<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Paraphrenia and can you explain it in depth? [/INST] Paraphrenia is a mental disorder characterized by an organized system of paranoid delusions with or without hallucinations (the positive symptoms of schizophrenia) and without deterioration of intellect or personality (its negative symptom).This disorder is also distinguished from schizophrenia by a lower hereditary occurrence, less premorbid maladjustment, and a slower rate of progression. Onset of symptoms generally occurs later in life, near the age of 60.  The prevalence of the disorder among the elderly is between 0.1% and 4%.Paraphrenia is not included in the DSM-5; psychiatrists often diagnose patients presenting with paraphrenia as having atypical psychosis, delusional disorder, psychosis not otherwise specified, schizoaffective disorders, and persistent persecutory states of older adults.  Recently, mental health professionals have also been classifying paraphrenia as very late-onset schizophrenia-like psychosis.In the Russian psychiatric manuals, paraphrenia (or paraphrenic syndrome) is the last stage of development of paranoid schizophrenia. "Systematized paraphrenia" (with systematized delusions i. e. delusions with complex logical structure) and "expansive-paranoid paraphrenia" (with expansive/grandiose delusions and persecutory delusions) are the variants of paranoid schizophrenia (F20.0). Sometimes systematized paraphrenia can be seen with delusional disorder (F22.0). The word is from Ancient Greek: παρά – beside, near + φρήν – intellect, mind.

Signs and symptoms
The main symptoms of paraphrenia are paranoid delusions and hallucinations.  The delusions often involve the individual being the subject of persecution, although they can also be erotic, hypochondriacal, or grandiose in nature.  The majority of hallucinations associated with paraphrenia are auditory, with 75% of patients reporting such an experience; however, visual, tactile, and olfactory hallucinations have also been reported.  The paranoia and hallucinations can combine in the form of “threatening or accusatory voices coming from neighbouring houses [and] are frequently reported by the patients as disturbing and undeserved".  Patients also present with a lack of symptoms commonly found in other mental disorders similar to paraphrenia.  There is no significant deterioration of intellect, personality, or habits and patients often remain clean and mostly self-sufficient.  Patients also remain oriented well in time and space.Paraphrenia is different from schizophrenia because, while both disorders result in delusions and hallucinations, individuals with schizophrenia exhibit changes and deterioration of personality whereas individuals with paraphrenia maintain a well-preserved personality and affective response.

Causes
Neurological
Paraphrenia is often associated with a physical change in the brain, such as a tumor, stroke, ventricular enlargement, or neurodegenerative process.   Research that reviewed the relationship between organic brain lesions and the development of delusions suggested that "brain lesions which lead to subcortical dysfunction could produce delusions when elaborated by an intact cortex".

Predisposing factors
Many patients who present with paraphrenia have significant auditory or visual loss, are socially isolated with a lack of social contact, do not have a permanent home, are unmarried and without children, and have maladaptive personality traits.  While these factors do not cause paraphrenia, they do make individuals more likely to develop the disorder later in life.

Diagnosis
While the diagnosis of paraphrenia is absent from recent revisions of the DSM and the ICD, many studies have recognized the condition as "a viable diagnostic entity that is distinct from schizophrenia, with organic factors playing a role in a significant portion of patients."  As such, paraphrenia is seen as being distinct from both schizophrenia and progressive dementia in old age.  Ravindran (1999) developed a list of criteria for the diagnosis of paraphrenia, which agrees with much of the research done up to the time it was published.

1.  A delusional disorder of at least six months duration characterized by the following:
a.  Preoccupation with one or more semisystematized delusions, often accompanied by auditory hallucinations.
b.  Affect notably well-preserved and appropriate.  Ability to maintain rapport with others.
c.  None of
i.  Intellectual deterioration
ii. Visual hallucinations
iii. Incoherence
iv. Flat or grossly inappropriate affect
v. Grossly disorganized behavior at times other than during the acute episode.
d.  Disturbance of behavior understandable in relation to the content of the delusions and hallucinations.
e. Only partly meets criterion A for schizophrenia.  No significant organic brain disorder.

Management
Research suggests that paraphrenics respond well to antipsychotic drug therapy if doctors can successfully achieve sufficient compliance.  Herbert found that Stelazine combined with Disipal was an effective treatment.  It promoted the discharging of patients and kept discharged patients from being readmitted later.  While behavior therapy may help patients reduce their preoccupation with delusions, psychotherapy is not currently of primary value.

Prognosis
Individuals who develop paraphrenia have a life expectancy similar to the normal population.  Recovery from the psychotic symptoms seems to be rare, and in most cases paraphrenia results in in-patient status for the remainder of the life of the patient.  Patients experience a slow deterioration of cognitive functions and the disorder can lead to dementia in some cases, but this development is no greater than the normal population.

Epidemiology
Studies suggest that the prevalence of paraphrenia in the elderly population is around 2–4%.

Sex differences
While paraphrenia can occur in both men and women, it is more common in women, even after the difference has been adjusted for life expectancies.  The ratio of women with paraphrenia to men with paraphrenia is anywhere from 3:1 to 45:2.

Age
It is seen mainly in patients over the age of 60, but has been known to occur in patients in their 40s and 50s.

Personality type and living situation
It is suggested that individuals who develop paraphrenia later in life have premorbid personalities, and can be described as “quarrelsome, religious, suspicious or sensitive, unsociable and cold-hearted.” Many patients were also described as being solitary, eccentric, isolated and difficult individuals; these characteristics were also long-standing rather than introduced by the disorder.  Most of the traits recognized prior to the onset of paraphrenia in individuals can be grouped as either paranoid or schizoid.  Patients presenting with paraphrenia were most often found to be living by themselves (either single, widowed, or divorced).  There have also been reports of low marriage rate among paraphrenics and these individuals also have few or no children (possibly because of this premorbid personality).

Physical factors
The development of paranoia and hallucinations in old age have been related to both auditory and visual impairment, and individuals with paraphrenia often present with one or both of these impairments. Hearing loss in paraphrenics is associated with early age of onset, long duration, and profound auditory loss.

History
The term paraphrenia was originally popularized by Karl Ludwig Kahlbaum in 1863 to describe the tendency of certain psychiatric disorders to occur during certain  transitional periods in life (describing paraphrenia hebetica as the insanity of the adolescence and paraphrenia senilis as the insanity of the elders.The term was also used by Sigmund Freud for a short time starting in 1911 as an alternative to the terms schizophrenia and dementia praecox, which in his estimation did not correctly identify the underlying condition, and by Emil Kraepelin in 1912/3, who changed its meaning to describe paraphrenia as it is understood today, as a small group of individuals that have many of the symptoms of schizophrenia with a lack of deterioration and thought disorder.  Kraepelins study was discredited by Wilhelm Mayer in 1921 when he conducted a follow-up study using Kraepelins data.  His study suggested that there was little to no discrimination between schizophrenia and paraphrenia; given enough time, patients presenting with paraphrenia will merge into the schizophrenic pool. However, Meyers data are open to various interpretations. In 1952, Roth and Morrissey conducted a large study in which they surveyed the mental hospital admissions of older patients.  They characterized patients as having "paraphrenic delusions which… occurred in each case in the setting of a well-preserved intellect and personality, were often ‘primary’ in character, and were usually associated with the passivity failings or other volitional disturbances and hallucinations in clear consciousness pathognomonic of schizophrenia".In recent medicine, the term paraphrenia has been replaced by the diagnosis of "very late-onset schizophrenia-like psychosis" and has also been called "atypical psychoses, delusional disorder, psychoses not otherwise specified, schizoaffective disorders, and persistent persecutory states of older adults" by psychotherapists. Current studies, however, recognize the condition as "a viable diagnostic entity that is distinct from schizophrenia, with organic factors playing a role in a significant portion of patients."

References
External links
Harris, M. J.; Jeste, D. V. (1988). "Late-onset schizophrenia: an overview". Schizophrenia Bulletin </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Placental insufficiency and can you explain it in depth? [/INST] Placental insufficiency or utero-placental insufficiency is the failure of the placenta to deliver sufficient nutrients to the fetus during pregnancy, and is often a result of insufficient blood flow to the placenta. The term is also sometimes used to designate late decelerations of fetal heart rate as measured by cardiotocography or an NST, even if there is no other evidence of reduced blood flow to the placenta, normal uterine blood flow rate being 600mL/min.

Causes
The following characteristics of placentas have been said to be associated with placental insufficiency, however all of them occur in normal healthy placentas and full term healthy births, so none of them can be used to accurately diagnose placental insufficiency:
Abnormally thin placenta (less than 1 cm)
Circumvallate placenta (1% of normal placentas)
Amnion cell metaplasia, (amnion nodosum) (present in 65% of normal placentas)
Increased syncytial knots
Calcifications
Infarcts due to focal or diffuse thickening of blood vessels
Villi capillaries occupying about 50% of the villi volume or when <40% of capillaries are on the villous peripheryPlacental insufficiency should not be confused with complete placental abruption, in which the placenta separates off the uterine wall, which immediately results in no blood flow to the placenta, which leads to immediate fetal demise. In the case of a marginal, incomplete placental abruption of less than 50%, usually weeks of hospitalization precedes delivery and outcomes are not necessarily affected by the partial abruption.

Pathophysiology
Maternal effects
Several aspects of maternal adaptation to pregnancy are affected by dysfunction of placenta. Maternal arteries fail to transform into low-resistance vessels (expected by 22–24 weeks of gestation).  This increases vascular resistance in fetoplacental vascular bed eventually leading to reduction in metabolically active mass of placenta like a vicious cycle.

Fetal effects
Placental insufficiency can affect the fetus, causing fetal distress. Placental insufficiency may cause oligohydramnios, preeclampsia, miscarriage or stillbirth. Placental insufficiency is most frequent cause of asymmetric IUGR.

Fetal metabolic changes
Metabolic changes occurring in uteroplacental insufficiency:

Fetal hormonal changes
Decrease in overall thyroid function is correlated with fetal hypoxemia. Serum glucagon, adrenaline, noradrenaline levels increase, eventually causing peripheral glycogenolysis and mobilization of fetal hepatic glycogen stores.

Fetal hematologic changes
Fetal hypoxemia triggers erythropoietin release. This stimulates RBC production from medullary and extramedullary sites and eventually results in polycythemia. Oxygen carrying capacity of blood is thus increased. Prolonged tissue hypoxemia may cause early release of erythrocytes from maturation sites and thus count of nucleated RBCs in blood increases. These factors, increase in blood viscosity, decrease in cell membrane fluidity and platelet aggregation are important precursors in accelerating placental vascular occlusion.

Fetal immunological changes
There is decrease in immunoglobulin, absolute B-cell counts  and total WBC count.  T-helper and cytotoxic T-cells are suppressed in proportion of degree of acidemia. These conditions lead to higher infection susceptibility of infant after delivery.

Fetal cardiovascular changes
There is decrease in magnitude of umbilical venous volume flow. In response to this, the proportion of umbilical venous blood diverted to fetal heart increases.  This eventually leads to elevation of pulmonary vascular resistance and increased right ventricular afterload. This fetal cerebral redistribution
of blood flow is an early response to placental insufficiency </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Tubulocystic renal cell carcinoma and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Keratomalacia and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Propionic acidemia and can you explain it in depth? [/INST] Propionic acidemia, also known as propionic aciduria or propionyl-CoA carboxylase deficiency (PCC deficiency), is a rare autosomal recessive metabolic disorder, classified as a branched-chain organic acidemia.The disorder presents in the early neonatal period with poor feeding, vomiting, lethargy, and lack of muscle tone. Without treatment, death can occur quickly, due to secondary hyperammonemia, infection, cardiomyopathy, or brain damage.

Symptoms and signs
Propionic acidemia is characterized almost immediately in newborns. Symptoms include poor feeding, vomiting, dehydration, acidosis, low muscle tone (hypotonia), seizures, and lethargy. The effects of propionic acidemia quickly become life-threatening.
Long-term complications can include chronic kidney disease, cardiomyopathy, and prolonged QTc interval.

Pathophysiology
In healthy individuals, enzyme propionyl-CoA carboxylase converts propionyl-CoA to methylmalonyl-CoA. This is one of many steps in the process of converting certain amino acids and fats into energy. Individuals with propionic acidemia cannot perform this conversion because the enzyme propionyl-CoA carboxylase is nonfunctional. The essential amino acids valine, methionine, isoleucine, and threonine can not be converted and this leads to a buildup of propionyl-CoA. Instead of being converted to methylmalonyl-CoA, propionyl-CoA is then converted into propionic acid, which builds up in the bloodstream. This in turn causes an accumulation of dangerous acids and toxins, which can cause damage to the organs.In many cases, propionic acidemia can damage the brain, heart, kidney, liver, cause seizures and delays to normal development such as walking or talking. The  patient may need to be hospitalized to prevent breakdown of proteins within the body. Dietary needs must be closely managed.Mutations in both copies of the PCCA or PCCB genes cause propionic acidemia. These genes contain instructions to form alpha- and beta-subunits of PCC, the enzyme called propionyl-CoA carboxylase.
PCC is required for the normal breakdown of the essential amino acids valine, isoleucine, threonine, and methionine, as well as certain odd-chained fatty-acids. Mutations in the PCCA or PCCB genes disrupt the function of the enzyme, preventing these acids from being metabolized. As a result, propionyl-CoA, propionic acid, ketones, ammonia, and other toxic compounds accumulate in the blood, causing the signs and symptoms of propionic acidemia. Hyperammonemia develops due to the inhibitory effects of propionyl-CoA on N-Acetylglutamate synthase, indirectly resulting in slowing of the urea cycle.

Diagnosis
Elevated metabolites of propionic acid (for example, 3-hydroxypropionate, methylcitrate, tiglylglycine, propionylglycine) found in blood and urine along with normal biotinidase levels.

Management
Patients with propionic acidemia should be started as early as possible on a low protein diet </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Sacrococcygeal teratoma and can you explain it in depth? [/INST] Sacrococcygeal teratoma (SCT) is a type of tumor known as a teratoma that develops at the base of the coccyx (tailbone) and is thought to be primarily derived from remnants of the primitive streak. Sacrococcygeal teratomas are benign 75% of the time, malignant 12% of the time, and the remainder are considered "immature teratomas" that share benign and malignant features. Benign sacrococcygeal teratomas are more likely to develop in younger children who are less than 5 months old, and older children are more likely to develop malignant sacrococcygeal teratomas.
The Currarino syndrome, due to an autosomal dominant mutation in the MNX1 gene, consists of a presacral mass (usually a mature teratoma or anterior meningocele), anorectal malformation and sacral dysgenesis.

Presentation
Complications
Maternal complications of pregnancy may include mirror syndrome.  Maternal complications of delivery may include a Cesarean section or, alternatively, a vaginal delivery with mechanical dystocia.Complications of the mass effect of a teratoma in general are addressed on the teratoma page.  Complications of the mass effect of a large SCT may include hip dysplasia, bowel obstruction, urinary obstruction, hydronephrosis and hydrops fetalis.  Even a small SCT can produce complications of mass effect, if it is presacral (Altman Type IV).  In the fetus, severe hydronephrosis may contribute to inadequate lung development.  Also in the fetus and newborn, the anus may be imperforate.Later complications of the mass effect and/or surgery may include neurogenic bladder, other forms of urinary incontinence, fecal incontinence, and other chronic problems resulting from accidental damage to or sacrifice of nerves and muscles within the pelvis.  Removal of the coccyx may include additional complications.  In one review of 25 patients, however, the most frequent complication was an unsatisfactory appearance of the surgical scar.

Late effects
Late effects are of two kinds:  consequences of the tumor itself, and consequences of surgery and other treatments for the tumor.Complications of not removing the coccyx may include both recurrence of the teratoma and metastatic cancer.  Late malignancies usually involve incomplete excision of the coccyx and are adenocarcinoma.Although functional disability in survivors is common, a small comparative study found a nonsignificant difference between SCT survivors and a matched control group.
In rare cases, pelvic scarring may necessitate that a pregnant woman who is a SCT survivor deliver her baby by Cesarean section.

Cause
SCT is seen in 1 in every 35,000 live births, and is the most common tumor presenting in newborn humans.  Most SCTs are found in babies and children, but SCTs have been reported in adults and the increasingly routine use of prenatal ultrasound exams has dramatically increased the number of diagnosed SCTs presenting in fetuses.  Like other teratomas, an SCT can grow very large.  Unlike other teratomas, an SCT sometimes grows larger than the rest of the fetus.
Sacrococcygeal teratomas are the most common type of germ cell tumors (both benign and malignant) diagnosed in neonates, infants, and children younger than 4 years.  SCTs occur more often in girls than in boys; ratios of 3:1 to 4:1 have been reported.Historically, sacrococcygeal teratomas present in 2 clinical patterns related to the childs age, tumor location, and likelihood of tumor malignancy.  With the advent of routine prenatal ultrasound examinations, a third clinical pattern is emerging.

Fetal tumors present during prenatal ultrasound exams, with or without maternal symptoms.  SCTs found during routine exams tend to be small and partly or entirely external.  The internal SCTs are not easily seen via ultrasound, unless they are large enough to reveal their presence by the abnormal position of the fetal urinary bladder and other organs, but large fetal SCTs frequently produce maternal complications which necessitate non-routine, investigative ultrasounds.
Neonatal tumors present at birth protruding from the sacral site and are usually mature or immature teratomas.
Among infants and young children, the tumor presents as a palpable mass in the sacropelvic region compressing the bladder or rectum. These pelvic tumors have a greater likelihood of being malignant. An early survey found that the rate of tumor malignancy was 48% for girls and 67% for boys older than 2 months at the time of sacrococcygeal tumor diagnosis, compared with a malignant tumor incidence of 7% for girls and 10% for boys younger than 2 months at the time of diagnosis. The pelvic site of the primary tumor has been reported to be an adverse prognostic factor, most likely caused by a higher rate of incomplete resection.
In older children and adults, the tumor may be mistaken for a pilonidal sinus, or it may be found during a rectal exam or other evaluation.

Diagnosis
During prenatal ultrasound, an SCT having an external component may appear as a fluid-filled cyst or a solid mass sticking out from the fetus body.  Fetal SCTs that are entirely internal may be undetected if they are small;  detection (or at least suspicion) is possible when the fetal bladder is seen in an abnormal position, due to the SCT pushing other organs out of place.
At birth, the usual presentation is a visible lump or mass under the skin at the top of the buttocks crease.  If not visible, it can sometimes be felt; gently prodded, it feels somewhat like a hardboiled egg.  A small SCT, if it is entirely inside the body, may not present for years, until it grows large enough to cause pain, constipation and other symptoms of a large mass inside the pelvis, or until it begins to extend out of the pelvis.  Even a relatively large SCT may be missed, if it is internal, because the bony pelvis conceals and protects it.  Mediastinal tumors, including teratomas, are similarly concealed and protected by the rib cage.
Some SCTs are discovered when a child begins to talk at about age 2 years and complains of their bottom hurting or feeling "poopy" when they ride in a car seat.
Other tumors can occur in the sacrococcygeal and/or presacral regions and hence must be ruled out to obtain a differential diagnosis.  These include extraspinal ependymoma, ependymoblastoma, neuroblastoma and rhabdomyosarcoma.
Smaller SCTs with an external component, seen in prenatal ultrasounds or at birth, often are mistaken for spina bifida.  Cystic SCT and terminal myelocystocele are especially difficult to distinguish;  for more accurate diagnosis, MRI has been recommended.

Treatment
The preferred first treatment for SCT is complete surgical removal (i.e., complete resection). The preferred approach to a small SCT is through the perineum; a large SCT may require an additional approach through the abdomen.  Resection should include the coccyx and may also include portions of the sacrum. The surgery should include reattachment of the small muscles and ligaments formerly attached to the coccyx, in effect reconstructing the posterior perineum.  If not, there is an increased risk of perineal hernia later in life.
SCTs are classified morphologically according to their relative extent outside and inside the body:

Altman type I — entirely outside, sometimes attached to the body only by a narrow stalk
Altman type II — mostly outside
Altman type III — mostly inside
Altman type IV — entirely inside;  this is also known as a presacral teratoma or retrorectal teratomaThe Altman type is significant in the contexts of management of labor and delivery, surgical approach, and complications of SCT </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Solitary cutaneous leiomyoma and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Amoebic liver abscess and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Carotid artery dissection and can you explain it in depth? [/INST] Carotid artery dissection is a separation of the layers of the artery wall supplying oxygen-bearing blood to the head and brain and is the most common cause of stroke in young adults.  (Dissection is a blister-like de-lamination between the outer and inner walls of a blood vessel, generally originating with a partial leak in the inner lining.)Dissection may occur after physical trauma to the neck, such as a blunt injury (e.g. traffic collision), strangulation, but may also happen spontaneously.

Signs and symptoms
The signs and symptoms of carotid artery dissection may be divided into ischemic and non-ischemic categories:Non-ischemic signs and symptoms:

Localised headache, particularly around one of the eyes
Neck pain
Swollen tongue
Decreased pupil size with drooping of the upper eyelid (Horner syndrome)
Pulsatile tinnitusIschemic signs and symptoms:

Temporary vision loss
Ischemic stroke

Causes
The causes of internal carotid artery dissection can be broadly categorized into two classes: spontaneous or traumatic.

Spontaneous
Once considered uncommon, spontaneous carotid artery dissection is an increasingly recognized cause of stroke that preferentially affects the middle-aged.The incidence of spontaneous carotid artery dissection is low, and incidence rates for internal carotid artery dissection have been reported to be 2.6 to 2.9 per 100,000.Observational studies and case reports published since the early 1980s show that patients with spontaneous internal carotid artery dissection may also have a history of stroke in their family and/or hereditary connective tissue disorders, such as Marfan syndrome, Ehlers-Danlos syndrome, autosomal dominant polycystic kidney disease, pseudoxanthoma elasticum, fibromuscular dysplasia, and osteogenesis imperfecta type I. IgG4-related disease involving the carotid artery has also been observed as a cause.However, although an association with connective tissue disorders does exist, most people with spontaneous arterial dissections do not have associated connective tissue disorders. Also, the reports on the prevalence of hereditary connective tissue diseases in people with spontaneous dissections are highly variable, ranging from 0% to 0.6% in one study to 5% to 18% in another study.Internal carotid artery dissection can also be associated with an elongated styloid process (known as Eagle syndrome when the elongated styloid process causes symptoms).

Traumatic
Carotid artery dissection is thought to be more commonly caused by severe violent trauma to the head and/or neck.  An estimated 0.67% of patients admitted to the hospital after major motor vehicle accidents were found to have blunt carotid injury, including intimal dissections, pseudoaneurysms, thromboses, or fistulas. Of these, 76% had intimal dissections, pseudoaneurysms, or a combination of the two. Sports-related activities such as surfing and Jiu-Jitsu have been reported as causes of carotid artery dissection.
The probable mechanism of injury for most internal carotid injuries is rapid deceleration, with resultant hyperextension and rotation of the neck, which stretches the internal carotid artery over the upper cervical vertebrae, producing an intimal tear. After such an injury, the patient may remain asymptomatic, have a hemispheric transient ischemic event, or have a stroke.Artery dissection has also been reported in association with some forms of neck manipulation. There is significant controversy about the level of risk of stroke from neck manipulation. It may be that manipulation can cause dissection, or it may be that the dissection is already present in some people who seek manipulative treatment </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Ebsteins anomaly and can you explain it in depth? [/INST] Ebsteins 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. It is classified as a critical congenital heart defect accounting for <1% of all congenital heart defects presenting in ≈1 per 200,000 live births </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Obturator hernia and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Tyrosinemia and can you explain it in depth? [/INST] Tyrosinemia or tyrosinaemia is an error of metabolism, usually inborn, in which the body cannot effectively break down the amino acid tyrosine. Symptoms of untreated tyrosinemia include liver and kidney disturbances </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Diplacusis and can you explain it in depth? [/INST] Diplacusis, also known as diplacusis binauralis, binauralis  disharmonica or interaural pitch difference (IPD), is a hearing disorder whereby a single auditory stimulus is perceived as different pitches between ears.  It is typically experienced as a secondary symptom of sensorineural hearing loss, although not all patients with sensorineural hearing loss experience diplacusis or tinnitus. The onset is usually spontaneous and can occur following an acoustic trauma, for example an explosive noise, or in the presence of an ear infection. Sufferers may experience the effect permanently, or it may resolve on its own. Diplacusis can be particularly disruptive to individuals working within fields requiring acute audition, such as musicians, sound engineers or performing artists.

Diplacusis of pure tones
The term diplacusis has been used in cases which people with unilateral cochlear hearing losses or asymmetrical hearing losses, the same tone presented alternately to the two ears may be perceived as having different pitches in the two ears. The magnitude of the shift can be measured by getting the subject to adjust the frequency of a tone in one ear until its pitch matches that of the tone in the other ear. On presentation of a single tone alternating between ears (i.e. 1000 Hz left, 1000 Hz right, 1000 Hz left, ...), a given person will consistently mismatch these sinusoids the same amount between trials if doing a pitch-matching task.  For example, a 1000 Hz tone in an unaffected ear may be heard as a slightly different pitch in the opposite ear, or have an imperfect tonal quality in the affected ear.

Biological explanation via theories of pitch of pure tones
There are two theories on the cause of diplacusis: place theory and temporal theory. Place theory posits that  the cause is looking for the edge of the wave for the pitch and could explain diplacusis as a small differences between the two cochleas.Temporal theory posits that the cause is from looking at the phase locking to tell what the pitch is.  This theory has a difficult time explaining diplacusis. There are some examples of pitch which do not have an "edge" on the basilar membrane, which this would account for—e.g., white noise, clicks, etc.  Both theories are under debate.

Effects of sensorineural hearing loss
Normal human ears can discriminate between two frequencies that differ by as little as 0.2%. If one ear has normal thresholds while the other has sensorineural hearing loss (SNHL),  diplacusis may be present, as much as 15–20% (for example 200 Hz one ear => 240 Hz in the other). The pitch may be difficult to match because the SNHL ear hears the sound "fuzzy". Bilateral SNHL gives less diplacusis, but pitch distortions may persist. This may cause problems with music and speech understanding.

Treatment
Treatment of diplacusis includes a full medical and audiological examination that may explain the nature of the problem. If needed, amplification may relieve the symptoms of diplacusis. Therapy in helping the patient understand the cause of the symptom and tinnitus retraining may provide some relief.  In at least some cases, amplification makes no difference and there is no treatment other than waiting for natural resolution. Some individuals may find the provided amplification also increases the audibility of their pitch discrepancy </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Trigeminal trophic syndrome and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Pulmonary contusion and can you explain it in depth? [/INST] A pulmonary contusion, also known as lung contusion, is a bruise of the lung, caused by chest trauma. As a result of damage to capillaries, blood and other fluids accumulate in the lung tissue.  The excess fluid interferes with gas exchange, potentially leading to inadequate oxygen levels (hypoxia).  Unlike pulmonary laceration, another type of lung injury, pulmonary contusion does not involve a cut or tear of the lung tissue.
A pulmonary contusion is usually caused directly by blunt trauma but can also result from explosion injuries or a shock wave associated with penetrating trauma. With the use of explosives during World Wars I and II, pulmonary contusion resulting from blasts gained recognition. In the 1960s its occurrence in civilians began to receive wider recognition, in which cases it is usually caused by traffic accidents. The use of seat belts and airbags reduces the risk to vehicle occupants.
Diagnosis is made by studying the cause of the injury, physical examination and chest radiography. Typical signs and symptoms include direct effects of the physical trauma, such as chest pain and coughing up blood, as well as signs that the body is not receiving enough oxygen, such as cyanosis.  The contusion frequently heals on its own with supportive care. Often nothing more than supplemental oxygen and close monitoring is needed; however, intensive care may be required. For example, if breathing is severely compromised, mechanical ventilation may be necessary. Fluid replacement may be required to ensure adequate blood volume, but fluids are given carefully since fluid overload can worsen pulmonary edema, which may be lethal.
The severity ranges from mild to severe: small contusions may have little or no impact on health, yet pulmonary contusion is the most common type of potentially lethal chest trauma. It occurs in 30–75% of severe chest injuries. The risk of death following a pulmonary contusion is between 14 and 40%. Pulmonary contusion is usually accompanied by other injuries. Although associated injuries are often the cause of death, pulmonary contusion is thought to cause death directly in a quarter to half of cases. Children are at especially high risk for the injury because the relative flexibility of their bones prevents the chest wall from absorbing force from an impact, causing it to be transmitted instead to the lung.  Pulmonary contusion is associated with complications including pneumonia and acute respiratory distress syndrome, and it can cause long-term respiratory disability.

Classification
Pulmonary contusion and laceration are injuries to the lung tissue. Pulmonary laceration, in which lung tissue is torn or cut, differs from pulmonary contusion in that the former involves disruption of the macroscopic architecture of the lung, while the latter does not. When lacerations fill with blood, the result is pulmonary hematoma, a collection of blood within the lung tissue. Contusion involves hemorrhage in the alveoli (tiny air-filled sacs responsible for absorbing oxygen), but a hematoma is a discrete clot of blood not interspersed with lung tissue.  A collapsed lung can result when the pleural cavity (the space outside the lung) accumulates blood (hemothorax) or air (pneumothorax) or both (hemopneumothorax). These conditions do not inherently involve damage to the lung tissue itself, but they may be associated with it.  Injuries to the chest wall are also distinct from but may be associated with lung injuries. Chest wall injuries include rib fractures and flail chest, in which multiple ribs are broken so that a segment of the ribcage is detached from the rest of the chest wall and moves independently.

Signs and symptoms
Presentation may be subtle; people with mild contusion may have no symptoms at all. However, pulmonary contusion is frequently associated with signs (objective indications) and symptoms (subjective states), including those indicative of the lung injury itself and  of accompanying injuries.  Because gas exchange is impaired, signs of low blood oxygen saturation, such as low concentrations of oxygen in arterial blood gas and cyanosis (bluish color of the skin and mucous membranes) are commonly associated.   Dyspnea (painful breathing or difficulty breathing) is commonly seen, and tolerance for exercise may be lowered. Rapid breathing and a rapid heart rate are other signs.  With more severe contusions, breath sounds heard through a stethoscope may be decreased, or rales (an abnormal crackling sound in the chest accompanying breathing) may be present. People with severe contusions may have bronchorrhea (the production of watery sputum). Wheezing and coughing are other signs. Coughing up blood or bloody sputum is present in up to half of cases. Cardiac output (the volume of blood pumped by the heart) may be reduced, and hypotension (low blood pressure) is frequently present. The area of the chest wall near the contusion may be  tender or painful due to associated chest wall injury.
Signs and symptoms take time to develop, and as many as half of cases are asymptomatic at the initial presentation. The more severe the injury, the more quickly symptoms become apparent. In severe cases, symptoms may occur as quickly as three or four hours after the trauma. Hypoxemia (low oxygen concentration in the arterial blood) typically becomes progressively worse over 24–48 hours after injury. In general, pulmonary contusion tends to worsen slowly over a few days, but it may also cause rapid deterioration or death if untreated.

Causes
Pulmonary contusion is the most common injury found in blunt chest trauma, occurring in 25–35% of cases. It is usually caused by the rapid deceleration that results when the moving chest strikes a fixed object. About 70% of cases result from motor vehicle collisions, most often when the chest strikes the inside of the car.  Falls, assaults, and sports injuries are other causes.  Pulmonary contusion can also be caused by explosions; the organs most vulnerable to blast injuries are those that contain gas, such as the lungs.  Blast lung is severe pulmonary contusion, bleeding, or edema with damage to alveoli and blood vessels, or a combination of these. This is the primary cause of death among people who initially survive an explosion.  Unlike other mechanisms of injury in which pulmonary contusion is often found alongside other injuries, explosions can cause pulmonary contusion without damage to the chest wall.In addition to blunt trauma, penetrating trauma can cause pulmonary contusion.  Contusion resulting from penetration by a rapidly moving projectile usually surrounds the path along which the projectile traveled through the tissue. The pressure wave forces tissue out of the way, creating a temporary cavity; the tissue readily moves back into place, but it is damaged.  Pulmonary contusions that accompany gun and knife wounds are not usually severe enough to have a major effect on outcome;  penetrating trauma causes less widespread lung damage than does blunt trauma. An exception is shotgun wounds, which can seriously damage large areas of lung tissue through a blast injury mechanism.

Mechanism
The physical processes behind pulmonary contusion are poorly understood. However, it is known that lung tissue can be crushed when the chest wall bends inward on impact. Three other possible mechanisms have been suggested: the inertial effect, the spalling effect, and the implosion effect.

In the inertial effect, the lighter alveolar tissue is sheared from the heavier hilar structures, an effect similar to diffuse axonal injury in head injury. It results from the fact that different tissues have different densities, and therefore different rates of acceleration or deceleration.
In the spalling effect, lung tissue bursts or is sheared where a shock wave meets the lung tissue, at interfaces between gas and liquid.  The alveolar walls form such a gas-liquid interface with the air in the alveoli.  The spalling effect occurs in areas with large differences in density; particles of the denser tissue are spalled (thrown) into the less dense particles.
The implosion effect occurs when a pressure wave passes through a tissue containing bubbles of gas: the bubbles first implode, then rebound and expand beyond their original volume. The air bubbles cause many tiny explosions, resulting in tissue damage; the overexpansion of gas bubbles stretches and tears alveoli.  This effect is thought to occur microscopically when the pressure in the airways increases sharply.Contusion usually occurs on the lung directly under the site of impact, but, as with traumatic brain injury, a contrecoup contusion may occur at the site opposite the impact as well. A blow to the front of the chest may cause contusion on the back of the lungs because a shock wave travels through the chest and hits the curved back of the chest wall; this reflects the energy onto the back of the lungs, concentrating it. (A similar mechanism may occur at the front of the lungs when the back is struck.)The amount of energy transferred to the lung is determined in a large part by the compliance (flexibility) of the chest wall. Childrens chests are more flexible because their ribs are more elastic and there is less ossification of their intercostal cartilage.  Therefore, their chest walls bend, absorbing less of the force and transmitting more of it to the underlying organs. An adults more bony chest wall absorbs more of the force itself rather than transmitting it. Thus children commonly get pulmonary contusions without fractures overlying them, while elderly people are more likely to develop fractures than contusions. One study found that pulmonary contusions were accompanied by fractures 62% of the time in children and 80% of the time in adults.

Pathophysiology
Pulmonary contusion results in bleeding and fluid leakage into lung tissue, which can become stiffened and lose its normal elasticity.  The water content of the lung increases over the first 72 hours after injury, potentially leading to frank pulmonary edema in more serious cases. As a result of these and other pathological processes, pulmonary contusion progresses over time and can cause hypoxia (insufficient oxygen).

Bleeding and edema
In contusions, torn capillaries leak fluid into the tissues around them. The membrane between alveoli and capillaries is torn; damage to this capillary–alveolar membrane and small blood vessels causes blood and fluids to leak into the alveoli and the interstitial space (the space surrounding cells) of the lung.  With more severe trauma, there is a greater amount of edema, bleeding, and tearing of the alveoli.  Pulmonary contusion is characterized by microhemorrhages (tiny bleeds) that occur when the alveoli are traumatically separated from airway structures and blood vessels. Blood initially collects in the interstitial space, and then edema occurs by an hour or two after injury. An area of bleeding in the contused lung is commonly surrounded by an area of edema. In normal gas exchange, carbon dioxide diffuses across the endothelium of the capillaries, the interstitial space, and across the alveolar epithelium; oxygen diffuses in the other direction. Fluid accumulation interferes with gas exchange, and can cause the alveoli to fill with proteins and collapse due to edema and bleeding. The larger the area of the injury, the more severe respiratory compromise will be.

Consolidation and collapse
Pulmonary contusion can cause parts of the lung to consolidate, alveoli to collapse, and atelectasis (partial or total lung collapse) to occur.  Consolidation occurs when the parts of the lung that are normally filled with air fill with material from the pathological condition, such as blood. Over a period of hours after the injury, the alveoli in the injured area thicken and may become consolidated. A decrease in the amount of surfactant produced also contributes to the collapse and consolidation of alveoli; inactivation of surfactant increases their surface tension. Reduced production of surfactant can also occur in surrounding tissue that was not originally injured.Inflammation of the lungs, which can result when components of blood enter the tissue due to contusion, can also cause parts of the lung to collapse.  Macrophages, neutrophils, and other inflammatory cells and blood components can enter the lung tissue and release factors that lead to inflammation, increasing the likelihood of respiratory failure.  In response to inflammation, excess mucus is produced, potentially plugging parts of the lung and leading to their collapse.  Even when only one side of the chest is injured, inflammation may also affect the other lung.  Uninjured lung tissue may develop edema, thickening of the septa of the alveoli, and other changes.  If this inflammation is severe enough, it can lead to dysfunction of the lungs like that seen in acute respiratory distress syndrome.

Ventilation/perfusion mismatch
Normally, the ratio of ventilation to perfusion is about one-to-one; the volume of air entering the alveoli (ventilation) is about equal to that of blood in the capillaries around them (perfusion).  This ratio is reduced in pulmonary contusion; fluid-filled alveoli cannot fill with air, oxygen does not fully saturate the hemoglobin, and the blood leaves the lung without being fully oxygenated. Insufficient inflation of the lungs, which can result from inadequate mechanical ventilation or an associated injury such as flail chest, can also contribute to the ventilation/perfusion mismatch. As the mismatch between ventilation and perfusion grows, blood oxygen saturation is reduced.  Pulmonary hypoxic vasoconstriction, in which blood vessels near the hypoxic alveoli constrict (narrow their diameter) in response to the lowered oxygen levels, can occur in pulmonary contusion.  The vascular resistance increases in the contused part of the lung, leading to a decrease in the amount of blood that flows into it,  directing blood to better-ventilated areas. Although reducing blood flow to the unventilated alveoli is a way to compensate for the fact that blood passing unventilated alveoli is not oxygenated, the oxygenation of the blood remains lower than normal.  If it is severe enough, the hypoxemia resulting from fluid in the alveoli cannot be corrected just by giving supplemental oxygen; this problem is the cause of a large portion of the fatalities that result from trauma.

Diagnosis
To diagnose pulmonary contusion, health professionals use clues from a physical examination, information about the event that caused the injury, and radiography.  Laboratory findings may also be used; for example, arterial blood gasses may show insufficient oxygen and excessive carbon dioxide even in someone receiving supplemental oxygen.  However, blood gas levels may show no abnormality early in the course of pulmonary contusion.

X-ray
Chest X-ray is the most common method used for diagnosis, and may be used to confirm a diagnosis already made using clinical signs.  Consolidated areas appear white on an X-ray film.  Contusion is not typically restricted by the anatomical boundaries of the lobes or segments of the lung.  The X-ray appearance of pulmonary contusion is similar to that of aspiration, and the presence of hemothorax or pneumothorax may obscure the contusion on a radiograph. Signs of contusion that progress after 48 hours post-injury are likely to be actually due to aspiration, pneumonia, or ARDS.Although chest radiography is an important part of the diagnosis, it is often not sensitive enough to detect the condition early after the injury. In a third of cases, pulmonary contusion is not visible on the first chest radiograph performed. It takes an average of six hours for the characteristic white regions to show up on a chest X-ray, and the contusion may not become apparent for 48 hours. When a pulmonary contusion is apparent in an X-ray, it suggests that the trauma to the chest was severe and that a CT scan might reveal other injuries that were missed with X-ray.

Computed tomography
Computed tomography (CT scanning) is a more sensitive test for pulmonary contusion, and it can identify abdominal, chest, or other injuries that accompany the contusion. In one study, chest X-ray detected pulmonary contusions in 16.3% of people with serious blunt trauma, while CT detected them in 31.2% of the same people. Unlike X-ray, CT scanning can detect the contusion almost immediately after the injury. However, in both X-ray and CT a contusion may become more visible over the first 24–48 hours after trauma as bleeding and edema into lung tissues progress. CT scanning also helps determine the size of a contusion, which is useful in determining whether a patient needs mechanical ventilation; a larger volume of contused lung on CT scan is associated with an increased likelihood that ventilation will be needed.  CT scans also help differentiate between contusion and pulmonary hematoma, which may be difficult to tell apart otherwise. However, pulmonary contusions that are visible on CT but not chest X-ray are usually not severe enough to affect outcome or treatment.

Ultrasound
Pulmonary ultrasound, performed at the bedside or on the accident scene, is being explored as a diagnosis for pulmonary contusion.  Its use is still not widespread, being limited to facilities which are comfortable with its use for other applications, like pneumothorax, airway management, and hemothorax.  Accuracy has been found to be comparable to CT scanning.

Prevention
Prevention of pulmonary contusion is similar to that of other chest trauma.  Airbags in combination with seat belts can protect vehicle occupants by preventing the chest from striking the interior of the vehicle during a collision, and by distributing forces involved in the crash more evenly across the body.  However, in rare cases, an airbag causes pulmonary contusion in a person who is not properly positioned when it deploys.  Child restraints such as carseats protect children in vehicle collisions from pulmonary contusion. Equipment exists for use in some sports to prevent chest and lung injury; for example, in softball the catcher is equipped with a chest protector.  Athletes who do not wear such equipment, such as basketball players, can be trained to protect their chests from impacts. Protective garments can also prevent pulmonary contusion in explosions. Although traditional body armor made from rigid plates or other heavy materials protects from projectiles generated by a blast, it does not protect against pulmonary contusion, because it does not prevent the blasts shock wave from being transferred to the lung.  Special body armor has been designed for military personnel at high risk for blast injuries; these garments can prevent a shock wave from being propagated across the chest wall to the lung, and thus protect wearers from blast lung injuries. These garments alternate layers of materials with high and low acoustic impedance (the product of a materials density and a waves velocity through it) in order to "decouple" the blast wave, preventing its propagation into the tissues.

Treatment
No treatment is known to speed the healing of a pulmonary contusion; the main care is supportive.   Attempts are made to discover injuries accompanying the contusion, to prevent additional injury, and to provide supportive care while waiting for the contusion to heal.  Monitoring, including keeping track of fluid balance, respiratory function, and oxygen saturation using pulse oximetry is also required as the patients condition may progressively worsen. Monitoring for complications such as pneumonia and acute respiratory distress syndrome is of critical importance. Treatment aims to prevent respiratory failure and to ensure adequate blood oxygenation.  Supplemental oxygen can be given and it may be warmed and humidified.  When the contusion does not respond to other treatments, extracorporeal membranous oxygenation may be used, pumping blood from the body into a machine that oxygenates it and removes carbon dioxide prior to pumping it back in.

Ventilation
Positive pressure ventilation, in which air is forced into the lungs, is needed when oxygenation is significantly impaired. Noninvasive positive pressure ventilation including continuous positive airway pressure (CPAP) and bi-level positive airway pressure (BiPAP), may be used to improve oxygenation and treat atelectasis: air is blown into the airways at a prescribed pressure via a face mask. Noninvasive ventilation has advantages over invasive methods because it does not carry the risk of infection that intubation does, and it allows normal coughing, swallowing, and speech. However, the technique may cause complications;  it may force air into the stomach or cause aspiration of stomach contents, especially when level of consciousness is decreased.People with  signs of inadequate respiration or oxygenation may need to be intubated and mechanically ventilated. Mechanical ventilation aims to reduce pulmonary edema and increase oxygenation. Ventilation can reopen collapsed alveoli, but it is harmful for them to be repeatedly opened, and positive pressure ventilation can also damage the lung by overinflating it.  Intubation is normally reserved for when respiratory problems occur, but most significant contusions do require intubation, and it may be done early in anticipation of this need. People with pulmonary contusion who are especially likely to need ventilation include those with prior severe lung disease or kidney problems; the elderly; those with a lowered level of consciousness; those with low blood oxygen or high carbon dioxide levels; and those who will undergo operations with anesthesia.  Larger contusions have been correlated with a need for ventilation for longer periods of time.Pulmonary contusion or its complications such as acute respiratory distress syndrome may cause lungs to lose compliance (stiffen), so higher pressures may be needed to give normal amounts of air and oxygenate the blood adequately. Positive end-expiratory pressure (PEEP), which delivers air at a given pressure at the end of the expiratory cycle, can reduce edema and keep alveoli from collapsing.  PEEP is considered necessary with mechanical ventilation; however, if the pressure is too great it can expand the size of the contusion and injure the lung. When the compliance of the injured lung differs significantly from that of the uninjured one, the lungs can be ventilated independently with two ventilators in order to deliver air at different pressures; this helps avoid injury from overinflation while providing adequate ventilation.

Fluid therapy
The administration of fluid therapy in individuals with pulmonary contusion is controversial. Excessive fluid in the circulatory system (hypervolemia) can worsen hypoxia because it can cause fluid leakage from injured capillaries (pulmonary edema), which are more permeable than normal. However, low blood volume (hypovolemia) resulting from insufficient fluid has an even worse impact, potentially causing hypovolemic shock; for people who have lost large amounts of blood, fluid resuscitation is necessary.  A lot of the evidence supporting the idea that fluids should be withheld from people with pulmonary contusion came from animal studies, not clinical trials with humans; human studies have had conflicting findings on whether fluid resuscitation worsens the condition.  Current recommendations suggest giving enough fluid to ensure sufficient blood flow but not giving any more fluid than necessary.  For people who do require large amounts of intravenous fluid, a catheter may be placed in the pulmonary artery to measure the pressure within it.  Measuring pulmonary artery pressure allows the clinician to give enough fluids to prevent shock without exacerbating edema.  Diuretics, drugs that increase urine output to reduce excessive fluid in the system, can be used when fluid overload does occur, as long as there is not a significant risk of shock.  Furosemide, a diuretic used in the treatment of pulmonary contusion, also relaxes the smooth muscle in the veins of the lungs, thereby decreasing pulmonary venous resistance and reducing the pressure in the pulmonary capillaries.

Supportive care
Retaining secretions in the airways can worsen hypoxia and lead to infections.  Thus, an important part of treatment is pulmonary toilet, the use of suction, deep breathing, coughing, and other methods to remove material such as mucus and blood from the airways.  Chest physical therapy makes use of techniques such as breathing exercises, stimulation of coughing, suctioning, percussion, movement, vibration, and drainage to rid the lungs of secretions, increase oxygenation, and expand collapsed parts of the lungs. People with pulmonary contusion, especially those who do not respond well to other treatments, may be positioned with the uninjured lung lower than the injured one to improve oxygenation. Inadequate pulmonary toilet can result in pneumonia. People who do develop infections are given antibiotics. No studies have yet shown a benefit of using antibiotics as a preventative measure before infection occurs, although some doctors do recommend prophylactic antibiotic use even without scientific evidence of its benefit. However, this can cause the development of antibiotic resistant strains of bacteria, so giving antibiotics without a clear need is normally discouraged. For people who are at especially high risk of developing infections, the sputum can be cultured to test for the presence of infection-causing bacteria; when they are present, antibiotics are used.Pain control is another means to facilitate the elimination of secretions. A chest wall injury can make coughing painful, increasing the likelihood that secretions will accumulate in the airways.  Chest injuries also contribute to hypoventilation (inadequate breathing) because the chest wall movement involved in breathing adequately is painful. Insufficient expansion of the chest may lead to atelectasis, further reducing oxygenation of the blood. Analgesics (pain medications) can be given to reduce pain. Injection of anesthetics into nerves in the chest wall, called nerve blockade, is another approach to pain management; this does not depress respiration the way some pain medications can.

Prognosis
Pulmonary contusion usually resolves itself without causing permanent complications; however it may also have long-term ill effects on respiratory function. Most contusions resolve in five to seven days after the injury.  Signs detectable by radiography are usually gone within 10 days after the injury—when they are not, other conditions, such as pneumonia, are the likely cause.  Chronic lung disease correlates with the size of the contusion and can interfere with an individuals ability to return to work. Fibrosis of the lungs can occur, resulting in dyspnea (shortness of breath), low blood oxygenation, and reduced functional residual capacity for as long as six years after the injury. As late as four years post-injury, decreased functional residual capacity has been found in most pulmonary contusion patients studied. During the six months after pulmonary contusion, up to 90% of people have difficulty breathing. In some cases, dyspnea persists for an indefinite period.  Contusion can also permanently reduce the compliance of the lungs.

Complications
Pulmonary contusion can result in respiratory failure—about half of such cases occur within a few hours of the initial trauma. Other severe complications, including infections and acute respiratory distress syndrome (ARDS) occur in up to half of cases.  Elderly people and those who have heart, lung, or kidney disease prior to the injury are more likely to stay longer in hospital and have complications from the injury. Complications occur in 55% of people with heart or lung disease and 13% of those without. Of people with pulmonary contusion alone, 17% develop ARDS, while 78% of people with at least two additional injuries develop the condition. A larger contusion is associated with an increased risk. In one study, 82% of people with 20% or more of the lung volume affected developed ARDS, while only 22% of people with less than 20% did so.Pneumonia, another potential complication, develops in as many as 20% of people with pulmonary contusion. Contused lungs are less able to remove bacteria than uninjured lungs, predisposing them to infection. Intubation and mechanical ventilation further increase the risk of developing pneumonia; the tube is passed through the nose or mouth into the airways, potentially tracking bacteria from the mouth or sinuses into them. Also, intubation prevents coughing, which would clear bacteria-laden secretions from the airways, and secretions pool near the tubes cuff and allow bacteria to grow. The sooner the endotracheal tube is removed, the lower the risk of pneumonia, but if it is removed too early and has to be put back in, the risk of pneumonia rises. People who are at risk for pulmonary aspiration (e.g. those with lowered level of consciousness due to head injuries) are especially likely to get pneumonia. As with ARDS, the chances of developing pneumonia increase with the size of the contusion. Children and adults have been found to have similar rates of complication with pneumonia and ARDS.

Associated injuries
A large amount of force is required to cause pulmonary contusion; a person injured with such force is likely to have other types of injuries as well. In fact, pulmonary contusion can be used to gauge the severity of trauma.  Up to three quarters of cases are accompanied by other chest injuries, the most common of these being hemothorax and pneumothorax.  Flail chest is usually associated with significant pulmonary contusion, and the contusion, rather than the chest wall injury, is often the main cause of respiratory failure in people with these injuries. Other indications of thoracic trauma may be associated, including fracture of the sternum and bruising of the chest wall.  Over half of fractures of the scapula are associated with pulmonary contusion.   The contusion is frequently found underlying fracture sites.  When accompanied by a fracture, it is usually concentrated into a specific location—the contusion is more diffuse when there is no fracture. Pulmonary lacerations may result from the same blunt or penetrating forces that cause contusion.  Lacerations can result in pulmonary hematomas; these are reported to develop in 4–11% of pulmonary contusions.

Epidemiology
Pulmonary contusion is found in 30–75% of severe cases of chest injury, making it the most common serious injury to occur in association with thoracic trauma. Of people who have multiple injuries with an injury severity score of over 15, pulmonary contusion occurs in about 17%. It is difficult to determine the death rate (mortality) because pulmonary contusion rarely occurs by itself. Usually, deaths of people with pulmonary contusion result from other injuries, commonly traumatic brain injury.  It is controversial whether pulmonary contusion with flail chest is a major factor in mortality on its own or whether it merely contributes to mortality in people with multiple injuries.  The estimated mortality rate of pulmonary contusion ranges from 14 to 40%, depending on the severity of the contusion itself and on associated injuries.  When the contusions are small, they do not normally increase the chance of death or poor outcome for people with blunt chest trauma; however, these chances increase with the size of the contusion.  One study found that 35% of people with multiple significant injuries including pulmonary contusion die. In another study, 11% of people with pulmonary contusion alone died, while the number rose to 22% in those with additional injuries.  Pulmonary contusion is thought to be the direct cause of death in a quarter to a half of people with multiple injuries (polytrauma) who die.  An accompanying flail chest increases the morbidity and mortality to more than twice that of pulmonary contusion alone.Pulmonary contusion is the most common cause of death among vehicle occupants involved in accidents, and it is thought to contribute significantly in about a quarter of deaths resulting from vehicle collisions.  As vehicle use has increased, so has the number of auto accidents, and with it the number of chest injuries. However an increase in the number of airbags installed in modern cars may be decreasing the incidence of pulmonary contusion.  Use of child restraint systems has brought the approximate incidence of pulmonary contusion in children in vehicle accidents from 22% to 10%.Differences in the bodies of children and adults lead to different manifestations of pulmonary contusion and associated injuries; for example, children have less body mass, so the same force is more likely to lead to trauma in multiple body systems.   Since their chest walls are more flexible, children are more vulnerable to pulmonary contusion than adults are, and thus suffer from the injury more commonly. Pulmonary contusion has been found in 53% of children with chest injuries requiring hospitalization. Children in forceful impacts suffer twice as many pulmonary contusions as adults with similar injury mechanisms, yet have proportionately fewer rib fractures.  The rates of certain types of injury mechanisms differ between children and adults; for example, children are more often hit by cars as pedestrians.  Some differences in childrens physiology might be advantageous (for example they are less likely to have other medical conditions), and thus they have been predicted to have a better outcome. However, despite these differences, children with pulmonary contusion have similar mortality rates to adults.

History
In 1761, the Italian anatomist Giovanni Battista Morgagni was first to describe a lung injury that was not accompanied by injury to the chest wall overlying it. Nonetheless, it was the French military surgeon Guillaume Dupuytren who is thought to have coined the term pulmonary contusion in the 19th century.  It still was not until the early 20th century that pulmonary contusion and its clinical significance began to receive wide recognition. With the use of explosives during World War I came many casualties with no external signs of chest injury but with significant bleeding in the lungs.  Studies of World War I injuries by D.R. Hooker showed that pulmonary contusion was an important part of the concussive injury that results from explosions.Pulmonary contusion received further attention during World War II, when the bombings of Britain caused blast injuries and associated respiratory problems in both soldiers and civilians. Also during this time, studies with animals placed at varying distances from a blast showed that protective gear could prevent lung injuries. These findings suggested that an impact to the outside of the chest wall was responsible for the internal lesions. In 1945, studies identified a phenomenon termed "wet lung", in which the lungs accumulated fluid and were simultaneously less able to remove it </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Dandruff and can you explain it in depth? [/INST] Dandruff is a skin condition that mainly affects the scalp. Symptoms include flaking and sometimes mild itchiness. It can result in social or self-esteem problems. A more severe form of the condition, which includes inflammation of the skin, is known as seborrhoeic dermatitis.The cause is unclear, but believed to involve a number of genetic and environmental factors; the condition may worsen in the winter. It is not due to poor hygiene, and the underlying mechanism involves the excessive growth of skin cells. Diagnosis is based on symptoms.There is no known cure for dandruff. Antifungal cream, such as ketoconazole, or salicylic acid may be used to try to improve the condition. Dandruff affects about half of adults, with males more often affected than females. In addition, people in all areas of the world are affected. Onset is usually at puberty, and it becomes less common after the age of 50.

Signs and symptoms
The main symptoms of dandruff are an itchy scalp and flakiness. Red and greasy patches of skin and a tingly feeling on the skin are also symptoms.

Causes
The cause is unclear but believed to involve a number of genetic and environmental factors.

As the skin layers continually replace themselves, cells are pushed outward where they die and flake off.  For most individuals, these flakes of skin are too small to be visible.  However, certain conditions cause cell turnover to be unusually rapid, especially in the scalp. It is hypothesized that for people with dandruff, skin cells may mature and be shed in 2–7 days, as opposed to around a month in people without dandruff.  The result is that dead skin cells are shed in large, oily clumps, which appear as white or grayish flakes on the scalp, skin and clothes.
According to one study, dandruff has been shown to be possibly the result of three factors:
Skin oil, commonly referred to as sebum or sebaceous secretions
The metabolic by-products of skin micro-organisms (most specifically Malassezia yeasts)
Individual susceptibility and allergy sensitivity.

Microorganisms
Older literature cites the fungus Malassezia furfur (previously known as Pityrosporum ovale) as the cause of dandruff. While this species does occur naturally on the skin surface of people both with and without dandruff, in 2007, it was discovered that the responsible agent is a scalp specific fungus, Malassezia globosa, that metabolizes triglycerides present in sebum by the expression of lipase, resulting in a lipid byproduct: oleic acid. During dandruff, the levels of Malassezia increase by 1.5 to 2 times its normal level. Oleic acid penetrates the top layer of the epidermis, the stratum corneum, and evokes an inflammatory response in susceptible people which disturbs homeostasis and results in erratic cleavage of stratum corneum cells.

Seborrhoeic dermatitis
In seborrhoeic dermatitis, redness and itching frequently occur around the folds of the nose and eyebrow areas, not just the scalp. Dry, thick, well-defined lesions consisting of large, silvery scales may be traced to the less common condition of scalp psoriasis. Inflammation can be characterized by redness, heat, pain or swelling, and can cause sensitivity.
Inflammation and extension of scaling outside the scalp exclude the diagnosis of dandruff from seborrhoeic dermatitis </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Specific phobia and can you explain it in depth? [/INST] Specific phobia is an anxiety disorder, characterized by an extreme, unreasonable, and irrational fear associated with a specific object, situation, or concept which poses little or no actual danger. Specific phobia can lead to avoidance of the object or situation, persistence of the fear, and significant distress or problems functioning associated with the fear. A phobia can be the fear of anything.
Although fears are common and normal, a phobia is an extreme type of fear where great lengths are taken to avoid being exposed to the particular danger. Phobias are considered the most common psychiatric disorder, affecting about 10% of the population in the US, according to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), (among children, 5%; among teens, 16%). About 75% of patients have more than one specific phobia.
It can be described as when patients are anxious about a particular situation. It causes a great load of difficulty in life. Patients have a lot of distress or interference when functioning in their daily life. Unreasonable or irrational fears get in the way of daily routines, work, and relationships due to the effort that a patient makes to avoid the terrifying feelings associated with the fear.Females are twice as likely to be diagnosed than males with a specific phobia (although this can depend on the stimulus).Children and adolescents who are diagnosed with a specific phobia are at an increased risk for additional psychopathology later in life.

Signs and symptoms
Fear, discomfort or anxiety may be triggered both by the presence and the anticipation of the specific object or situation. The main behavioral sign of a specific phobia is avoidance. The fear or anxiety associated with specific phobia can also manifest in physical symptoms such as an increased heart rate, shortness of breath, muscle tension, sweating, or a desire to escape the situation.

Causes
The exact cause of specific phobias is not known. The mechanisms for development of specific phobias can be distinguished between innate (genetic and neurobiological) factors, and learned factors.
In neurobiology, one explanation proposed for specific phobia is that the typical activation of the amygdala in response to stimuli may be exaggerated due to pathological changes. According to this theory, a deficiency in amygdala habituation may also contribute to the persistence of non-experiential phobia. Certain phobias that are less lethal (e.g. dogs) seem to be more frequently observed and easily acquired in comparison to potentially lethal fears which are more relevant to developed human society (e.g. cars and guns). This was theorised to be due to biological adaptation being passed through evolution which makes recent threats less prone to easy acquisition. However, a 2014 study found evidence against this evolutionary theory, which stated: "Our findings are inconsistent with the hypothesis that fears/phobias of individual stimuli result from genetic and environmental factors unique to that stimulus. Instead, we observed substantial sharing of risk factors across individual fears." There is also evidence for the validity of a genetic component contributing to blood-injection-injury phobias and animal phobias, although this evidence did not support the idea that other specific phobias had genetic influence. Blood-injection-injury phobias are also believed to be the most heritable among specific phobias.The classical conditioning model of learning has also been used to suggest that a phobia will be learned when an event that causes a fear or anxiety reaction is paired with a neutral event. An example of this model is when being near a dog (neutral event) is paired with the emotional experience of being bitten by a dog, resulting in a chronic fear which is described as a specific phobia to dogs. An alternative proposed mechanism of association is through observational learning. According to this theory, a person may internalize another persons fears about a specific object or situation through observation of their reactions.

Diagnosis
Diagnosis in the ICD or the DSM requires a marked fear, anxiety or avoidance that is long-lasting (greater than six months) and consistently occurs in the presence of the feared object or situation. The DSM-5 that the fears should be out of proportion to the danger posed, compared to the ICD-10 which specifies that the symptoms must be excessive or unreasonable. Minor differences have persisted between the ICD-11 and DSM-5.In the DSM-5, there are several types which specific phobia can be classified under:

Animal type – Including fear of spiders (arachnophobia), insects (entomophobia), or dogs (cynophobia).
Natural environment type – Including fear of water (aquaphobia), heights (acrophobia), lightning and thunderstorms (astraphobia), or aging (gerascophobia).
Situational type – Including the fear of small confined spaces (claustrophobia), or the dark (nyctophobia).
Blood/injection/injury type – Including fear of medical procedures, including needles and injections (trypanophobia), fear of blood (hemophobia) and fear of getting injured (traumatophobia).
Other – Situations which can lead to choking or vomiting, and childrens fears of loud sounds or costumed characters.Although the avoidance resulting from specific phobia is comparable to other anxiety disorders, differential diagnosis is done through examining underlying causes for the behavior. Agoraphobia is also considered distinct from specific phobia, along with substance use disorders, and avoidant personality disorder. The occurrence of panic attacks is not itself a symptom of specific phobias and falls under the criteria of panic disorder.

Treatment
There are a variety of treatment options available for specific phobias, most of which focus on psychosocial interventions. Different psychological treatments have varying levels of effects depending on the specific phobia being addressed.

Cognitive behavioral therapy (CBT)
Cognitive behavioral therapy is a short term, skills-focused therapy that aims to help people diffuse unhelpful emotional responses by helping people consider them differently or change their behavior. CBT represents the gold standard and first line of therapy in specific phobias. CBT is effective in treating specific phobias primarily through exposure and cognitive strategies to overcome a persons anxiety. Computer-assisted treatment programs, self-help manuals, and delivery by a trained practitioner are all methods of accessing CBT. A single session of CBT in one of these modalities can be effective for individuals who have a specific phobia.

Exposure therapy
Exposure therapy is a particularly effective form of CBT for many specific phobias, however, treatment acceptance and high drop-out rates have been noted as concerns. In addition, a third of people who complete exposure therapy as a treatment for specific phobia may not respond, regardless of the type of exposure therapy. Other interventions have been successful for particular types of specific phobia, such as virtual reality exposure therapy (VRET) for spider, dental, and height phobias, applied muscle tension (AMT) for needle phobia, and psychoeducation with relaxation exercises for fear of childbirth. With exposure therapy, a type of cognitive-behavioural therapy, clinically significant improvement was experienced by up to 90% of patients. While very long-term outcomes remain unknown, many of the benefits of exposure therapy persisted after one year. Treatment may be more successful at reducing symptoms in people with low trait anxiety, high motivation, and high self-efficacy entering exposure therapy. In addition, high cortisol levels, high heart rate variation, evoking disgust, avoiding relaxation, focusing on cognitive changes, context variation, sleep, and memory-enhancing drugs can also reduce symptoms following exposure therapy.Exposure can be "live"(in real life) or imaginal (in ones imagination) and can involve:

Systematic desensitization—A therapy that exposes the person to increasing levels of vivid stimuli gradually and frequently, while instructed to relax.
Flooding—A therapy that exposes the person with a specific phobia to the most fearful stimulus first (i.e. the most intense part of the phobia). Patients are at great risk for dropping out of treatment as this method repeatedly exposes the patient to the fear.
Modeling—This method includes the clinician approaching the feared stimuli while the patient observes and tries to repeat the approach themselves.Exposures that are imaginal are less effective.Specifically for acrophobia, in-vivo exposure (exposure to real-world height-scenarios while maintaining anxiety at controlled levels) has been shown to significantly improve measures of anxiety in the short-term, but this effect decreased over a longer term. Likewise, virtual reality exposure was statistically significant in some measures of anxiety reduction, but not others.

Pharmacotherapeutics
As of late 2020, there is limited evidence for the use of pharmacotherapy in the treatment of specific phobia. Pharmacological treatments are typically used in combination with behaviorally-focused psychotherapy, as introducing pharmacological interventions independently may result in relapsing of symptoms. Different treatments are better suited for certain types of specific phobia. For instance, beta blockers are useful in those with performance anxiety.  The selective serotonin re-uptake inhibitors (SSRIs), paroxetine and escitalopram, have shown preliminary efficacy in small randomized controlled clinical trials. However, these trials were too small to show any definitive benefits of anxiolytic medication alone in treating phobia. Benzodiazepines are occasionally used for acute symptom relief, but have not been shown to be effective for long-term treatment. There are some findings suggesting that adjuvant use of the NMDA receptor partial agonist, d-cycloserine, with virtual reality exposure therapy may improve specific phobia symptoms more than virtual reality exposure therapy alone. As of 2020, studies on the use of adjunct d-cycloserine are inconclusive.

Prognosis
The majority of those that develop a specific phobia first experience symptoms in childhood. Often individuals will experience symptoms periodically with periods of remission before complete remission occurs. However, specific phobias that continue into adulthood are likely to experience a more chronic course. Specific phobias in older adults has been linked with a decrease in quality of life. Those with specific phobias are at an increased risk of suicide. Greater impairment is found in those that have multiple phobias </s>


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<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Blue baby syndrome and can you explain it in depth? [/INST] Blue baby syndrome can refer to conditions that cause cyanosis, or blueness of the skin, in babies as a result of low oxygen levels in the blood. This term has traditionally been applied to cyanosis as a result of:
Cyanotic heart disease, which is a category of congenital heart defect that results in low levels of oxygen in the blood. This can be caused by either reduced blood flow to the lungs or mixing of oxygenated and deoxygenated blood.
Methemoglobinemia, which is a disease defined by high levels of methemoglobin in the blood. Increased levels of methemoglobin prevent oxygen from being released into the tissues and result in hypoxemia.Although these are the most common causes of cyanosis, there are other potential factors that can cause a blue tint to a babys skin or mucous membranes. These factors include hypoventilation, perfusion or ventilation differences in the lungs, and poor cardiac output of oxygenated blood, among others. The blue baby syndrome or cyanosis occurs when absolute amount of deoxygenated hemoglobin >3g/dL which is typically reflected with an O2 saturation of <85%.Both of these conditions cause cyanosis, or a bluish discoloration of skin or mucous membranes. Normally, oxygenated blood appears red and deoxygenated blood has more of a blue appearance. In babies with low levels of oxygen or mixing of oxygenated and deoxygenated blood, the blood can have a blue or purple color, causing cyanosis.

Signs and symptoms
The main sign of blue baby syndrome is cyanosis. Depending on the underlying cause of the cyanosis, additional symptoms may be:
Rapid heartbeat
Rapid respiratory rate
Failure to thrive
Shortness of breath
Nasal flaring
Lethargy
Seizures

Causes
Blue baby syndrome has been attributed to cyanotic congenital heart diseases and methemoglobinemia, however there are additional causes that could result in a baby becoming cyanotic, such as:
Decreased blood perfusion
Pulmonary/lung disorders (ex: Pulmonary hypertension, cystic fibrosis)
Disordered control of breathing (ex: Cyanotic breath-holding spells, seizures)
Airway obstruction
Respiratory distress syndrome

Mechanism
Cyanotic heart disease
Specific types of congenital heart defects that cause blood to pass directly from the right side of the heart to the left side result in cyanosis. In these defects, some of the blood that is pumped to the body has not been oxygenated by the lungs and therefore will appear more blue. Infants with these types of heart defects may have a constant bluish tint to their skin, or they may have temporary episodes of cyanosis. The degree of cyanosis is dependent on how much deoxygenated blood is mixed with oxygenated blood before being pumped to the body.
Cardiac conditions in which there is decreased blood flow to the lungs such as, tetralogy of Fallot or pulmonary valve atresia, result in less blood becoming oxygenated. There are also cardiac conditions such as transposition of the great arteries or truncus arteriosus, that results in an overall increase in blood flow to the lungs but with limited flow of the oxygenated blood to the rest of the body. Conditions in which there is poor blood flow to the systemic circulation, such as coarctation of the aorta suggests that the body does not receive the oxygenated blood it requires with resultant cyanosis.The five most common cyanotic heart defects that may result in Blue Baby Syndrome include the following:

Methemoglobinemia
Methemoglobinemia which can be acquired or congenital, occurs when the iron in hemoglobin is oxidized from Fe2+ to Fe3+, leading to poor binding of oxygen. Additionally, the oxygen that is already bound is held more tightly to the hemoglobin due to a higher affinity, resulting in less oxygen delivery. A methemoglobin level >1.5g/dL causes cyanosis. The most common congenital cause is a deficiency in the enzyme cytochrome b5 reductase which reduces methemoglobin in the blood. However, in infants the most common cause of methemoglobinemia is acquired through the ingestion of nitrates through well water or foods. Infants younger than 4 months are at greater risk given that they drink more water per body weight, they have a lower NADH- cytochrome b5 reductase activity, and they have a higher level of fetal hemoglobin which converts more easily to methemoglobin. Additionally, infants are at an increased risk after an episode of gastroenteritis due to the production of nitrites by bacteria. The sources of nitrate can include fertilizers used in agricultural lands, waste dumps or pit latrines. For example, nitrate levels are subject to monitoring to comply with drinking water quality standards in the United States and other countries. The link between blue baby syndrome and nitrates in drinking water is widely accepted, but some studies indicate that other contaminants, or dietary nitrate sources, may also play a role in the syndrome.

Diagnosis
When diagnosing blue baby syndrome, it is important to perform a thorough history and physical exam. When obtaining the history, it is important to determine the timing of symptoms and to ask about risk factors/exposures, such as prenatal history or access to well-water.

On physical exam it is important to visualize where the cyanosis is present to differentiate between peripheral and central cyanosis. Central cyanosis is typically visible as a blueish discoloration over the entire body and mucous membranes. In contrast, peripheral cyanosis typically has a blueish discoloration over the extremities. Cyanosis can be noted in babies around the lips, tongue, and sublingual area, where the skin is thinnest. In addition, it is important to observe the infant for signs of respiratory distress, visualized as nasal flaring, subcostal retractions, etc. Examination should include a respiratory and cardiac assessment.One of the key tools in diagnosing is a pulse oximeter to determine oxygen saturation. While severe cyanosis can be easily noticed, an oxygen saturation as low as 80% causes only mild clinical cyanosis that is difficult to see. Additionally an arterial blood gas is useful, for example in the case of methemoglobinemia the PO2 can be expected to be normal even with a low oxygen saturation. Additional work up includes a complete blood count, blood glucose, blood culture, chest x-ray, and an echocardiography.Babies with cyanosis due to congenital heart disease usually present with symptoms hours to days after birth. In addition to cyanosis, they often show signs of tachypnea (fast breathing), a heart murmur, and decreased peripheral pulses. If congenital heart disease is suspected in a newborn, doctors will likely perform several tests to evaluate the heart, including a chest x-ray, echocardiogram, and electrocardiogram. In tetralogy of Fallot, episodes in which infants become cyanotic are called tet spells, typically occurring during feeding or crying. When older, children may squat to feel relief since this increases the systemic vascular resistance causing more blood to go towards the lungs, resulting in increased oxygenation.Babies with cyanosis due to methemoglobinemia also usually present with cyanosis in the neonatal period, but pulse oximetry may be falsely elevated and does not always reveal low blood oxygen saturation. . A co-oximeter can be used to detect levels of methemoglobin in the blood if methemoglobinemia is suspected, by seeing the difference between oxygen saturation on an arterial blood gas and the measurement on a co-oximeter. Additionally, a direct methemoglobin level can be obtained.

Prevention/Screening
The United States Environmental Protection Agency has established a maximum contaminant level of 10 mg/L for nitrate and 1 mg/L for nitrite due to the potential harmful effects in infants.A screening tool has been developed to screen for critical cardiac defects, which refers to cardiac lesions that require surgery or intervention in the 1st year of life. Screening for critical congenital heart defect should be done on all newborns after 24hours or shortly before discharge. Oxygen saturation is measured in the right hand and either foot.A screening is considered positive if:

Oxygen saturation <90% in either extremity,
Oxygen saturation 90-94% in both extremities on 3 measurements separated by an hour each,
Oxygen saturation difference >3% between both extremities on 3 measurements separated by an hour each.

Management
Treatment for blue baby syndrome will depend on the underlying cause.
When evaluating a patient for cyanosis or respiratory distress, vital signs should be monitored, especially the patients heart rate and oxygen saturation. It is beneficial to have vascular access established. In newborns, the pulse oximeter is typically placed on the right hand to determine pre-ductal oxygenation, referring to oxygenation before the ductus arteriosus (connection between aorta and pulmonary artery). This gives the oxygenation level the heart and brain receive. Traditionally, supplemental oxygen is given in an escalating manner beginning with free-flowing oxygen, progressing to positive pressure ventilation or continuous positive airway pressure, and ending with mechanical intubation. The goal oxygen saturation is between 85 and 95%. If an infant requires supplemental oxygen for a prolonged time it should be heated and humidified to avoid heat loss.

Cyanotic heart disease
Some babies born with cyanotic heart disease are treated with prostaglandin E1 after birth to keep the ductus arteriosus open and allow for more oxygenated blood to be pumped to the body. Many also receive oxygen therapy to increase the percentage of oxygen in the blood. Most of these babies will require surgery during infancy to correct their structural heart defect.

Severe methemoglobinemia
The first-line treatment for severe methemoglobinemia is methylene blue, a medication that will reduce methemoglobin in the blood. This is possible because methylene blue oxidizes NADPH, which in turn can convert methemoglobin back to hemoglobin.

Epidemiology
Out of all the babies born with congenital heart defects, about 25% have cyanosis as a result. Tetralogy of Fallot is the most common cyanotic cardiac heart defect.Methemoglobinemia is considered to be rare, with acquired methemoglobinemia encountered more than the congenital form.

Outcomes
In the case of cyanotic causing heart defects, about 75% of infants survive to 1 year of age and 69% survive to 18 years of age </s>


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