined by a health care professional who is able to rule out oral cancer (e.g. a dentist, oral physician, oral surgeon, or maxillofacial surgeon). If there have been previous ulcers which have healed, then this again makes cancer unlikely.

An ulcer that keeps forming on the same site and then healing may be caused by a nearby sharp surface, and ulcers that heal and then recur at different sites are likely to be RAS. Malignant ulcers are likely to be single in number, and conversely, multiple ulcers are very unlikely to be oral cancer. The size of the ulcers may be helpful in distinguishing the types of RAS, as can the location (minor RAS mainly occurs on non-keratinizing mucosa, major RAS occurs anywhere in the mouth or oropharynx). Induration, contact bleeding and rolled margins are features of a malignant ulcer. There may be nearby causative factor, e.g. a broken tooth with a sharp edge that is traumatizing the tissues. Otherwise, the person may be asked about problems elsewhere, e.g. ulceration of the genital mucous membranes, eye lesions or digestive problems, swollen glands in neck (lymphadenopathy) or a general unwell feeling.

The diagnosis comes mostly from the history and examination, but the following special investigations may be involved: blood tests (vitamin deficiency, anemia, leukemia, Epstein-Barr virus, HIV infection, diabetes) microbiological swabs (infection), or urinalysis (diabetes). A biopsy (minor procedure to cut out a small sample of the ulcer to look at under a microscope) with or without immunofluorescence may be required, to rule out cancer, but also if a systemic disease is suspected. Ulcers caused by local trauma are painful to touch and sore. They usually have an irregular border with erythematous margins and the base is yellow. As healing progresses, a keratotic (thickened, white mucosa) halo may occur.

Diagnosis is mostly based on the clinical appearance and the medical history. The most important diagnostic feature is a history of recurrent, self healing ulcers at fairly regular intervals. Although there are many causes of oral ulceration, "recurrent" oral ulceration has relatively few causes, most commonly aphthous stomatitis, but rarely Behçet's disease, erythema multiforme, ulceration associated with gastrointestinal disease, and recurrent intra-oral herpes simplex infection. A systemic cause is more likely in adults who suddenly develop recurrent oral ulceration with no prior history.

Special investigations may be indicated to rule out other causes of oral ulceration. These include blood tests to exclude anemia, deficiencies of iron, folate or vitamin B12 or celiac disease. However, the nutritional deficiencies may be latent and the peripheral blood picture may appear relatively normal. Some suggest that screening for celiac disease should form part of the routine work up for individuals complaining of recurrent oral ulceration. Many of the systemic diseases cause other symptoms apart from oral ulceration, which is in contrast to aphthous stomatitis where there is isolated oral ulceration. Patch testing may be indicated if allergies are suspected (e.g. a strong relationship between certain foods and episodes of ulceration). Several drugs can cause oral ulceration (e.g. nicorandil), and a trial substitution to an alternative drug may highlight a causal relationship.

Tissue biopsy is not usually required, unless to rule out other suspected conditions such as oral squamous cell carcinoma. The histopathologic appearance is not pathognomonic (the microscopic appearance is not specific to the condition). Early lesions have a central zone of ulceration covered by a fibrinous membrane. In the connective tissue deep to the ulcer there is increased vascularity and a mixed inflammatory infiltrate composed of lymphocytes, histiocytes and polymorphonuclear leukocytes. The epithelium on the margins of the ulcer shows spongiosis and there are many mononuclear cells in the basal third. There are also lymphocytes and histiocytes in the connective tissue surrounding deeper blood vessels near to the ulcer, described histologically as "perivascular cuffing".

Two of the most common differential diagnoses are haemophilia B which is a deficiency in Factor IX and von Willebrand Disease which is a deficiency in von Willebrand factor (needed for the proper functioning of Factor VIII), haemophilia C is also a possible, differential diagnosis.

Treatment is directed at the prevention of haemorrhagic shock. Standard dose prednisolone does not increase the platelet count. High-dose methylprednisolone therapy in children with Onyalai has been shown to improve platelet count and reduce the requirement for transfusions. Vincristine sulphate may be of benefit to some patients. Splenectomy is indicated in patients with severe uncontrollable haemorrhage. High-dose intravenous gammaglobulin may help in increasing the platelet count and cessation of haemorrhage.

A 2015 Cochrane systematic review assessing the prevention of chemotherapy-induced oral mucositis concluded that oral cryotherapy leads to large reductions in the incidence of oral mucositis of all severities in adults receiving 5-FU treatment for solid cancers. The evidence also indicates a reduction of oral mucositis in adults receiving high-dose melphalan-based cancer treatment prior to haematopoietic stem cell transplantation, although there is uncertainty regarding the size of the reduction in this instance. No evidence was found for use of this preventive measure in children. Oral cryotherapy involves the placement of rounded ice chips in the mouth, which cools the oral tissues and causes vasoconstriction. This decreases blood flow to the region and, hence, also restricts the amounts of the chemotherapy drugs delivered to the tissues.

The Kleihauer–Betke test is a blood test used to measure the amount of foetal hemoglobin transferred from a foetus to its mother's bloodstream. It takes advantage of the differential resistance of foetal hemoglobin to acid. A standard blood smear is prepared from the mother's blood, and exposed to an acid bath. This removes adult hemoglobin, but not foetal hemoglobin, from the red blood cells. Subsequent staining, using Shepard's method, makes fetal cells (containing foetal hemoglobin) appear rose-pink in color, while adult red blood cells are only seen as "ghosts". 2000 cells are counted under the microscope and a percentage of foetal to maternal cells is calculated.

Foetal-maternal haemorrhage can also be diagnosed by flow cytometry, using anti-foetal hemoglobin antibodies (anti-HbF).

Inadequate nutrition or the consumption of tainted food are suspected. Both IgG and IgM autoantibodies to platelet and to glycoprotein IIb/IIIa is found in majority of patients.

Both sex are equally affected

Any age group can develop a parapheryngeal abscess but it is most commonly seen in children and adolescents. Adults who are immunocompromised are also at high risk.

Treatment is cause-related, but also symptomatic if the underlying cause is unknown or not correctable. It is also important to note that most ulcers will heal completely without any intervention. Treatment can range from simply smoothing or removing a local cause of trauma, to addressing underlying factors such as dry mouth or substituting a problem medication. Maintaining good oral hygiene and use of an antiseptic mouthwash or spray (e.g. chlorhexidine) can prevent secondary infection and therefore hasten healing. A topical analgesic (e.g. benzydamine mouthwash) may reduce pain. Topical (gels, creams or inhalers) or systemic steroids may be used to reduce inflammation. An antifungal drug may be used to prevent oral candidiasis developing in those who use prolonged steroids. People with mouth ulcers may prefer to avoid hot or spicy foods, which can increase the pain. Self-inflicted ulceration can be difficult to manage, and psychiatric input may be required in some people.

The severity of oral candidiasis is subject to great variability from one person to another and in the same person from one occasion to the next. The prognosis of such infection is usually excellent after the application of topical or systemic treatments. However, oral candidiasis can be recurrent. Individuals continue to be at risk of the condition if underlying factors such as reduced salivary flow rate or immunosuppression are not rectifiable.

Candidiasis can be a marker for underlying disease, so the overall prognosis may also be dependent upon this. For example, a transient erythematous candidiasis that developed after antiobiotic therapy usually resolves after antibiotics are stopped (but not always immediately), and therefore carries an excellent prognosis—but candidiasis may occasionally be a herald of a more sinister undiagnosed pathology, such as HIV/AIDS or leukemia.

It is possible for candidiasis to spread to/from the mouth, from sites such as the pharynx, esophagus, lungs, liver, anogenital region, skin or the nails. The spread of oral candidiasis to other sites usually occurs in debilitated individuals. It is also possible that candidiasis is spread by sexual contact. Rarely, a superficial candidal infection such as oral candidiasis can cause invasive candidiasis, and even prove fatal. The observation that Candida species are normally harmless commensals on the one hand, but are also occasionally capable of causing fatal invasive candidiases has led to the description "Dr Jekyll and Mr Hyde".

The role of thrush in the hospital and ventilated patients is not entirely clear however there is a theoretical risk of positive interaction of candida with topical bacteria that could increase the risk for Ventilator Associated Pneumonia and other diseases.

The diagnosis can typically be made from the clinical appearance alone, but not always. As candidiasis can be variable in appearance, and present with white, red or combined white and red lesions, the differential diagnosis can be extensive. In pseudomembraneous candidiasis, the membranous slough can be wiped away to reveal an erythematous surface underneath. This is helpful in distinguishing pseudomembraneous candidiasis from other white lesions in the mouth that cannot be wiped away, such as lichen planus, oral hairy leukoplakia. Erythematous candidiasis can mimic geographic tongue. Erythematous candidiasis usually has a diffuse border that helps distinguish it from erythroplakia, which normally has a sharply defined border.

Special investigations to detect the presence of candida species include oral swabs, oral rinse or oral smears. Smears are collected by gentle scraping of the lesion with a spatula or tongue blade and the resulting debris directly applied to a glass slide. Oral swabs are taken if culture is required. Some recommend that swabs be taken from 3 different oral sites. Oral rinse involves rinsing the mouth with phosphate-buffered saline for 1 minute and then spitting the solution into a vessel that examined in a pathology laboratory. Oral rinse technique can distinguish between commensal candidal carriage and candidiasis. If candidal leukoplakia is suspected, a biopsy may be indicated. Smears and biopsies are usually stained with periodic acid-Schiff, which stains carbohydrates in fungal cell walls in magenta. Gram staining is also used as Candida stains are strongly Gram positive.

Sometimes an underlying medical condition is sought, and this may include blood tests for full blood count and hematinics.

If a biopsy is taken, the histopathologic appearance can be variable depending upon the clinical type of candidiasis. Pseudomembranous candidiasis shows hyperplastic epithelium with a superficial parakeratotic desquamating (i.e., separating) layer. Hyphae penetrate to the depth of the stratum spinosum, and appear as weakly basophilic structures. Polymorphonuclear cells also infiltrate the epithelium, and chronic inflammatory cells infiltrate the lamina propria.

Atrophic candidiasis appears as thin, atrophic epithelium, which is non-keratinized. Hyphae are sparse, and inflammatory cell infiltration of the epithelium and the lamina propria. In essence, atrophic candidiasis appears like pseudomembranous candidiasis without the superficial desquamating layer.

Hyperplastic candidiasis is variable. Usually there is hyperplastic and acanthotic epithelium with parakeratosis. There is an inflammatory cell infiltrate and hyphae are visible. Unlike other forms of candidiasis, hyperplastic candidiasis may show dysplasia.

Oral and maxillofacial pathology, previously termed oral pathology, is a speciality involved with the diagnosis and study of the causes and effects of diseases affecting the oral and maxillofacial regions (i.e. the mouth, the jaws and the face). It can be considered a speciality of dentistry and pathology. Oral pathology is a closely allied speciality with oral and maxillofacial surgery and oral medicine.

The clinical evaluation and diagnosis of oral mucosal diseases are in the scope of oral & maxillofacial pathology specialists and oral medicine practitioners, both disciplines of dentistry.

When a microscopic evaluation is needed, a biopsy is taken, and microscopically observed by a pathologist. The American Dental Association uses the term oral and maxillofacial pathology, and describes it as "the specialty of dentistry and pathology which deals with the nature, identification, and management of diseases affecting the oral and maxillofacial regions. It is a science that investigates the causes, processes and effects of these diseases."

In some parts of the world, oral and maxillofacial pathologists take on responsibilities in forensic odontology.

By definition, there is no serious underlying medical condition, and most importantly, the ulcers do not represent oral cancer nor are they infectious. However, aphthae are capable of causing significant discomfort. There is a spectrum of severity, with symptoms ranging from a minor nuisance to disabling. Due to pain during eating, weight loss may develop as a result of not eating in severe cases of aphthous stomatitis. Usually, the condition lasts for several years before spontaneously disappearing in later life.

If ongoing and rapid haemorrhage is occurring then immediate delivery of the foetus may be indicated if the fetus is sufficiently developed. If the haemorrhage has already occurred and now stopped, an inutero transfusion of red cells to the foetus may be recommended.

Cerebral vasospasm is the prolonged, intense vasoconstriction of the larger conducting arteries in the subarachnoid space which is initially surrounded by a clot.

Significant narrowing develops gradually over the first few days after the aneurysmal rupture. This spasm usually is maximal in about a week's time following haemorrhage.

Vasospasm is the one of the leading causes of death after the aneurysmal rupture along with the effect of the initial haemorrhage and later bleeding.

The diagnosis for hemophilia B can be done via the following tests/methods:

- Coagulation screening test

- Bleeding scores

- Coagulation factor assays

Parapharyngeal abscess is a deep neck abscess. It is also known as abscess of pharyngomaxillary or lateral pharyngeal space. Parapharyngeal abscess involve the parapharyngeal space.

Parapharyngeal space is lateral to the superior pharyngeal constrictor and medial to the masseter muscle, this space is divided by styloid process into anterior and posterior compartment. This space contains the carotid artery, internal jugular vein, numerous nerves.